Panel of 6 docs replaces tainted MCI
'
MCI DISSOLVED
Panel of 6 docs replaces tainted MCI
Tainted with charges of corruption, the 76-year-old Medical Council of India was on Saturday dissolved and replaced by a six-member panel of eminent doctors to carry out its duties.
An ordinance dissolving the all-powerful body, formed to regulate medical education in the country, was signed by President Pratibha Patil and notified by the law ministry.
The Union Cabinet had discussed the ordinance on Thursday following which it had gone to the law ministry for consultations.
The six-member panel is headed by eminent gastroenterologist from Delhi Dr S K Sarin. The other five members are: former director of National Institute of Immunology Prof Ranjit Roy Chowdhary, Dr Sita Naik from SGPGIMS, Dr Gautam Sen, cardiac surgeon, Dr Devi Shetty and former head of Safdarjung hospital Dr R L Salhan.
Union health secretary K Sujatha Rao told TOI, "This committee will not have an advisory role but will actively run the MCI including issuing licences and permissions, conducting inspections and regulating medical education, for a maximum of one year. It will also suggest ways to reform MCI which will help in preparing the bill which we plan to introduce in the monsoon session of Parliament."
MCI till now was the sole body that granted recognition to medical degrees, gave accreditation to medical colleges, registered medical practitioners and monitored medical practice in the country.
However, allegations of corruption against the MCI have been rife for years now. On April 22, MCI's president Dr Ketan Desai was arrested by the CBI for allegedly taking a bribe of Rs 2 crore to recognize a medical college in Punjab though it did not meet MCI standards. The ministry said it plans to bring in a new law for the formation of an overarching body to regulate medical education in the country.
According to Rao, the draft law for the formation of such a body would be formulated within a month. Sources say MCI would be made a body to regulate medical professionals, which would be in line with the original mandate of the MCI.
An earlier effort by the ministry to amend the Indian Medical Council Act of 1956, giving more powers to the ministry, was turned down by the parliamentary standing committee on health, which argued that the move would destroy the council's autonomy. Health minister Ghulam Nabi Azad said the ordinance "was required as there is no law that empowers us to take action against MCI as it was created by an act of Parliament."
Saturday, May 15, 2010
Sunday, May 2, 2010
teriparatite- forteo
Teriparatide (trade name Forteo) is a medication to treat osteoporosis that works in a different way than other drugs for osteoporosis. It is the first drug to cause new bone to be formed. Teriparatide has been FDA approved to treat osteoporosis in postmenopausal women and in men with hypogonadal or idiopathic osteoporosis who are at high risk for fracture.
Osteoporosis-related fractures are a serious problem for older people. It is often a hip fracture that leads to decline in the health of the elderly. A third of all hip fractures occur in men, and almost 38% of those men will die in the following year. Osteoporosis in men is underdiagnosed. Generally defined as the thinning of bone tissue and decrease in density, osteoporosis is the most common type of bone disease.
The existing treatments for osteoporosis are medications that prevent bone resorption. Bisphosphonates alendronate (Fosamax) and risedronate (Actonel) are oral medications. Other treatments include salmon calcitonin (Miacalsin) which is available as a nasal spray or injection. Raloxifene (Evista) is a selective estrogen receptor modulator. By preventing bone resorption, these medications are used to prevent bone loss.
Teriparatide is a synthetic form of the naturally occuring parathyroid hormone. Unlike other osteoporosis drugs, it actually causes bone density to increase. In the body, parathyroid hormone is released by the parathyroid glands in the neck (behine the thyroid glands) and is an important regulator in the bloodstream's levels of calcium and phosphorus. Laboratory tests can determine the level of this hormone in the blood.
The most important endpoint for treatment with any of these drugs is prevention of fractures, especially hip and vertebral fractures.
Bone metabolism is a complex process. Bone remodels throughout a person’s life, so that there is new bone being made along with bone resorption. Among the substances that affect bone metabolism are vitamin D, calcium, estrogen, testosterone, and parathyroid hormone which regulates the calcium and bone formation in the body. Other external factors influence bone metabolism and increase the risk of osteoporosis, including prolonged use of corticosteroids, alcoholism, smoking, and in men, hypogonadism.
Early trials of teriparatide leading to its FDA approval were completed separately for men and women. Evaluation of drugs for osteoporosis are complicated by the difficulty of knowing how severe the bone loss is, and also because treatment is needed not just to prevent thinning bone but to definitively protect against fracture.
One randomized trial of postmenopausal women who had already fractured vertebra compared teriparatide at either 20 or 40 micrograms per day with placebo. After about 19 months, 14% of the women taking placebo had new vertebral fractures, as compared with 5% of the women taking 20 micrograms of teriparatide and 4% of the women taking 40 micrograms. There were also a statistically significant lower number of non-vertebral fractures in the teriparatide treated group. 20 micrograms of teriparatide increased spine and hip bone mineral density. However, this study had to be terminated because 1.6% of the women taking 40 micrograms of teriparatide and 0.2% of those taking 20 micrograms developed significant increases in serum calcium, the amount of calcium in the blood, which can be dangerous.
Another trial compared 40 micrograms of teriparatide to alendronate. After about 14 months later, bone density increased more in the spine and femoral neck (part of the hip) in the patients treated with teriparatide. Bone density in the wrist decreased with teriparatide. Fewer patients treated with teriparatide suffered nonvertebral fractures.
A randomized trial using teriparatide to treat men with osteoporosis (half of whom had low testosterone levels) showed that teriparatide doses of both 20 micrograms and 40 micrograms increased bone density in the lumbar spine and the femoral neck. In this study bone density in the wrist decreased.
Side Effects of Teriparatide
Generally, teriparatide is well tolerated.
The most common side effects, among others, are dizziness, nausea, heartburn, diarrhea, headache and leg cramps, pain, weakness, and depression. Lowered blood pressure (hypotension) when standing can occur with the first few doses but does go away in a matter of hours. Patients may be told to lie down after the injection. There have been some cases of slightly elevated serum calcium, and elevated calcium in the urine (which can lead to kidney stones). Ooccasionally transient hypercalcemia occurs 4 to 6 hours after injection, reducing blood serum calcium concentrations.
If any of these side effects persist or worsen, the prescribing doctor should be informed. More serious reactions have included chest pain, fainting, difficulty breathing, more severe nausea, vomiting, constipation, and muscle weakness. Allergic reactions can occur, from itching at the injection site to more serious symptoms of allergy including swelling, and difficulty breathing. Serious side effects warrant immediate medical attention.
When teriparatide was given to growing young rats, they developed osteogenic sarcoma, a very malignant tumor. The drug should not be given to anyone at risk for developing this bony cancer. That would include patients with Paget’s disease, those with elevated alkaline phosphatase (which could indicate a problem in bone), patients who had radiation therapy to their bones, or children and young adults whose bones are still growing.
At this time, the recommended length of treatment is two years. There are many ongoing clinical trials to determine the best way to use teriparatide, with other medicines like alendronate, how long treatment should last, and which patients with osteoporosis will benefit the most from it. There have been attempts to deliver the medication as a nasal spray instead of injection. It is also being tested for other conditions. One, called osteogenesis imperfecta is a genetic bone disease causing brittle bones. Teriparatide is being tried as a treatment for adults with osteogenesis imperfecta. It is also being tested as an aid to fracture healing. There are some 50 trials in various stages at this time, and new uses for teriparatide will probably be found.
The approved dose (20Fg daily by subcutaneous injection) and duration of treatment have not been found to be associated with an increased
Osteoporosis-related fractures are a serious problem for older people. It is often a hip fracture that leads to decline in the health of the elderly. A third of all hip fractures occur in men, and almost 38% of those men will die in the following year. Osteoporosis in men is underdiagnosed. Generally defined as the thinning of bone tissue and decrease in density, osteoporosis is the most common type of bone disease.
The existing treatments for osteoporosis are medications that prevent bone resorption. Bisphosphonates alendronate (Fosamax) and risedronate (Actonel) are oral medications. Other treatments include salmon calcitonin (Miacalsin) which is available as a nasal spray or injection. Raloxifene (Evista) is a selective estrogen receptor modulator. By preventing bone resorption, these medications are used to prevent bone loss.
Teriparatide is a synthetic form of the naturally occuring parathyroid hormone. Unlike other osteoporosis drugs, it actually causes bone density to increase. In the body, parathyroid hormone is released by the parathyroid glands in the neck (behine the thyroid glands) and is an important regulator in the bloodstream's levels of calcium and phosphorus. Laboratory tests can determine the level of this hormone in the blood.
The most important endpoint for treatment with any of these drugs is prevention of fractures, especially hip and vertebral fractures.
Bone metabolism is a complex process. Bone remodels throughout a person’s life, so that there is new bone being made along with bone resorption. Among the substances that affect bone metabolism are vitamin D, calcium, estrogen, testosterone, and parathyroid hormone which regulates the calcium and bone formation in the body. Other external factors influence bone metabolism and increase the risk of osteoporosis, including prolonged use of corticosteroids, alcoholism, smoking, and in men, hypogonadism.
Early trials of teriparatide leading to its FDA approval were completed separately for men and women. Evaluation of drugs for osteoporosis are complicated by the difficulty of knowing how severe the bone loss is, and also because treatment is needed not just to prevent thinning bone but to definitively protect against fracture.
One randomized trial of postmenopausal women who had already fractured vertebra compared teriparatide at either 20 or 40 micrograms per day with placebo. After about 19 months, 14% of the women taking placebo had new vertebral fractures, as compared with 5% of the women taking 20 micrograms of teriparatide and 4% of the women taking 40 micrograms. There were also a statistically significant lower number of non-vertebral fractures in the teriparatide treated group. 20 micrograms of teriparatide increased spine and hip bone mineral density. However, this study had to be terminated because 1.6% of the women taking 40 micrograms of teriparatide and 0.2% of those taking 20 micrograms developed significant increases in serum calcium, the amount of calcium in the blood, which can be dangerous.
Another trial compared 40 micrograms of teriparatide to alendronate. After about 14 months later, bone density increased more in the spine and femoral neck (part of the hip) in the patients treated with teriparatide. Bone density in the wrist decreased with teriparatide. Fewer patients treated with teriparatide suffered nonvertebral fractures.
A randomized trial using teriparatide to treat men with osteoporosis (half of whom had low testosterone levels) showed that teriparatide doses of both 20 micrograms and 40 micrograms increased bone density in the lumbar spine and the femoral neck. In this study bone density in the wrist decreased.
Side Effects of Teriparatide
Generally, teriparatide is well tolerated.
The most common side effects, among others, are dizziness, nausea, heartburn, diarrhea, headache and leg cramps, pain, weakness, and depression. Lowered blood pressure (hypotension) when standing can occur with the first few doses but does go away in a matter of hours. Patients may be told to lie down after the injection. There have been some cases of slightly elevated serum calcium, and elevated calcium in the urine (which can lead to kidney stones). Ooccasionally transient hypercalcemia occurs 4 to 6 hours after injection, reducing blood serum calcium concentrations.
If any of these side effects persist or worsen, the prescribing doctor should be informed. More serious reactions have included chest pain, fainting, difficulty breathing, more severe nausea, vomiting, constipation, and muscle weakness. Allergic reactions can occur, from itching at the injection site to more serious symptoms of allergy including swelling, and difficulty breathing. Serious side effects warrant immediate medical attention.
When teriparatide was given to growing young rats, they developed osteogenic sarcoma, a very malignant tumor. The drug should not be given to anyone at risk for developing this bony cancer. That would include patients with Paget’s disease, those with elevated alkaline phosphatase (which could indicate a problem in bone), patients who had radiation therapy to their bones, or children and young adults whose bones are still growing.
At this time, the recommended length of treatment is two years. There are many ongoing clinical trials to determine the best way to use teriparatide, with other medicines like alendronate, how long treatment should last, and which patients with osteoporosis will benefit the most from it. There have been attempts to deliver the medication as a nasal spray instead of injection. It is also being tested for other conditions. One, called osteogenesis imperfecta is a genetic bone disease causing brittle bones. Teriparatide is being tried as a treatment for adults with osteogenesis imperfecta. It is also being tested as an aid to fracture healing. There are some 50 trials in various stages at this time, and new uses for teriparatide will probably be found.
The approved dose (20Fg daily by subcutaneous injection) and duration of treatment have not been found to be associated with an increased
Massive Blood transfusion
Massive Transfusion is usually defined as the need to transfuse from one to two times the patient's normal blood volume. In a "normal" adult, this is the equivalent of 10-20 units. Potential complications from this include coagulopathy, citrate toxicity, hypothermia, acid-base disturbances and changes in serum potassium concentration.
________________________________________
Coagulopathy is common with massive transfusion. The most common cause of bleeding following a large volume transfusion is dilutional thrombocytopenia. This should be suspected and treated first before moving on to factor deficiencies as the cause of coagulopathy.
Citrate toxicity results when the citrate in the transfused blood begins to bind calcium in the patient's body. Clinically significant hypocalcemia does not usually occur unless the rate of transfusion exceeds one unit every five minutes or so. Citrate metabolism is primarily hepatic - so hepatic disease or dysfunction can cause this effect to be more pronounced. Treatment is with intravenous calcium administration - but identification of the problem requires a high index of suspicion.
Hypothermia should not occur on a regular basis. Massive transfusion is an absolute indication for the warming of all blood and fluid to body temperature as it is being given.
Acid-Base balance can be seen after massive transfusion. The most common abnormality is a metabolic alkalosis. Patients may initially be acidotic because the blood load itself is acidic and there may be a prevailing lactic acidosis from hypoperfusion. However, once normal perfusion is restored, any metabolic acidosis resolves and the citrate and lactate are then converted to bicarbonate in the liver.
Serum potassium can rise as blood is given. The potassium concentration in stored blood increases steadily with time. The amount of potassium is typically less than 4 milliequivalents per unit - so you can see that large amounts of blood at a high rate of delivery is required to raise serum levels of potassium.
________________________________________
Infectious Agents can be passed along with blood transfusion as well.
o Hepatitis
o AIDS
o Other viral agents (CMV, EBV, HTLV)
o Parasites and bacteria
Hepatitis has been an ongoing problem. Until recently, the incidence of hepatitis following transfusion was as high as 10% with the overwhelming majority of these infections caused by hepatitis C. Now that this virus is identified and tested for, the risk is decreased. Currently the risk from transfusion is estimated to be in the range of 1:1,000,000 for hepatitis A, 1:30,000 - 250,000 for hepatitis B and 1:30,000 - 150,000 for hepatitis C.
AIDS is a feared disease but the actual risk is quite low. All blood is tested for the anti-HIV-1 antibody which is a marker for infectivity. Unfortunately, there is a 6-8 week period required for a person to develop the antibody after they are infected with HIV and therefore infectious units can go undetected. The current risk for HIV infection due to transfusion is estimated to be 1:200,000 to 2,000,000.
CMV and EBV are usually the cause of only asymptomatic infection or mild systemic illness. Unfortunately, some of these people become asymptomatic carriers of the viruses and the white blood cells in blood units are capable of transmitting either virus. Immunocompromised and immunosuppressed patients are particularly susceptible to CMV and should receive CMV negative units only.
Human T cell Lymphocytic Viruses (HTLV-1 responsible for tropical spastic paresis and HTLV-II) are leukemia and lymphoma retro-viruses that have been reported to be transmitted via transfusion. Screening is done for these, but again those in the window before antibodies are made can be missed. Current risk is estimated at 1:250,000 - 2,000,000.
Parvovirus B19 has been reported to be transmitted by factor concentrates and occurs in approximately 1:10,000 transfusions. It is associated with aplastic anemia and liver failure, especially inimmunologically compromised children.
Parasitic diseases reported to be transmitted via blood transfusion include malaria, toxoplasmosis, and Chagas' disease. Fortunately, such cases are rare and the prevalence of these diseases is very low in the United States. Therefore, these are of very little concern in this country.
Both gram-positive and gram-negative bacteria can rarely contaminate blood transfusions. To avoid the possibility of significant bacterial contamination, blood should be administered over a period of shorter than four hours.
________________________________________
Coagulopathy is common with massive transfusion. The most common cause of bleeding following a large volume transfusion is dilutional thrombocytopenia. This should be suspected and treated first before moving on to factor deficiencies as the cause of coagulopathy.
Citrate toxicity results when the citrate in the transfused blood begins to bind calcium in the patient's body. Clinically significant hypocalcemia does not usually occur unless the rate of transfusion exceeds one unit every five minutes or so. Citrate metabolism is primarily hepatic - so hepatic disease or dysfunction can cause this effect to be more pronounced. Treatment is with intravenous calcium administration - but identification of the problem requires a high index of suspicion.
Hypothermia should not occur on a regular basis. Massive transfusion is an absolute indication for the warming of all blood and fluid to body temperature as it is being given.
Acid-Base balance can be seen after massive transfusion. The most common abnormality is a metabolic alkalosis. Patients may initially be acidotic because the blood load itself is acidic and there may be a prevailing lactic acidosis from hypoperfusion. However, once normal perfusion is restored, any metabolic acidosis resolves and the citrate and lactate are then converted to bicarbonate in the liver.
Serum potassium can rise as blood is given. The potassium concentration in stored blood increases steadily with time. The amount of potassium is typically less than 4 milliequivalents per unit - so you can see that large amounts of blood at a high rate of delivery is required to raise serum levels of potassium.
________________________________________
Infectious Agents can be passed along with blood transfusion as well.
o Hepatitis
o AIDS
o Other viral agents (CMV, EBV, HTLV)
o Parasites and bacteria
Hepatitis has been an ongoing problem. Until recently, the incidence of hepatitis following transfusion was as high as 10% with the overwhelming majority of these infections caused by hepatitis C. Now that this virus is identified and tested for, the risk is decreased. Currently the risk from transfusion is estimated to be in the range of 1:1,000,000 for hepatitis A, 1:30,000 - 250,000 for hepatitis B and 1:30,000 - 150,000 for hepatitis C.
AIDS is a feared disease but the actual risk is quite low. All blood is tested for the anti-HIV-1 antibody which is a marker for infectivity. Unfortunately, there is a 6-8 week period required for a person to develop the antibody after they are infected with HIV and therefore infectious units can go undetected. The current risk for HIV infection due to transfusion is estimated to be 1:200,000 to 2,000,000.
CMV and EBV are usually the cause of only asymptomatic infection or mild systemic illness. Unfortunately, some of these people become asymptomatic carriers of the viruses and the white blood cells in blood units are capable of transmitting either virus. Immunocompromised and immunosuppressed patients are particularly susceptible to CMV and should receive CMV negative units only.
Human T cell Lymphocytic Viruses (HTLV-1 responsible for tropical spastic paresis and HTLV-II) are leukemia and lymphoma retro-viruses that have been reported to be transmitted via transfusion. Screening is done for these, but again those in the window before antibodies are made can be missed. Current risk is estimated at 1:250,000 - 2,000,000.
Parvovirus B19 has been reported to be transmitted by factor concentrates and occurs in approximately 1:10,000 transfusions. It is associated with aplastic anemia and liver failure, especially inimmunologically compromised children.
Parasitic diseases reported to be transmitted via blood transfusion include malaria, toxoplasmosis, and Chagas' disease. Fortunately, such cases are rare and the prevalence of these diseases is very low in the United States. Therefore, these are of very little concern in this country.
Both gram-positive and gram-negative bacteria can rarely contaminate blood transfusions. To avoid the possibility of significant bacterial contamination, blood should be administered over a period of shorter than four hours.
Sunday, April 25, 2010
LAST 10 YEARS DNB QUESTIONS
DNB Orthopaedics Theory December 2009
Paper 1
1. Post-operative pain management. Describe patient control analgesia.
2. Clinical features and management of stove in chest.
3. Indications of Limb salvage surgery in malignant bone tumors. Describe the techniques of limb salvage in osteosarcoma.
4. Uses of botulinum neurotoxin in Orthopaedic surgery.
5. Define pigmented villonodular synovitis. Describe pathology, clinical features, diagnosis & its treatment.
6. Give a functional classification of muscles around the shoulder. Enumerate the indications for shoulder arthrodesis. What are the pre-requisites for a good result? Describe any one technique of shoulder arthrodesis.
7. Describe pathophysiology of nerve compression (entrapment) syndromes. Enumerate various syndromes of nerve entrapment. Give an outline of the management of Tarsal Tunnel Syndrome.
8. What is traumatic arthrotomy of the knee joint? What is fluid challenge test to confirm the diagnosis in doubtful cases? Outline the principles of management.
9. What are the various causes of late onset paraplegia in tuberculosis of spine? Describe the investigative modalities and outline the principles of management.
10. Describe the management of unicompartmental osteoarthrosis knee.
Paper 2
1. Management of septic arthritis in children,
2. Pathophysiology, types and clinical features of Osteogenesis Imperfecta
3. Prognostic factors and outcome in the treatment of Perthe’s disease
4. Describe Madelung deformity, classification, clinical features and management of Perthe’s disease
5. Classify congenital dislocation of knee. Comment on differential diagnosis and management
6. Draw a diagram of Floor Reaction Orthosis, What is a good indication for its use. Describe mechanism of action
7. Orthopaedic manifestation of neurofibromatosis
8. Describe muscular dynamics in calcaneovalgus deformity. Describe management in patients before and after attaining skeletal maturity
9. Classification of neurogenic bladder and management
10. What are closed chain and open chain exercises and discuss ACL rehabilitation protocol
Paper 3
1. Classification, management and complication of fractures of the femoral head and neck in children
2. What are Monteggia equivalents, discuss the principles of management of Monteggia fracture dislocation in children
3. Principles of management of a pulseless hand after supracondylar fractures in children
4. Role of ultrasound in fracture healing
5. Subacromial impingement syndrome
6. Describe indications for amputation, Principles of lower limb amputation in children
7. What is Mangled Extremity severity score(MESS), describe principles of flap coverage in proximal one third of tibia
8. Classify ankle fractures, which pattern has syndesmotic instability, what is their management?
9. What are biodegradable implants, what is their chemical composition? Mention the indications of their use, advantage and disadvantage of their use
10. What is central cord syndrome, describe its clinical presentation. How will you manage such a case?
Paper 4
1. Osteochondral allograft transplantation. Mention indications for the procedure
2. Role of Pamidronate in bone metastasis
3. What do you understand by patellar instability, describe the principles of management, before and after skeletal maturity?
4. Enumerate modalities leading to biological enhancement of fracture healing. Mention the methods of preservation of allogenic bone grafts. Comment on mode of action, advantages and disadvantages
5. Describe the pathogenesis of hallux valgus deformity; describe the role of metatarsus primary varus in the pathogenesis. How will you manage an adolescent girl with severe hallux valgus?
6. Describe various types of rickets; describe biochemical changes and clinical presentation of various types of rickets!
7. Define osteoporosis. Comment on types, causes and management
8. What is highly cross linked polyethylene? How is it manufactured? How has it affected modern total hip arthroplasty?
9. Anatomy of Lisfranc joint, and management of injuries around the joint
10. Describe gate control theory of pain. What is transcutaneous nerve stimulation and its indications?
JUNE 2009
Paper – I
1) Briefly describe the stages of fracture healing. Discuss physical or chemical modalities to enhance fracture healing.
2) Discuss prophylaxis against secondary complications of patient with polytrauma.
3) Ganz antishock pelvic fixator.
4) Describe musculoskeletal manifestations of HIV infected patients.
5) Describe pathogenesis of medial compartment osteoarthrosis. Discuss pros & cons of HTO vs unicondylar replacement.
6) Femoroacetabular impingement syndrome.
7) Osteofibrous Dysplasia
8) Enumerate indications & various techniques for shoulder arthrodesis. What are the prerequisites for a good result?
9) What is malalignment test? Discuss principles of focal dome osteotomy.
10) Gene therapy in Orthopedics.
Paper II
1) Enumerate the causes of intoeing gait. How will you treat intoeing gait because of hip disorders.
2) What is congenital coxa vara? Describe its pathophysiology and outline principles of management.
3) Ober’s test.
4) Briefly discuss the clinical features and pathology of Ewing’s Sarcoma. Outline the principles of treatment in a case of Ewing’s Sarcoma of upper end of humerus.
5) How will you evaluate a child with genu valgum deformity? Outline the principles of management. What is timed epiphysiodesis?
6) Thermoplastic splints
7) Classify nerve injuries. What is the role of electrodiagnosis in differentiating various nerve lesions?
8) Discuss the principles of rehabilitation of a paraplegic patient.
9) Briefly describe the principles & steps of Ponsetti’s method of CTEV correction.
10) Enumerate various causes of claw hand. What is the pathogenesis of clawing? Discuss the principles of surgical correction.
Paper – III
1) Classify fractures of calcaneum. Outline the principles of management.
2) Elaborate the principles of LCP. What are the applications in periarticular fractures?
3) Classify epiphyseal injuries. Describe the complications. What is Langenskiold’s procedure?
4) Current concepts in the management of fracture neck & head of radius in children and adults.
5) Classify flexor tendon injuries of the hand. Describe the treatment of neglected ruptures of flexor tendons in Zone II.
6) Outline the principles of management in a case of infected non union of a long bone. How will you treat infected non union of tibia?
7) Classify fractures of the acetabulum. Discuss radiographic evaluation of acetabular trauma.
8) How will you manage a case of knee dislocation with absent distal pulsations?
9) Describe instability patterns after wrist trauma. Discuss the management of VISI (Volar Intercalated Segment Instability)
10) How will you differentiate between the cerebral sign as a result of head injury vs fat embolism syndrome? Describe in brief management of fat embolism syndrome.
Paper – IV
1) Autologous Transfusion.
2) Describe the anatomy of Distal Radio Ulnar Joint. Describe indications & technique of performing Kapandji’s procedure.
3) Sexual Dimorphism in orthopedic practice.
4) Brown Tumor.
5) Surgical Dislocation of Hip.
6) Describe anatomical classification of chronic osteomyelitis. Discuss the principles of management based on this classification. How will you fill the dead space after excision of infected tissue?
7) Describe the presentation of tourniquet palsy and its causes. What precautions are taken to prevent it?
8) Describe the anatomy of PCL. Discuss its significance in Total Knee Arthroplasty.
9) Describe the basic principle of PET scan and discuss its role in orthopedics.
10) What is pelvic support osteotomy? Outline its principles and operative technique.
Dec. 2008
Paper – I
1. Discuss Anatomy of rotator cuff. What is rotator cuff disease?
Discuss its pathogenesis and management.
2. Define and classify Rickets. Describe pathogenesis, clinical
features and management of hypophosphatemic rickets.
3. What are Biochemical markers for bone formation and bone
resorption. Discuss their role in management of osteoporosis.
4. Discuss causes of loosening after a total hip replacement.
Discuss its clinical features, diagnosis and management.
5. Discuss various methods available for treatment of Giant cell
tumor of proximal tibia in a 30 yr. old man.
6. What is claudication? Classify it and discuss its cause specific
management.
7. Discuss the etiology, Pathology , diagnosis, and management of
Gas Gangrene of the Lower Extremity.
8. Discuss approach to find out a primary tumor in a 65 yr. old
man presenting with vertebral metastasis and low backache.
9. Discuss differential diagnosis in a 25 yr. old male presenting
with mono-articular arthritis of knee joint. Tabulate the
management in an algorithmic manner.
10. What is Marfan’s syndrome? What is its orthopaedic
management?
Paper – II
1) Classify elbow dislocation. How will you manage an unreduced
posterior dislocation elbow in 10 yr. old child?
2) Define and classify cerebral palsy. Describe crouched gait and
its management in a 10 yr. old child.
3) Describe various systems, implants available for limb length
equalization. Discuss their underlying principle.
4) Give one example each of concentric and eccentric contraction
during gait cycle. How will paralysis of tibialis anterior affect
normal gait.
5) Describe Salter’s osteotomy. What are its indications, merits
and demerits.
6) What is thoracic outlet syndrome? Discuss its Anatomy . How
will you diagnose it in OPD?
7) Discuss sexual and bladder rehabilitation of a 30 yr. old male
following a complete spinal injury at D12 vertebral level.
8) Discuss indications, merits and demerits of talectomy.
9) Discuss orthotic management in a High Radial Nerve Palsy.
10) Discuss various functions of hand. How will you attain key pinch
in a quadriplegic with no useful power?
Dec. 2008 Paper – III
1) What is Polytrauma? Describe the scoring method & principles
of management of a patient with polytrauma in accident &
emergency department.
2) Describe clinical features, diagnostic criteria and treatment of
fat embolism syndrome.
3) What is floating knee? Discuss its management in a 25 yr. old
adult.
4) Describe various clinical methods to diagnose anterior cruciate
ligament injury. Describe post operative management of ACL
reconstruction by a bone patellar tendon bone graft.
5) Discuss the principles of management of Non-Union fracture
Neck of Femur in an adult.
6) What is a Toddler’s fracture? Discuss its differential diagnosis
and management.
7) How will you transport an organ after amputation to a
sterilized centre for re-implantation? What is the order of
implantation in a below elbow amputation?
8) Classify peri prosthetic fracture following a total hip
replacement. Discuss their management.
9) Discuss the principles and the biomechanics of intra-medullary
nailing.
10) Classify Pilon fractures and discuss their management.
Dec. 2008 Paper – IV
1) What is multi system organ failure? What are indicators of
mortality? Write briefly about diagnosis and management.
2) Define and classify VIC. Describe its surgical and orthotic
management in Grade II VIC of forearm.
3) Describe arches of foot. Classify Flat Foot & briefly discuss the
management principles of flat feet in a child.
4) What are the anatomical & physiological differences between
neck shaft angle and version in a child and adult?
5) Discuss principle of chondroplasty in osteoarthritis of knee joint.
6) Define multidirectional instability of shoulder joint. Discuss its
management.
7) Discuss the role of injectable steroids following spinal injury.
8) Discuss various methods of preventing deep vein thrombosis
following total knee replacement. Discuss their merits &
demerits.
9) What are indications of arthrography in a hip? Discuss various
approaches to aspirate the hip joint.
10) What is the indication & principle behind parathormone
therapy for treatment of osteoporosis? What are its merits &
demerits?
June 2008 Paper – I
1) Femoro acetabular impingement syndrome.
2) Chronic recurrent multifocal osteomyelitis. Diagnosis and
management.
3) Management of Brachial artery injury in association with
supracondylar fracture of humerus.
4) Differentiating features between Osteonecrosis and transient
migratory osteoporosis.
5) Discuss the diagnosis and clinical features of DVT in orthopedic
surgery. Outline the management. What special precautions
are required if post-operative epidural analgesia is used for 4 –
5 days.
6) Discuss the approach to a patient with suspected bony
metastasis with unknown primary tumor.
7) Enumerate the radiological types of Tuberculosis Hip. How does
this classification help us in prognostication?
8) Discuss the approach to a patient of pelvic fracture with a
suspected abdominal injury.
9) Enumerate various methods of ACL Reconstruction. Discuss the
pros & cons of each method.
10) Bone defects encountered during total knee replacement and
their management.
June 2008 Paper – II
1) Discuss the types of equines contracture in cerebral palsy and
its management.
2) Describe the Anatomy of iliotibial band and the effect of its
contracture on the lower limb. How do you clinically detect the
contracture?
3) Renal Osteodystrophy
4) Scheurmans disease.
5) Pathophysiology of claw hand and its treatment.
6) Discuss the management of flexor tendon injury in zone II.
7) Describe the orthotic management of an asensate foot
particularly in reference to leprosy.
8) What are the various types of exercises? Discuss the benefits
and indications of isometric exercises.
9) What is paraffin wax? How is it useful in treatment of
orthopedic conditions? What are the indications and
contraindications of wax bath therapy?
10)Define ankle foot orthosis. What are the plastic materials used
in fabrication. Describe indications and care during daily use.
June 2008 Paper – III
1) Describe the causes of ulnar wrist pain after healing of a
distal radial fracture and discuss the management.
2) Damage control orthopaedics .
3) Classify fractures of acetabulum and role of conventional
radiology in the classification
4) Classify ankle injuries. Which fracture patterns have
syndesmotic instability & how do you manage it?
5) Classify fractures of the proximal humerus. What is the
relevance of blood supply of humerus in planning
management? How will you treat four part fractures?
6) Discuss the advances in the management of periarticular
fractures.
7) Describe the mechanism of injury & clinical presentation of
various incomplete spinal cord syndromes.
8) Differentiating features in the patho Anatomy &
management of intracapsular fracture neck of femur in
children & adults.
9) Advances in treatment of osteoporotic fractures.
10)Discuss the clinical features & management of Achilles
tendinopathy in athletes.
June 2008 Paper – IV
1) Biological therapy in inflammatory arthritis.
2) Trochanteric flip osteotomy in surgical exposures of the hip
joint.
3) Rationale for using metallic implants in osteoarticular
tuberculosis.
4) Clinical differentiation between pre-ganglionic and postganglionic
lesions of brachial plexus & its effect on the
management.
5) Transcutaneous nerve stimulation.
6) Define femoral anteversion. How do you detect it clinically?
Discuss the role of anteversion in orthopaedics diagnosis &
management
7) Pathophysiology of lumbar canal stenosis.
8) What are bisphosphonates? Discuss the role of
Bisphosphonates in various orthopedic disorders.
9) Describe the blood supply of a long bone. Discuss the effects
of various modalities of internal fixation on the blood supply.
10)Biodegradable orthopedic implants
Dec 2007
2007 DEC Paper I
1. management of multiple rib fracture with Haemopneumothorax
2. filum terminale syndrome
3. management of skeletal metastasis
4. round cell tumour. Discuss the management of multiple myeloma
5. osteoporosis
6. management of fat embolism
7. exertional compartment syndrome
8. management of haemarthrosis of knee developing in an injury
9. role of labeled WBC and multiphasic bone scan in bone Pathology
10. tuberculosis of hip joint
2007 Dec Paper II
1. etiology and pathological Anatomy of DDH
2. Mid carpal instability
3. surgical principles of flexor tendon repair
4. klippel feil syndrome
5. indications of amputation. Describe surgical principles of
amputation in children and adults
6. pes planus
7. role and mode of action of pharmacological treatment in CP
8. Calcaneovalgus
deformity. Disscuss the treatment issues in mature and immature
foot
9. madelung deformity
10. shoulder instability
2007 Dec Paper III
1. indications of Valgus osteotomy for fracture neck of femur. Discuss
the preoperative planning, Implant choice, advantages and
disadvantages of the procedure/
2. guiding principles of removal of orthopaedic implants after
fracture union. What are the current recommendations for
removal of implant in commonly encountered fractures
3. classify Periprosthetic fractures around the knee. Outline the
treatment strategy
4. Classify fractures of the Capitullumn and discuss the management
of each type
5. Surgical Anatomy of AC joint along with classification of AC joint
injuries. Briefly discuss the management.
6. what are the various protocols which have been used for
pharmacological intervention in spinal cord injuries.what is the
current opinion on pharmacological intervention
7. classify fractures of pelvis briefly discuss the management of
rotationally unstable and vertically stable injuries
8. Various methods of fixing severely osteoporotic fractures.
9. what is LISS. Discuss its role in stabilizing fractures of distal femur.
10. what is ballistics. Briefly describe the current management of
ballistic injuries of the spine.
2007 Dec. Paper IV
1. Biological enhancement of fracture healing
2. Bearing surface of total hip arthroplasty
3. Causes and treatment of thoracic outlet syndrome
4. what are the musculo skeletal manifestations of retroviral
infection
5. high tibial osteotomy
6. discuss the pharmacological treatment of rheumatoid arthritis
7. Structure and function of articular cartilage
8. Sickle cell disease
9. Classify Spondylolisthesis. Describe the management
10. Renal Rickets.
June 2007
2007 June Paper I
1. DIC
2. Enumerate bleeding disorders . How will you manage a grossly
arthritic Knee in haemophilia?
3. Tension Pneumothorax
4. Decribe the various myocutaneous flaps used to cover tibia in
different levels.
5. primitive neuroectodermal tumours
6. pathogenesis of lumbar canal stenosis? What is the differentiating
ffeature between vascular & neurogenic claudication
7. Briefly discuss the principles and priorities in managing polytrauma
8. loose bodies in knee – etiology? How will u manage a case of 30
year old sportsmanwho presents with locked knee due to
loose body
9. how will u differentiate structural scoliosis from nonstructural
scoliosis?describe infantile idiopathic scoliosis. What is the
importance of rib vertebral angle?
10. how will u manage a case of recalcitrant tennis elbow?
2007 June PaperII
1. Classify radial club hand. Describe the pathological Anatomy &
management of a 1 yr old child?
2. Classify Coxa Vara. Describe the management of adolescent coax
vara
3. describe the DD of cystic lesion in upper end of humerus in a 10
year old child. Describe the management of SBC in same
child
4. Classify fracture neck of femur in children. Describe its
management and complications briefly
5. Define Gait. Describe the aetiopathogenesis and causes of
trendleberg gait
6. what is symes amputation? Desribe the indications and
complications. What is the prosthesis suitable for symes
amputation?
7. Describe briefly the clinical features and management of SCFE?
8. Neurological deficit in caries spine; types, pathogenesis and
prognostic factors?
9. A one year old child has been successfully treated for CTEV.
Describe the orthotic management from this time to the
completion of treatment?
10. Describe the pathological Anatomy of the bursae of the hand.
Discuss the etiology, clinical feature and management of acute
infection in those bursae?
June 2007 Paper III
1. Peritalar dislocation
2. Chronic compartment syndrome
3. Hanging cast 4. what is unstable trochanteric fracture? Briefly
describe the various methods of managing unstable trochanteric
fracture
5. discuss the indications pros and cons of reamed Vs unreamed
intramedullary nailing
6. discuss the management of closed fracture shaft of humerus with
radial nerve palsy
7. Carpal instability – types, clinical features and radiological
assessment
8. Describe the Anatomy of Subacromial space. What is the
morphology of acromion process in the pathogenesis of rotator cuff
tears? How will you manage full thickness tear?
9. what is locked compression plate? Discuss the principles, clinical
situations where it is particularly usefull
10. how will you manage a case of acute Hemarthrosis Knee?
June 2007 Paper IV
1. Describe Bone remodeling unit. Briefly describe the drugs which
influence remodeling
2. PET Scan
3. Wallerian degeneration
4. Briefly describe the relevant biomechanics of the lower limb,
particularly in relation to bone cuts in total knee replacement
5. gate control theory of pain
6. what is neuropraxia? How will you differentiate it from
axonometsis during first few days of injury
7. tribology
8. tumour induced osteomalacia
9. describe the histological zones of growth plate. Discuss the
anatomical changes which takes place in rickets and Slipped
capital femoral epiphysis
10. Discuss the pathogenesis of acute hematogenous osteomyelitis.
How does it differ in different age groups
Dec 2006
Paper – I
1) Autologous Chondrocyte Implantation
2) Features which differentiate head injury from the cerebral
symptoms of Fat Embolism syndrome.
3) Synovioma
4) Otto Pelvis
5) Principles of surface replacement arthroplasty of hip. What
do you think are the reasons of failure of previous historical
designs compared to the modern successful design?
6) What are the various methods of closing gaps between nerve
ends during nerve repair?
7) What are the indications of spinal osteotomy in ankylosing
spondylitis? Describe the various techniques.
8) Pathophysiology of septic shock.
9) Management of a patient having fracture pelvis with urinary
retention. Restrict yourself to the management of his urinary
problem.
10)Kienbock’s disease.
2006 Dec. Paper – II
1) Name the prehensile movements of hand. What are the
tendon transfers described for opponens deficit hand?
2) Describe briefly indications, contraindications and principle
technical steps of Salter’s osteotomy.
3) How do principles of amputation differ in children as
compared to adults? What is pylon prosthesis? What are
advantages and disadvantages?
4) What is the pathological Anatomy of carpal tunnel? Describe
briefly the diagnosis and management of carpal tunnel
syndrome.
5) What are the hand deformities in rheumatoid arthritis?
Describe the pathological Anatomy and treatment of
Boutannaire’s deformity.
6) Describe briefly the aetiology, clinical features and principles
of treatment of Tom Smith arthritis.
7) Outline the calcium metabolism. What do you mean by
Vitamin D resistant rickets? Describe its clinical features and
management.
8) What is crutch palsy? Describe the orthotic management of
wrist drop.
9) Describe the pathological Anatomy , clinical features and
management of post polio calcaneus deformity in a 12 yr. old
patient.
10)What is Floor Reaction Orthosis? Describe its parts and
mechanism of function. What are its indications and
contraindications?
Paper – III
1) Describe the mechanism of injury and clinical presentation of
various incomplete spinal cord syndromes.
2) What is Lisfranc joint? Classify injuries around this joint and
principles of management.
3) Classify calcaneal fractures. Discuss the management based
on classification system. Enumerate the complications.
4) Enumerate Biodegradable implants. What are the advantages
and disadvantages of their use?
5) Classify periprosthetic fractures around the knee and discuss
their management.
6) Classify fracture acetabulum and outline the indications of
surgical treatment.
7) Classify ankle injuries. Which fracture patterns have
syndesmotic instability and how do you manage that?
8) Classify fractures of the proximal humerus in elderly. What is
the relevance of blood supply of the humeral head in
planning management? How will you treat four part
fracture?
9) What is Gas Gangrene? Discuss the clinical features,
bacteriology and principles of management.
10)Describe the causes of ulnar wrist pain after healing of distal
radius fractures. Discuss the management of DRUJ disorders.
Paper – IV
1) Describe the Physiology of micturition. Briefly discuss the
management of automatic bladder in spinal injuries.
2) Describe the arches of foot. Discuss the clinical features and
management of peroneospastic flat foot.
3) Describe the blood supply of femoral head. How does it differ
in children and adults?
4) Describe the properties of synovial fluids. How does it help in
differentiating various types of arthritis?
5) What are the stages of fracture healing? Discuss the factors
regulating fracture healing.
6) What are bone graft substitutes? How do they work?
7) Describe the metabolism of Vitamin D and its clinical
significance.
8) What are Giant cell variants? Describe in brief their
differential diagnosis.
9) What is DOTS? What is its rationale?
10)Pathoanatomy, radiology and diagnosis of Congenital vertical
Talus.
June 2006
Paper – I
1) Discuss the Pathology of osteoarthritis of knee with special
reference to the role of ACL rupture in the pathogenesis of
osteoarthritis knee.
2) Briefly describe the clinical features, types and management
of osteoid osteoma.
3) Describe in detail the synovial fluid analysis. How do you
differentiate various types of arthritides based on the
analysis?
4) Video Assisted Thoracoscopy
5) Osteochondritis Dessicans
6) Transient Migratory Osteoporosis of the hips
7) Describe various types of skin grafts. Discuss the stages of
biological incorporation of skin grafts.
8) Discuss the pathogenesis of neurospinal claudication.
9) Automatic Dysreflexia.
10)Control of air quality in a modern orthopaedic operation
theatre.
June 2006
Paper – II
1) Anterior Interosseous Nerve syndrome – Aetiology, clinical
features, differential diagnosis and management.
2) Dwyer’s osteotomy for CTEV – Indications, steps and
complications.
3) Sprengel’s Deformity. Etio pathogenesis, clinical features and
management.
4) Coxa Plana – Clinical, Radiological features, Differential
diagnosis and principles of treatment.
5) Boutannaire deformity – etiology, pathomechanics and
management.
6) Ultrasonic Therapy – Physiological effects, clinical
applications and contraindications.
7) Quadriceps Paralysis Gait – pathomechanics, compensation
employed and corrective measures.
8) Suction Socket Prosthesis – principles, indications and
advantages over conventional prosthesis and main points in
its construction.
9) Bowing of Tibia in children – Causes, types and management
of Congenital Bowing
10)Equinus Deformity in cerebral palsy – Etiopathogenesis,
evaluation and treatment.
June 2006
Paper – III
1) Fracture Talus.
2) Bennet’s Fracture dislocation
3) Hangman’s Fracture.
4) Motor March
5) Principles of Tendon Transfer.
6) Anterior Cruciate Ligament Injury.
7) Acromio clavicular Disruption
8) Lateral Condyle fracture of Humerus
9) Perilunar Dislocation.
10)Fracture Disease.
June 2006 Paper – IV
1) Etiopathogenesis, Pathology and management of DIC.
2) Congenital postural deformities associated with in-utero
position.
3) Raloxifene.
4) Biomechanics of Knee in relation to total knee replacement.
5) Structure and Biochemistry of articular cartilage.
6) Bryant’s Traction.
7) Biochemical markers of Bone formation and resorption.
8) Describe pathological Anatomy and radiology in CTEV.
9) Stewart and Harnaley ankle arthrodesis.
10)Enumerate various deformities of foot and ankle seen in Post
Polio Residual Paralysis (PPRP). Describe in detail the
management of Talipes Calcaneus
Dec. 2005 Paper – I
1) Define entrapment syndrome. Enumerate various entrapment
syndromes. Discuss the entrapment syndrome in relation to
the ulnar nerve in detail.
2) Bony changes in hyperparathyroidism and
hypoparathyroidism along with relevant pathophysiology.
3) Sports related injuries to soft tissues.
4) Suture Materials.
5) Finger Injuries.
6) Enumerate various classical levels of lower limb amputations.
Discuss AK amputation in detail. What is the difference in
energy consumption by the patient in AK amputation as
compared to a BK amputation?
7) Respiratory Distress Syndrome.
Cool Intravenous Regional Anaesthesia in orthopedic practice.
9) Day Care Surgery.
10)Surgical audit.
Dec. 2005 Paper – II
1) Congenital vertical Talus – Etiology, Pathology , clinical,
radiological features and management.
2) Chiari Osteotomy – indications, advantages, steps of surgery.
3) Claw Hand – Etiology, patho-mechanics,principles of various
corrective procedures.
4) Bowing of Tibia in children – Causes, types, clinical features &
management of congenital bowing of tibia.
5) Klippel-Fiel syndrome – Etiology, Pathology , clinical &
radiological features, differential diagnosis & management.
6) Microwave Diathermy – its physiogical effects, clinical
applications & contraindications.
7) Describe various types of Crutches ; gait pattern with crutches.
Cool Skew Flap Amputation – indications, advantages of
conventional amputation,steps of operation and complications.
9) Post – polio equinus deformity of foot – etiopathology,
evaluation & management.
10)Floor reaction Orthosis – indications, principles and advantages.
Dec. 2005 Paper – III
1) Enumerate the types of spinal cord lesions following fracture
dislocation of C5-6 vertebrae and discuss clinical features,
treatment and prognosis of each type of lesion in adult. 25 marks
2) Describe the following in brief 15 marks each
i) Treatment of fractures of distal end of radius.
ii) Management of fracture of fracture shaft of femur that
has become infected after intramedullary fixation
iii) Treatment of radial head and neck fractures in children
iv) Management of Trochnanteric fractures in elderly.
v) Principles of management of Lisfranc injuries of foot.
Dec. 2005 Paper – IV
1) Massive Transfusion.
2) Harmon’s approach of Tibia with applied Anatomy .
3) Strength – Duration Curve.
4) Biomechanics of hip joint and its clinical applications.
5) Radionuclide bone scanning
6) Allopurinol
7) Tension band principle and its application in treatment of
fractures using a wire and plate.
Cool Pathology of tuberculous arthritis and correlation with clinical
staging.
9) Growth plate - Anatomy and pathological states affecting it.
10) Radiological and biochemical features of renal osteodystrophy and
their interpretation.
June 2005 Paper – I
Part A
1) Draw a flow chart of disaster planning at state level. What is the
concept of triage?
2) Pathology , clinical features and management of diabetic foot.
3) Nosocomial infection on orthopaedics – common organism and
preventive measures.
4) Post operative DVT – Prevention, clinical features and treatment.
5) Post Menopausal Osteoporosis – Prevention and management.
Part B
1) Crystal Synovitis.
2) Incoporation of Bone Grafts. How does it differ for cancellous and
cortical grafts?
3) Preparation and precautions required to operate HIV positive
patients.
4) Chemotherapy for osteosarcoma.
5) How does a neurological claudication differ from vascular
claudication? Enumerate the etiology of the two.
June 2005 Paper – II
Part A
1) Clinical features and management of slipped capital femoral
epiphysis.
2) Ewing’s Sarcoma
3) Pollicisation – Indications and prerequisites
4) What are parts of a shoe? Describe the modifications of a CTEV
shoe.
5) What is modified Jone’s transfer for a high radial nerve palsy?
How does it differ from original transfer?
Part B
1) Pylon prosthesis – Indications, prerequisites and advantages.
2) Botulin in cerebral palsy patients.
3) PTB prosthesis – Indications and principles.
4) Radial club hand.
5) Salter osteotomy for DDH.
June 2005 Paper – III
1) Describe the biology of fracture healing and the influence of intra
medullary rods and plates in healing. Discuss the role of various
modalities in stimulation of osteogenesis
(25 marks)
2) Describe in brief on the following (15 marks each)
i) Treatment of odontoid fracture in adults.
ii) Enumerate the complications of femoral neck fractures in
children and discuss the management in any one of the
complications.
iii) Classification and treatment of acromioclavicular dislocation.
iv) Stress, Strain, Modulus of elasticity and strength in relation
to metallic implants.
v) Rotator cuff injury in sportsmen.
June 2005 Paper – IV
Part A
1) Trendelenberg test with its anatomical basis and clinical
applications
2) Madura foot.
3) Synovial fluid and its analysis in various arthritis
4) Blood supply of head of femur and its clinical significance.
5) Morbid Anatomy , radiological and laboratory features of Multiple
Myeloma
Part B
1) Thompsons approach of radius with applied Anatomy .
2) Paralytic Bladder.
3) Methotrexae as a DMARD.
4) Therapeutic ultrasound.
5) Prophylaxis in thrombo-embolic disease.
Dec. 2004 Paper – I
1) Describe etiopathogenesis of thoracic outlet syndrome and its
management
2) Short notes on
i) Shock
ii) Haemophiliac arthropathy
iii) Compartment syndrome
iv) Ehler-Danlos syndrome
v) Acute rupture of Achilles Tendon
Dec. 2004 Paper – II
1) Discuss etiology, pathogenesis and management of Perthe’s
disease.
2) Write short notes on
i) Principles of amputation of lower limb in children
ii) Dupuytren’s contracture
iii) Carpal Tunnel Syndrome
v) Nuclear Imaging.
iv) F.R.O.
Dec. 2004 Paper – III
1) Classify pelvic fractures and discuss the management.
2) Write short notes on
i) Fracture Talus
ii) Calcaneovalgus Deformity
iii) Myositis Ossificans
iv) Biomechanics of Hip
v) Habitual Dislocation of Patella
Dec.2004 Paper – IV
1) Describe calcium metabolism. Discuss the etiology, clinical
features, diagnosis and management of nutritional rickets.
2) Write short notes on
i) Arches of foot
ii) Core decompression
iii) Bone graft substitutes
iv) Pathology of osteoarthritis
v) Sudeck’s osteodystrophy
June 2004 Paper – I
1) Osteoporosis – Definition, Etiology, Clinical features,
Investigations, Prevention and Treatment.
2) Short notes on
i) Surgery for habitual dislocation of patella
ii) Triple arthrodesis for equinus
iii) Shoe modification for valgoid tilt
iv) Fascio-cutaneous skin graft
v) Ideal stump
June 2004 Paper – II
1) Discuss the merits & demerits of operative & non-operative
treatment of simple diaphyseal fracture of tibia.
2) Short notes on
i) Bristow’s procedure
ii) Classification of Distal Radius fracture
iii) Classification of Rotatory knee instability
iv) Management of Pelvic fractures
v) Old metacarpo phalangeal dislocation
June 2004 Paper – III
1) Discuss mechanism & classification of injury around ankle joint.
Discuss diagnosis and treatment.
2) Short notes on
i) Discuss Pathology & management of infected non-union.
ii) Fracture Neck of Femur – Classification and treatment
iii) Compression & Distraction in Orthopaedics
iv) Role of Ligamentotaxis in fractures
v) Tension band wiring principle.
June 2004 Paper – IV
1) Describe bone tumour. Classification, diagnosis and treatment
modalities for Multiple Myeloma.
2) Short notes on
i) Bone Cement
ii) Intrinsic Hand
iii) Shoulder Hand Syndrome
iv) Gait Cycle
v) Osteoclast.
Dec. 2003 Paper I
1) Define Gangrene. Describe the aetiological classification & Mx
of gas gangerene?
2) Short Notes on :
i) Skin grafting
ii) Madura foot
iii) Mortons metatarsalgia
iv) DVT
v) Ewings tumour
Dec. 2003 Paper II
1. Management of ankle fractures in children
2. Pathophysiology & presentation of TB spine in children
3. Juvenile Chronic arthritis - DD & investigations
4. Osteochondritis dessicans
5. Congenital amputations of lower limb in children
6. Haemophilia knee
7. Compound palmar ganglia
8. Ulnar claw hand
9. Pes planus
10. Mono ostotoc fibrous dysplasia
Dec. 2003 Paper III
1) Recent advances in the management of intraarticular
fractures of upper end of tibia
2) Short notes on :
i) Rationale of surgical treatment of recurrent dislocation of
shoulder
ii) Hangmans fracture
iii) Calcaneum fracture
iv) Orthopaedic complications of high dose steroid
v) Sudeks Osteodystrophy
Dec.2003 Paper IV
1) Describe the mechanism of calcium homeostasis by parathyroid
hormone and the skeletal changes that occur as a result of
hyperparathyroidism. Discuss the uses and limitations of lab
investigations in the diagnosis of primary hyperparathyroidism
2) Short notes on :
i) BMP
ii) 2nd line of ATT
iii) Acute ankle sprain
iv) Growth plate & its functions
v) Stress, strain & modulus of elasticity in relationship to
implants.
Dec. 2002 Paper I
1) Aetiology, Pathology & Mx of Spinal canal stenosis
2) Short notes on :
i) Tension pneumpthorax
ii) Non specific synovitis
iii) Painful arc syndrome
iv) metastatic lesion of bone & tis management
v) Crush Syndrome
Dec. 2002 Paper II
1) Pathogenesis, Clinical features & management of Caries spine
in a child 10 yrs old
2) Short notes on :
i) Intrinsic muscles hand
ii) fibrous dysplasia
iii) Habittual dislocation patella
iv) LASER Therapy
v) Amputations in children
Dec. 2002 PAPER III
1) Management of fracture pelvis and their complications
2) Short notes on :
i) Cerebral diplegia? Line of Management?
ii) Multiple myelpma – Investigations & Management?
iii) Pes Planus –etiology & Management?
iv) Investigations of Pain in Hand?
v) Rationale of surgical Rx for recurrent anterior dislocation
shoulder?
Dec. 2002 Paper IV
1) Blood supply of head of femur in diff age groups?Management of
Idiopathic AVN of Femur?
2) Short notes on :
i) Osteogenesis imperfecta
ii) Cubitus Varus
iii) Renal Rickets
iv) Sudecks dystrophy
v) Neurogenic Bladder
June 2002 Paper I
1) Describe the various approaches to the spine
2) Short notes on :
i) Recurrent dislocation of patella
ii) Compression plating
iii) Hallux valgus
iv) Volkmans ischaemic contracture
v) Ewings sarcoma
June 2002 Paper II
1) Describe the management of claw hand
2) Short notes on :
i) CTEV
ii) Septic arthritis of hip in a child below 5 years and above
3years
iii) Epiphyseal injuries
iv) Principles of amputation in children
v) Calcaneovalgus foot
June 2002 PAPER III
1.Treatment of ununited fracture neck of femur
2.Treatment of intercondylar fracture of humerus
3.Investigation of collapse of a vertebra
4.Osteomalacia
5.Osteogenesis imperfecta
6.Post Polio Residual Paralysis
7.Diagnostic criteria of osteolytic lesion in upper end tibia
8.Pilon fracture
9.Brodies abscess
10. Costo clavicular syndrome
Paper IV
1) Describe the Anatomy of recurrent dislocation shoulder? Discuss
Management
2) Short notes on :
i) Ceramics In Orthopaedics
ii) Bone grafts
iii) Hyper parathyroidism
iv) Pigmented villonodular synovitis
v) Pes planus
2001 Paper I
1. OA Knee – pathophysiology. Discuss rationale of surgical
management of OA Knee
2. Short notes on :
i) Renal Rickets – Pathophysiology
ii) Thoracic Outlet Syndrome
iii) Hand to Knee gait in Polio
iv) Wallerian Degenration
v) Endotoxic Shock
2001 PaperII
1. Pathomechanics, Clincal features & Management of various
deformities in RA – hand?
2. Short notes on :
i) Pseudoarthrosis
ii) Neglected Cong. Talipes Equino varus
iii) Electromyography
iv) Osteochondromatosis
v) Suction socket prosthesis
2001 Paper III
1.Discuss the pathological alterations of femoral neck & head in
neglected & ununited femoral neck fractures
and their management?
2. Short notes on :
i) Traumatic paraplegia
ii) Fractures at the upper end of humerus
iii) Intercarpal instability
iv) Two level fracture of shaft of tibia
v) Fractures and dislocation of talus
2001 PAPER IV
1. Describe the development of vertebral column.Pathogenesis and
management of potts paraplegia. Discuss the treatment of resistant
cases?
2. Short notes on :
i) Biodegradable implants
ii) Rigid flat foot
iii) wrist drop
iv) Compartment Syndrome
v) Symes amputation
Paper 1
1. Post-operative pain management. Describe patient control analgesia.
2. Clinical features and management of stove in chest.
3. Indications of Limb salvage surgery in malignant bone tumors. Describe the techniques of limb salvage in osteosarcoma.
4. Uses of botulinum neurotoxin in Orthopaedic surgery.
5. Define pigmented villonodular synovitis. Describe pathology, clinical features, diagnosis & its treatment.
6. Give a functional classification of muscles around the shoulder. Enumerate the indications for shoulder arthrodesis. What are the pre-requisites for a good result? Describe any one technique of shoulder arthrodesis.
7. Describe pathophysiology of nerve compression (entrapment) syndromes. Enumerate various syndromes of nerve entrapment. Give an outline of the management of Tarsal Tunnel Syndrome.
8. What is traumatic arthrotomy of the knee joint? What is fluid challenge test to confirm the diagnosis in doubtful cases? Outline the principles of management.
9. What are the various causes of late onset paraplegia in tuberculosis of spine? Describe the investigative modalities and outline the principles of management.
10. Describe the management of unicompartmental osteoarthrosis knee.
Paper 2
1. Management of septic arthritis in children,
2. Pathophysiology, types and clinical features of Osteogenesis Imperfecta
3. Prognostic factors and outcome in the treatment of Perthe’s disease
4. Describe Madelung deformity, classification, clinical features and management of Perthe’s disease
5. Classify congenital dislocation of knee. Comment on differential diagnosis and management
6. Draw a diagram of Floor Reaction Orthosis, What is a good indication for its use. Describe mechanism of action
7. Orthopaedic manifestation of neurofibromatosis
8. Describe muscular dynamics in calcaneovalgus deformity. Describe management in patients before and after attaining skeletal maturity
9. Classification of neurogenic bladder and management
10. What are closed chain and open chain exercises and discuss ACL rehabilitation protocol
Paper 3
1. Classification, management and complication of fractures of the femoral head and neck in children
2. What are Monteggia equivalents, discuss the principles of management of Monteggia fracture dislocation in children
3. Principles of management of a pulseless hand after supracondylar fractures in children
4. Role of ultrasound in fracture healing
5. Subacromial impingement syndrome
6. Describe indications for amputation, Principles of lower limb amputation in children
7. What is Mangled Extremity severity score(MESS), describe principles of flap coverage in proximal one third of tibia
8. Classify ankle fractures, which pattern has syndesmotic instability, what is their management?
9. What are biodegradable implants, what is their chemical composition? Mention the indications of their use, advantage and disadvantage of their use
10. What is central cord syndrome, describe its clinical presentation. How will you manage such a case?
Paper 4
1. Osteochondral allograft transplantation. Mention indications for the procedure
2. Role of Pamidronate in bone metastasis
3. What do you understand by patellar instability, describe the principles of management, before and after skeletal maturity?
4. Enumerate modalities leading to biological enhancement of fracture healing. Mention the methods of preservation of allogenic bone grafts. Comment on mode of action, advantages and disadvantages
5. Describe the pathogenesis of hallux valgus deformity; describe the role of metatarsus primary varus in the pathogenesis. How will you manage an adolescent girl with severe hallux valgus?
6. Describe various types of rickets; describe biochemical changes and clinical presentation of various types of rickets!
7. Define osteoporosis. Comment on types, causes and management
8. What is highly cross linked polyethylene? How is it manufactured? How has it affected modern total hip arthroplasty?
9. Anatomy of Lisfranc joint, and management of injuries around the joint
10. Describe gate control theory of pain. What is transcutaneous nerve stimulation and its indications?
JUNE 2009
Paper – I
1) Briefly describe the stages of fracture healing. Discuss physical or chemical modalities to enhance fracture healing.
2) Discuss prophylaxis against secondary complications of patient with polytrauma.
3) Ganz antishock pelvic fixator.
4) Describe musculoskeletal manifestations of HIV infected patients.
5) Describe pathogenesis of medial compartment osteoarthrosis. Discuss pros & cons of HTO vs unicondylar replacement.
6) Femoroacetabular impingement syndrome.
7) Osteofibrous Dysplasia
8) Enumerate indications & various techniques for shoulder arthrodesis. What are the prerequisites for a good result?
9) What is malalignment test? Discuss principles of focal dome osteotomy.
10) Gene therapy in Orthopedics.
Paper II
1) Enumerate the causes of intoeing gait. How will you treat intoeing gait because of hip disorders.
2) What is congenital coxa vara? Describe its pathophysiology and outline principles of management.
3) Ober’s test.
4) Briefly discuss the clinical features and pathology of Ewing’s Sarcoma. Outline the principles of treatment in a case of Ewing’s Sarcoma of upper end of humerus.
5) How will you evaluate a child with genu valgum deformity? Outline the principles of management. What is timed epiphysiodesis?
6) Thermoplastic splints
7) Classify nerve injuries. What is the role of electrodiagnosis in differentiating various nerve lesions?
8) Discuss the principles of rehabilitation of a paraplegic patient.
9) Briefly describe the principles & steps of Ponsetti’s method of CTEV correction.
10) Enumerate various causes of claw hand. What is the pathogenesis of clawing? Discuss the principles of surgical correction.
Paper – III
1) Classify fractures of calcaneum. Outline the principles of management.
2) Elaborate the principles of LCP. What are the applications in periarticular fractures?
3) Classify epiphyseal injuries. Describe the complications. What is Langenskiold’s procedure?
4) Current concepts in the management of fracture neck & head of radius in children and adults.
5) Classify flexor tendon injuries of the hand. Describe the treatment of neglected ruptures of flexor tendons in Zone II.
6) Outline the principles of management in a case of infected non union of a long bone. How will you treat infected non union of tibia?
7) Classify fractures of the acetabulum. Discuss radiographic evaluation of acetabular trauma.
8) How will you manage a case of knee dislocation with absent distal pulsations?
9) Describe instability patterns after wrist trauma. Discuss the management of VISI (Volar Intercalated Segment Instability)
10) How will you differentiate between the cerebral sign as a result of head injury vs fat embolism syndrome? Describe in brief management of fat embolism syndrome.
Paper – IV
1) Autologous Transfusion.
2) Describe the anatomy of Distal Radio Ulnar Joint. Describe indications & technique of performing Kapandji’s procedure.
3) Sexual Dimorphism in orthopedic practice.
4) Brown Tumor.
5) Surgical Dislocation of Hip.
6) Describe anatomical classification of chronic osteomyelitis. Discuss the principles of management based on this classification. How will you fill the dead space after excision of infected tissue?
7) Describe the presentation of tourniquet palsy and its causes. What precautions are taken to prevent it?
8) Describe the anatomy of PCL. Discuss its significance in Total Knee Arthroplasty.
9) Describe the basic principle of PET scan and discuss its role in orthopedics.
10) What is pelvic support osteotomy? Outline its principles and operative technique.
Dec. 2008
Paper – I
1. Discuss Anatomy of rotator cuff. What is rotator cuff disease?
Discuss its pathogenesis and management.
2. Define and classify Rickets. Describe pathogenesis, clinical
features and management of hypophosphatemic rickets.
3. What are Biochemical markers for bone formation and bone
resorption. Discuss their role in management of osteoporosis.
4. Discuss causes of loosening after a total hip replacement.
Discuss its clinical features, diagnosis and management.
5. Discuss various methods available for treatment of Giant cell
tumor of proximal tibia in a 30 yr. old man.
6. What is claudication? Classify it and discuss its cause specific
management.
7. Discuss the etiology, Pathology , diagnosis, and management of
Gas Gangrene of the Lower Extremity.
8. Discuss approach to find out a primary tumor in a 65 yr. old
man presenting with vertebral metastasis and low backache.
9. Discuss differential diagnosis in a 25 yr. old male presenting
with mono-articular arthritis of knee joint. Tabulate the
management in an algorithmic manner.
10. What is Marfan’s syndrome? What is its orthopaedic
management?
Paper – II
1) Classify elbow dislocation. How will you manage an unreduced
posterior dislocation elbow in 10 yr. old child?
2) Define and classify cerebral palsy. Describe crouched gait and
its management in a 10 yr. old child.
3) Describe various systems, implants available for limb length
equalization. Discuss their underlying principle.
4) Give one example each of concentric and eccentric contraction
during gait cycle. How will paralysis of tibialis anterior affect
normal gait.
5) Describe Salter’s osteotomy. What are its indications, merits
and demerits.
6) What is thoracic outlet syndrome? Discuss its Anatomy . How
will you diagnose it in OPD?
7) Discuss sexual and bladder rehabilitation of a 30 yr. old male
following a complete spinal injury at D12 vertebral level.
8) Discuss indications, merits and demerits of talectomy.
9) Discuss orthotic management in a High Radial Nerve Palsy.
10) Discuss various functions of hand. How will you attain key pinch
in a quadriplegic with no useful power?
Dec. 2008 Paper – III
1) What is Polytrauma? Describe the scoring method & principles
of management of a patient with polytrauma in accident &
emergency department.
2) Describe clinical features, diagnostic criteria and treatment of
fat embolism syndrome.
3) What is floating knee? Discuss its management in a 25 yr. old
adult.
4) Describe various clinical methods to diagnose anterior cruciate
ligament injury. Describe post operative management of ACL
reconstruction by a bone patellar tendon bone graft.
5) Discuss the principles of management of Non-Union fracture
Neck of Femur in an adult.
6) What is a Toddler’s fracture? Discuss its differential diagnosis
and management.
7) How will you transport an organ after amputation to a
sterilized centre for re-implantation? What is the order of
implantation in a below elbow amputation?
8) Classify peri prosthetic fracture following a total hip
replacement. Discuss their management.
9) Discuss the principles and the biomechanics of intra-medullary
nailing.
10) Classify Pilon fractures and discuss their management.
Dec. 2008 Paper – IV
1) What is multi system organ failure? What are indicators of
mortality? Write briefly about diagnosis and management.
2) Define and classify VIC. Describe its surgical and orthotic
management in Grade II VIC of forearm.
3) Describe arches of foot. Classify Flat Foot & briefly discuss the
management principles of flat feet in a child.
4) What are the anatomical & physiological differences between
neck shaft angle and version in a child and adult?
5) Discuss principle of chondroplasty in osteoarthritis of knee joint.
6) Define multidirectional instability of shoulder joint. Discuss its
management.
7) Discuss the role of injectable steroids following spinal injury.
8) Discuss various methods of preventing deep vein thrombosis
following total knee replacement. Discuss their merits &
demerits.
9) What are indications of arthrography in a hip? Discuss various
approaches to aspirate the hip joint.
10) What is the indication & principle behind parathormone
therapy for treatment of osteoporosis? What are its merits &
demerits?
June 2008 Paper – I
1) Femoro acetabular impingement syndrome.
2) Chronic recurrent multifocal osteomyelitis. Diagnosis and
management.
3) Management of Brachial artery injury in association with
supracondylar fracture of humerus.
4) Differentiating features between Osteonecrosis and transient
migratory osteoporosis.
5) Discuss the diagnosis and clinical features of DVT in orthopedic
surgery. Outline the management. What special precautions
are required if post-operative epidural analgesia is used for 4 –
5 days.
6) Discuss the approach to a patient with suspected bony
metastasis with unknown primary tumor.
7) Enumerate the radiological types of Tuberculosis Hip. How does
this classification help us in prognostication?
8) Discuss the approach to a patient of pelvic fracture with a
suspected abdominal injury.
9) Enumerate various methods of ACL Reconstruction. Discuss the
pros & cons of each method.
10) Bone defects encountered during total knee replacement and
their management.
June 2008 Paper – II
1) Discuss the types of equines contracture in cerebral palsy and
its management.
2) Describe the Anatomy of iliotibial band and the effect of its
contracture on the lower limb. How do you clinically detect the
contracture?
3) Renal Osteodystrophy
4) Scheurmans disease.
5) Pathophysiology of claw hand and its treatment.
6) Discuss the management of flexor tendon injury in zone II.
7) Describe the orthotic management of an asensate foot
particularly in reference to leprosy.
8) What are the various types of exercises? Discuss the benefits
and indications of isometric exercises.
9) What is paraffin wax? How is it useful in treatment of
orthopedic conditions? What are the indications and
contraindications of wax bath therapy?
10)Define ankle foot orthosis. What are the plastic materials used
in fabrication. Describe indications and care during daily use.
June 2008 Paper – III
1) Describe the causes of ulnar wrist pain after healing of a
distal radial fracture and discuss the management.
2) Damage control orthopaedics .
3) Classify fractures of acetabulum and role of conventional
radiology in the classification
4) Classify ankle injuries. Which fracture patterns have
syndesmotic instability & how do you manage it?
5) Classify fractures of the proximal humerus. What is the
relevance of blood supply of humerus in planning
management? How will you treat four part fractures?
6) Discuss the advances in the management of periarticular
fractures.
7) Describe the mechanism of injury & clinical presentation of
various incomplete spinal cord syndromes.
8) Differentiating features in the patho Anatomy &
management of intracapsular fracture neck of femur in
children & adults.
9) Advances in treatment of osteoporotic fractures.
10)Discuss the clinical features & management of Achilles
tendinopathy in athletes.
June 2008 Paper – IV
1) Biological therapy in inflammatory arthritis.
2) Trochanteric flip osteotomy in surgical exposures of the hip
joint.
3) Rationale for using metallic implants in osteoarticular
tuberculosis.
4) Clinical differentiation between pre-ganglionic and postganglionic
lesions of brachial plexus & its effect on the
management.
5) Transcutaneous nerve stimulation.
6) Define femoral anteversion. How do you detect it clinically?
Discuss the role of anteversion in orthopaedics diagnosis &
management
7) Pathophysiology of lumbar canal stenosis.
8) What are bisphosphonates? Discuss the role of
Bisphosphonates in various orthopedic disorders.
9) Describe the blood supply of a long bone. Discuss the effects
of various modalities of internal fixation on the blood supply.
10)Biodegradable orthopedic implants
Dec 2007
2007 DEC Paper I
1. management of multiple rib fracture with Haemopneumothorax
2. filum terminale syndrome
3. management of skeletal metastasis
4. round cell tumour. Discuss the management of multiple myeloma
5. osteoporosis
6. management of fat embolism
7. exertional compartment syndrome
8. management of haemarthrosis of knee developing in an injury
9. role of labeled WBC and multiphasic bone scan in bone Pathology
10. tuberculosis of hip joint
2007 Dec Paper II
1. etiology and pathological Anatomy of DDH
2. Mid carpal instability
3. surgical principles of flexor tendon repair
4. klippel feil syndrome
5. indications of amputation. Describe surgical principles of
amputation in children and adults
6. pes planus
7. role and mode of action of pharmacological treatment in CP
8. Calcaneovalgus
deformity. Disscuss the treatment issues in mature and immature
foot
9. madelung deformity
10. shoulder instability
2007 Dec Paper III
1. indications of Valgus osteotomy for fracture neck of femur. Discuss
the preoperative planning, Implant choice, advantages and
disadvantages of the procedure/
2. guiding principles of removal of orthopaedic implants after
fracture union. What are the current recommendations for
removal of implant in commonly encountered fractures
3. classify Periprosthetic fractures around the knee. Outline the
treatment strategy
4. Classify fractures of the Capitullumn and discuss the management
of each type
5. Surgical Anatomy of AC joint along with classification of AC joint
injuries. Briefly discuss the management.
6. what are the various protocols which have been used for
pharmacological intervention in spinal cord injuries.what is the
current opinion on pharmacological intervention
7. classify fractures of pelvis briefly discuss the management of
rotationally unstable and vertically stable injuries
8. Various methods of fixing severely osteoporotic fractures.
9. what is LISS. Discuss its role in stabilizing fractures of distal femur.
10. what is ballistics. Briefly describe the current management of
ballistic injuries of the spine.
2007 Dec. Paper IV
1. Biological enhancement of fracture healing
2. Bearing surface of total hip arthroplasty
3. Causes and treatment of thoracic outlet syndrome
4. what are the musculo skeletal manifestations of retroviral
infection
5. high tibial osteotomy
6. discuss the pharmacological treatment of rheumatoid arthritis
7. Structure and function of articular cartilage
8. Sickle cell disease
9. Classify Spondylolisthesis. Describe the management
10. Renal Rickets.
June 2007
2007 June Paper I
1. DIC
2. Enumerate bleeding disorders . How will you manage a grossly
arthritic Knee in haemophilia?
3. Tension Pneumothorax
4. Decribe the various myocutaneous flaps used to cover tibia in
different levels.
5. primitive neuroectodermal tumours
6. pathogenesis of lumbar canal stenosis? What is the differentiating
ffeature between vascular & neurogenic claudication
7. Briefly discuss the principles and priorities in managing polytrauma
8. loose bodies in knee – etiology? How will u manage a case of 30
year old sportsmanwho presents with locked knee due to
loose body
9. how will u differentiate structural scoliosis from nonstructural
scoliosis?describe infantile idiopathic scoliosis. What is the
importance of rib vertebral angle?
10. how will u manage a case of recalcitrant tennis elbow?
2007 June PaperII
1. Classify radial club hand. Describe the pathological Anatomy &
management of a 1 yr old child?
2. Classify Coxa Vara. Describe the management of adolescent coax
vara
3. describe the DD of cystic lesion in upper end of humerus in a 10
year old child. Describe the management of SBC in same
child
4. Classify fracture neck of femur in children. Describe its
management and complications briefly
5. Define Gait. Describe the aetiopathogenesis and causes of
trendleberg gait
6. what is symes amputation? Desribe the indications and
complications. What is the prosthesis suitable for symes
amputation?
7. Describe briefly the clinical features and management of SCFE?
8. Neurological deficit in caries spine; types, pathogenesis and
prognostic factors?
9. A one year old child has been successfully treated for CTEV.
Describe the orthotic management from this time to the
completion of treatment?
10. Describe the pathological Anatomy of the bursae of the hand.
Discuss the etiology, clinical feature and management of acute
infection in those bursae?
June 2007 Paper III
1. Peritalar dislocation
2. Chronic compartment syndrome
3. Hanging cast 4. what is unstable trochanteric fracture? Briefly
describe the various methods of managing unstable trochanteric
fracture
5. discuss the indications pros and cons of reamed Vs unreamed
intramedullary nailing
6. discuss the management of closed fracture shaft of humerus with
radial nerve palsy
7. Carpal instability – types, clinical features and radiological
assessment
8. Describe the Anatomy of Subacromial space. What is the
morphology of acromion process in the pathogenesis of rotator cuff
tears? How will you manage full thickness tear?
9. what is locked compression plate? Discuss the principles, clinical
situations where it is particularly usefull
10. how will you manage a case of acute Hemarthrosis Knee?
June 2007 Paper IV
1. Describe Bone remodeling unit. Briefly describe the drugs which
influence remodeling
2. PET Scan
3. Wallerian degeneration
4. Briefly describe the relevant biomechanics of the lower limb,
particularly in relation to bone cuts in total knee replacement
5. gate control theory of pain
6. what is neuropraxia? How will you differentiate it from
axonometsis during first few days of injury
7. tribology
8. tumour induced osteomalacia
9. describe the histological zones of growth plate. Discuss the
anatomical changes which takes place in rickets and Slipped
capital femoral epiphysis
10. Discuss the pathogenesis of acute hematogenous osteomyelitis.
How does it differ in different age groups
Dec 2006
Paper – I
1) Autologous Chondrocyte Implantation
2) Features which differentiate head injury from the cerebral
symptoms of Fat Embolism syndrome.
3) Synovioma
4) Otto Pelvis
5) Principles of surface replacement arthroplasty of hip. What
do you think are the reasons of failure of previous historical
designs compared to the modern successful design?
6) What are the various methods of closing gaps between nerve
ends during nerve repair?
7) What are the indications of spinal osteotomy in ankylosing
spondylitis? Describe the various techniques.
8) Pathophysiology of septic shock.
9) Management of a patient having fracture pelvis with urinary
retention. Restrict yourself to the management of his urinary
problem.
10)Kienbock’s disease.
2006 Dec. Paper – II
1) Name the prehensile movements of hand. What are the
tendon transfers described for opponens deficit hand?
2) Describe briefly indications, contraindications and principle
technical steps of Salter’s osteotomy.
3) How do principles of amputation differ in children as
compared to adults? What is pylon prosthesis? What are
advantages and disadvantages?
4) What is the pathological Anatomy of carpal tunnel? Describe
briefly the diagnosis and management of carpal tunnel
syndrome.
5) What are the hand deformities in rheumatoid arthritis?
Describe the pathological Anatomy and treatment of
Boutannaire’s deformity.
6) Describe briefly the aetiology, clinical features and principles
of treatment of Tom Smith arthritis.
7) Outline the calcium metabolism. What do you mean by
Vitamin D resistant rickets? Describe its clinical features and
management.
8) What is crutch palsy? Describe the orthotic management of
wrist drop.
9) Describe the pathological Anatomy , clinical features and
management of post polio calcaneus deformity in a 12 yr. old
patient.
10)What is Floor Reaction Orthosis? Describe its parts and
mechanism of function. What are its indications and
contraindications?
Paper – III
1) Describe the mechanism of injury and clinical presentation of
various incomplete spinal cord syndromes.
2) What is Lisfranc joint? Classify injuries around this joint and
principles of management.
3) Classify calcaneal fractures. Discuss the management based
on classification system. Enumerate the complications.
4) Enumerate Biodegradable implants. What are the advantages
and disadvantages of their use?
5) Classify periprosthetic fractures around the knee and discuss
their management.
6) Classify fracture acetabulum and outline the indications of
surgical treatment.
7) Classify ankle injuries. Which fracture patterns have
syndesmotic instability and how do you manage that?
8) Classify fractures of the proximal humerus in elderly. What is
the relevance of blood supply of the humeral head in
planning management? How will you treat four part
fracture?
9) What is Gas Gangrene? Discuss the clinical features,
bacteriology and principles of management.
10)Describe the causes of ulnar wrist pain after healing of distal
radius fractures. Discuss the management of DRUJ disorders.
Paper – IV
1) Describe the Physiology of micturition. Briefly discuss the
management of automatic bladder in spinal injuries.
2) Describe the arches of foot. Discuss the clinical features and
management of peroneospastic flat foot.
3) Describe the blood supply of femoral head. How does it differ
in children and adults?
4) Describe the properties of synovial fluids. How does it help in
differentiating various types of arthritis?
5) What are the stages of fracture healing? Discuss the factors
regulating fracture healing.
6) What are bone graft substitutes? How do they work?
7) Describe the metabolism of Vitamin D and its clinical
significance.
8) What are Giant cell variants? Describe in brief their
differential diagnosis.
9) What is DOTS? What is its rationale?
10)Pathoanatomy, radiology and diagnosis of Congenital vertical
Talus.
June 2006
Paper – I
1) Discuss the Pathology of osteoarthritis of knee with special
reference to the role of ACL rupture in the pathogenesis of
osteoarthritis knee.
2) Briefly describe the clinical features, types and management
of osteoid osteoma.
3) Describe in detail the synovial fluid analysis. How do you
differentiate various types of arthritides based on the
analysis?
4) Video Assisted Thoracoscopy
5) Osteochondritis Dessicans
6) Transient Migratory Osteoporosis of the hips
7) Describe various types of skin grafts. Discuss the stages of
biological incorporation of skin grafts.
8) Discuss the pathogenesis of neurospinal claudication.
9) Automatic Dysreflexia.
10)Control of air quality in a modern orthopaedic operation
theatre.
June 2006
Paper – II
1) Anterior Interosseous Nerve syndrome – Aetiology, clinical
features, differential diagnosis and management.
2) Dwyer’s osteotomy for CTEV – Indications, steps and
complications.
3) Sprengel’s Deformity. Etio pathogenesis, clinical features and
management.
4) Coxa Plana – Clinical, Radiological features, Differential
diagnosis and principles of treatment.
5) Boutannaire deformity – etiology, pathomechanics and
management.
6) Ultrasonic Therapy – Physiological effects, clinical
applications and contraindications.
7) Quadriceps Paralysis Gait – pathomechanics, compensation
employed and corrective measures.
8) Suction Socket Prosthesis – principles, indications and
advantages over conventional prosthesis and main points in
its construction.
9) Bowing of Tibia in children – Causes, types and management
of Congenital Bowing
10)Equinus Deformity in cerebral palsy – Etiopathogenesis,
evaluation and treatment.
June 2006
Paper – III
1) Fracture Talus.
2) Bennet’s Fracture dislocation
3) Hangman’s Fracture.
4) Motor March
5) Principles of Tendon Transfer.
6) Anterior Cruciate Ligament Injury.
7) Acromio clavicular Disruption
8) Lateral Condyle fracture of Humerus
9) Perilunar Dislocation.
10)Fracture Disease.
June 2006 Paper – IV
1) Etiopathogenesis, Pathology and management of DIC.
2) Congenital postural deformities associated with in-utero
position.
3) Raloxifene.
4) Biomechanics of Knee in relation to total knee replacement.
5) Structure and Biochemistry of articular cartilage.
6) Bryant’s Traction.
7) Biochemical markers of Bone formation and resorption.
8) Describe pathological Anatomy and radiology in CTEV.
9) Stewart and Harnaley ankle arthrodesis.
10)Enumerate various deformities of foot and ankle seen in Post
Polio Residual Paralysis (PPRP). Describe in detail the
management of Talipes Calcaneus
Dec. 2005 Paper – I
1) Define entrapment syndrome. Enumerate various entrapment
syndromes. Discuss the entrapment syndrome in relation to
the ulnar nerve in detail.
2) Bony changes in hyperparathyroidism and
hypoparathyroidism along with relevant pathophysiology.
3) Sports related injuries to soft tissues.
4) Suture Materials.
5) Finger Injuries.
6) Enumerate various classical levels of lower limb amputations.
Discuss AK amputation in detail. What is the difference in
energy consumption by the patient in AK amputation as
compared to a BK amputation?
7) Respiratory Distress Syndrome.
Cool Intravenous Regional Anaesthesia in orthopedic practice.
9) Day Care Surgery.
10)Surgical audit.
Dec. 2005 Paper – II
1) Congenital vertical Talus – Etiology, Pathology , clinical,
radiological features and management.
2) Chiari Osteotomy – indications, advantages, steps of surgery.
3) Claw Hand – Etiology, patho-mechanics,principles of various
corrective procedures.
4) Bowing of Tibia in children – Causes, types, clinical features &
management of congenital bowing of tibia.
5) Klippel-Fiel syndrome – Etiology, Pathology , clinical &
radiological features, differential diagnosis & management.
6) Microwave Diathermy – its physiogical effects, clinical
applications & contraindications.
7) Describe various types of Crutches ; gait pattern with crutches.
Cool Skew Flap Amputation – indications, advantages of
conventional amputation,steps of operation and complications.
9) Post – polio equinus deformity of foot – etiopathology,
evaluation & management.
10)Floor reaction Orthosis – indications, principles and advantages.
Dec. 2005 Paper – III
1) Enumerate the types of spinal cord lesions following fracture
dislocation of C5-6 vertebrae and discuss clinical features,
treatment and prognosis of each type of lesion in adult. 25 marks
2) Describe the following in brief 15 marks each
i) Treatment of fractures of distal end of radius.
ii) Management of fracture of fracture shaft of femur that
has become infected after intramedullary fixation
iii) Treatment of radial head and neck fractures in children
iv) Management of Trochnanteric fractures in elderly.
v) Principles of management of Lisfranc injuries of foot.
Dec. 2005 Paper – IV
1) Massive Transfusion.
2) Harmon’s approach of Tibia with applied Anatomy .
3) Strength – Duration Curve.
4) Biomechanics of hip joint and its clinical applications.
5) Radionuclide bone scanning
6) Allopurinol
7) Tension band principle and its application in treatment of
fractures using a wire and plate.
Cool Pathology of tuberculous arthritis and correlation with clinical
staging.
9) Growth plate - Anatomy and pathological states affecting it.
10) Radiological and biochemical features of renal osteodystrophy and
their interpretation.
June 2005 Paper – I
Part A
1) Draw a flow chart of disaster planning at state level. What is the
concept of triage?
2) Pathology , clinical features and management of diabetic foot.
3) Nosocomial infection on orthopaedics – common organism and
preventive measures.
4) Post operative DVT – Prevention, clinical features and treatment.
5) Post Menopausal Osteoporosis – Prevention and management.
Part B
1) Crystal Synovitis.
2) Incoporation of Bone Grafts. How does it differ for cancellous and
cortical grafts?
3) Preparation and precautions required to operate HIV positive
patients.
4) Chemotherapy for osteosarcoma.
5) How does a neurological claudication differ from vascular
claudication? Enumerate the etiology of the two.
June 2005 Paper – II
Part A
1) Clinical features and management of slipped capital femoral
epiphysis.
2) Ewing’s Sarcoma
3) Pollicisation – Indications and prerequisites
4) What are parts of a shoe? Describe the modifications of a CTEV
shoe.
5) What is modified Jone’s transfer for a high radial nerve palsy?
How does it differ from original transfer?
Part B
1) Pylon prosthesis – Indications, prerequisites and advantages.
2) Botulin in cerebral palsy patients.
3) PTB prosthesis – Indications and principles.
4) Radial club hand.
5) Salter osteotomy for DDH.
June 2005 Paper – III
1) Describe the biology of fracture healing and the influence of intra
medullary rods and plates in healing. Discuss the role of various
modalities in stimulation of osteogenesis
(25 marks)
2) Describe in brief on the following (15 marks each)
i) Treatment of odontoid fracture in adults.
ii) Enumerate the complications of femoral neck fractures in
children and discuss the management in any one of the
complications.
iii) Classification and treatment of acromioclavicular dislocation.
iv) Stress, Strain, Modulus of elasticity and strength in relation
to metallic implants.
v) Rotator cuff injury in sportsmen.
June 2005 Paper – IV
Part A
1) Trendelenberg test with its anatomical basis and clinical
applications
2) Madura foot.
3) Synovial fluid and its analysis in various arthritis
4) Blood supply of head of femur and its clinical significance.
5) Morbid Anatomy , radiological and laboratory features of Multiple
Myeloma
Part B
1) Thompsons approach of radius with applied Anatomy .
2) Paralytic Bladder.
3) Methotrexae as a DMARD.
4) Therapeutic ultrasound.
5) Prophylaxis in thrombo-embolic disease.
Dec. 2004 Paper – I
1) Describe etiopathogenesis of thoracic outlet syndrome and its
management
2) Short notes on
i) Shock
ii) Haemophiliac arthropathy
iii) Compartment syndrome
iv) Ehler-Danlos syndrome
v) Acute rupture of Achilles Tendon
Dec. 2004 Paper – II
1) Discuss etiology, pathogenesis and management of Perthe’s
disease.
2) Write short notes on
i) Principles of amputation of lower limb in children
ii) Dupuytren’s contracture
iii) Carpal Tunnel Syndrome
v) Nuclear Imaging.
iv) F.R.O.
Dec. 2004 Paper – III
1) Classify pelvic fractures and discuss the management.
2) Write short notes on
i) Fracture Talus
ii) Calcaneovalgus Deformity
iii) Myositis Ossificans
iv) Biomechanics of Hip
v) Habitual Dislocation of Patella
Dec.2004 Paper – IV
1) Describe calcium metabolism. Discuss the etiology, clinical
features, diagnosis and management of nutritional rickets.
2) Write short notes on
i) Arches of foot
ii) Core decompression
iii) Bone graft substitutes
iv) Pathology of osteoarthritis
v) Sudeck’s osteodystrophy
June 2004 Paper – I
1) Osteoporosis – Definition, Etiology, Clinical features,
Investigations, Prevention and Treatment.
2) Short notes on
i) Surgery for habitual dislocation of patella
ii) Triple arthrodesis for equinus
iii) Shoe modification for valgoid tilt
iv) Fascio-cutaneous skin graft
v) Ideal stump
June 2004 Paper – II
1) Discuss the merits & demerits of operative & non-operative
treatment of simple diaphyseal fracture of tibia.
2) Short notes on
i) Bristow’s procedure
ii) Classification of Distal Radius fracture
iii) Classification of Rotatory knee instability
iv) Management of Pelvic fractures
v) Old metacarpo phalangeal dislocation
June 2004 Paper – III
1) Discuss mechanism & classification of injury around ankle joint.
Discuss diagnosis and treatment.
2) Short notes on
i) Discuss Pathology & management of infected non-union.
ii) Fracture Neck of Femur – Classification and treatment
iii) Compression & Distraction in Orthopaedics
iv) Role of Ligamentotaxis in fractures
v) Tension band wiring principle.
June 2004 Paper – IV
1) Describe bone tumour. Classification, diagnosis and treatment
modalities for Multiple Myeloma.
2) Short notes on
i) Bone Cement
ii) Intrinsic Hand
iii) Shoulder Hand Syndrome
iv) Gait Cycle
v) Osteoclast.
Dec. 2003 Paper I
1) Define Gangrene. Describe the aetiological classification & Mx
of gas gangerene?
2) Short Notes on :
i) Skin grafting
ii) Madura foot
iii) Mortons metatarsalgia
iv) DVT
v) Ewings tumour
Dec. 2003 Paper II
1. Management of ankle fractures in children
2. Pathophysiology & presentation of TB spine in children
3. Juvenile Chronic arthritis - DD & investigations
4. Osteochondritis dessicans
5. Congenital amputations of lower limb in children
6. Haemophilia knee
7. Compound palmar ganglia
8. Ulnar claw hand
9. Pes planus
10. Mono ostotoc fibrous dysplasia
Dec. 2003 Paper III
1) Recent advances in the management of intraarticular
fractures of upper end of tibia
2) Short notes on :
i) Rationale of surgical treatment of recurrent dislocation of
shoulder
ii) Hangmans fracture
iii) Calcaneum fracture
iv) Orthopaedic complications of high dose steroid
v) Sudeks Osteodystrophy
Dec.2003 Paper IV
1) Describe the mechanism of calcium homeostasis by parathyroid
hormone and the skeletal changes that occur as a result of
hyperparathyroidism. Discuss the uses and limitations of lab
investigations in the diagnosis of primary hyperparathyroidism
2) Short notes on :
i) BMP
ii) 2nd line of ATT
iii) Acute ankle sprain
iv) Growth plate & its functions
v) Stress, strain & modulus of elasticity in relationship to
implants.
Dec. 2002 Paper I
1) Aetiology, Pathology & Mx of Spinal canal stenosis
2) Short notes on :
i) Tension pneumpthorax
ii) Non specific synovitis
iii) Painful arc syndrome
iv) metastatic lesion of bone & tis management
v) Crush Syndrome
Dec. 2002 Paper II
1) Pathogenesis, Clinical features & management of Caries spine
in a child 10 yrs old
2) Short notes on :
i) Intrinsic muscles hand
ii) fibrous dysplasia
iii) Habittual dislocation patella
iv) LASER Therapy
v) Amputations in children
Dec. 2002 PAPER III
1) Management of fracture pelvis and their complications
2) Short notes on :
i) Cerebral diplegia? Line of Management?
ii) Multiple myelpma – Investigations & Management?
iii) Pes Planus –etiology & Management?
iv) Investigations of Pain in Hand?
v) Rationale of surgical Rx for recurrent anterior dislocation
shoulder?
Dec. 2002 Paper IV
1) Blood supply of head of femur in diff age groups?Management of
Idiopathic AVN of Femur?
2) Short notes on :
i) Osteogenesis imperfecta
ii) Cubitus Varus
iii) Renal Rickets
iv) Sudecks dystrophy
v) Neurogenic Bladder
June 2002 Paper I
1) Describe the various approaches to the spine
2) Short notes on :
i) Recurrent dislocation of patella
ii) Compression plating
iii) Hallux valgus
iv) Volkmans ischaemic contracture
v) Ewings sarcoma
June 2002 Paper II
1) Describe the management of claw hand
2) Short notes on :
i) CTEV
ii) Septic arthritis of hip in a child below 5 years and above
3years
iii) Epiphyseal injuries
iv) Principles of amputation in children
v) Calcaneovalgus foot
June 2002 PAPER III
1.Treatment of ununited fracture neck of femur
2.Treatment of intercondylar fracture of humerus
3.Investigation of collapse of a vertebra
4.Osteomalacia
5.Osteogenesis imperfecta
6.Post Polio Residual Paralysis
7.Diagnostic criteria of osteolytic lesion in upper end tibia
8.Pilon fracture
9.Brodies abscess
10. Costo clavicular syndrome
Paper IV
1) Describe the Anatomy of recurrent dislocation shoulder? Discuss
Management
2) Short notes on :
i) Ceramics In Orthopaedics
ii) Bone grafts
iii) Hyper parathyroidism
iv) Pigmented villonodular synovitis
v) Pes planus
2001 Paper I
1. OA Knee – pathophysiology. Discuss rationale of surgical
management of OA Knee
2. Short notes on :
i) Renal Rickets – Pathophysiology
ii) Thoracic Outlet Syndrome
iii) Hand to Knee gait in Polio
iv) Wallerian Degenration
v) Endotoxic Shock
2001 PaperII
1. Pathomechanics, Clincal features & Management of various
deformities in RA – hand?
2. Short notes on :
i) Pseudoarthrosis
ii) Neglected Cong. Talipes Equino varus
iii) Electromyography
iv) Osteochondromatosis
v) Suction socket prosthesis
2001 Paper III
1.Discuss the pathological alterations of femoral neck & head in
neglected & ununited femoral neck fractures
and their management?
2. Short notes on :
i) Traumatic paraplegia
ii) Fractures at the upper end of humerus
iii) Intercarpal instability
iv) Two level fracture of shaft of tibia
v) Fractures and dislocation of talus
2001 PAPER IV
1. Describe the development of vertebral column.Pathogenesis and
management of potts paraplegia. Discuss the treatment of resistant
cases?
2. Short notes on :
i) Biodegradable implants
ii) Rigid flat foot
iii) wrist drop
iv) Compartment Syndrome
v) Symes amputation
Saturday, February 20, 2010
The use of absorbable materials in
surgery is not new, as gut suture
was described in the writings of
Galen in the second century. However,
recent improvements in polymer
science have led to the development
of new orthopaedic implants
made of bioabsorbable materials.
The chief advantage of these implants
is that there is initial stability
adequate for healing and then gradual
resorption after biologic fixation
has been established. In addition,
these materials limit stress shielding
of bone, gradually apply load as
they degrade, obviate hardware
removal procedures, and facilitate
postoperative radiologic imaging.
Polymers made from lactic acid,
glycolic acid, and dioxanone, as
well as copolymers of these materials,
have been studied and are readily
available for clinical use as implants
for both bone and soft-tissue
fixation.
Basic Science of
Bioabsorbable Implants
By definition, bioabsorbable implants
are degraded in a biologic
environment, and their breakdown
products are incorporated into normal
cellular physiologic and biochemical
processes. These materials
must also be biocompatible, with
degradation products that are well
tolerated by the host with no immunogenic
or mutagenic tendency. In
addition, for musculoskeletal applications,
these materials must maintain
adequate strength and not degrade
too rapidly, so that fixation is not lost
before adequate healing can occur.
The perfect bioabsorbable material
for orthopaedic use would initially
have mechanical characteristics
equal to those of standard stainless
steel implants. It would degrade
with the healing process so that load
is gradually transferred to the healing
tissue. The currently available
polymers still do not have mechanical
characteristics equal to those of
metal implants1-3 (Table 1), but
improvements continue to be made,
particularly with the use of reinforcing
techniques.
Polymer Science
Most research on the clinical applications
of bioabsorbable materials
has focused on the use of polymers
known as alpha-polyesters or poly-
(alpha-hydroxy) acids. These include
polylactic acid (PLA), polyglycolic
acid (PGA), and polydioxanone
(PDS). Combinations of these
materials allow optimization of
Dr. Ciccone is in private practice in Colorado
Springs, Colo. Dr. Motz is in private practice in
San Diego, Calif. Dr. Bentley is in private practice
in San Diego. Dr. Tasto is Associate Clinical
Professor of Orthopaedics, University of
California, San Diego.
One or more of the authors or the departments
with which they are affiliated have received
something of value from a commercial or other
party related directly or indirectly to the subject
of this article.
Reprint requests: Dr. Tasto, San Diego Sports
Medicine & Orthopaedic Center, #200, 6719
Alvarado Road, San Diego, CA 92120.
Abstract
The use of bioabsorbable implants in orthopaedic surgical procedures is becoming
more frequent. Advances in polymer science have allowed the production of
implants with the mechanical strength necessary for such procedures.
Bioabsorbable materials have been utilized for the fixation of fractures as well as
for soft-tissue fixation. These implants offer the advantages of gradual load
transfer to the healing tissue, reduced need for hardware removal, and radiolucency,
which facilitates postoperative radiographic evaluation. Reported complications
with the use of these materials include sterile sinus tract formation,
osteolysis, synovitis, and hypertrophic fibrous encapsulation. Further study is
required to determine the clinical situations in which these materials are of most
benefit.
J Am Acad Orthop Surg 2001;9:280-288
Bioabsorbable Implants in Orthopaedics:
New Developments and Clinical Applications
William J. Ciccone II, MD, Cary Motz, MD, Christian Bentley, MD, and James P. Tasto, MD
Perspectives on Modern Orthopaedics
William J. Ciccone II, MD, et al
Vol 9, No 5, September/October 2001 281
their biomechanical properties for
specific clinical uses.
Polymers are composed of covalently
bonded subunits that form
large macromolecules.4 These repeating
subunits are referred to as
monomers. A polymer made of a single
repeating monomer is a homopolymer.
A combination of two or
more different monomers results in a
copolymer. The various monomeric
units in a copolymer may be arranged
randomly (random copolymer)
or in long regions of one subunit
alternating with another (block
copolymer). The biomechanical
and biochemical properties of a
copolymer differ from those of its
constituent monomers.5
The polymer chains that constitute
the implant may be linear,
branched, or cross-linked to neighboring
chains. The microstructural
organization of the chains may be
amorphous or crystalline, as determined
by the orientation of the polymer
chains. The overall crystallinity
of a polymer affects its biomechanical
and degradation proerties. These
properties can be influenced by the
manufacturing technique, with elevated
temperatures and a slow rate
of cooling allowing the polymeric
chains to align themselves in an
ordered solid structure.6 Most bioabsorbable
implants are made of
“semicrystalline” materials containing
both amorphous and crystalline
regions, each of which plays a role in
strength and absorption rates.5,7,8
Many of the physical properties
of a polymer are dependent on the
chemical composition, the molecular
weight, and the arrangement of
the polymer chains. Polymers utilized
in orthopaedics are viscoelastic
in nature; therefore, their physical
properties change with the rate
of load application and are timedependent.
Increased molecular
weight implies an increased intrinsic
viscosity within the polymer,
leading to less deformability (i.e.,
less flow) with an applied load. In
general, high- to average-molecularweight
polymers that are highly viscous
will undergo slower biodegradation
than those of lesser molecular
weight and viscosity.
The mechanical properties of a
polymer are further influenced by
temperature. The glass-transition
temperature (Tg) is the temperature
below which the polymer is stiff and
hard and above which it is soft and
rubbery. The Tg will vary with the
chemical composition of the polymer,
the molecular weight, and the
percentage of the polymer involved
in amorphous domains. As a polymeric
implant is able to withstand
more load at temperatures below its
Tg, most polymers utilized clinically
have a Tg above body temperature.
Lactic acid is a small, hydrophobic
three-carbon molecule that
plays an important role in cellular
energy production. Due to the asymmetry
of the molecule, it has both a
dextrorotatory (D) and a levorotatory
(L) configuration. The D-form is
readily produced, but the L-isomer
is the biologically active form. Polymerized
L-lactic acid is referred to as
poly-L-lactic acid (PLLA). The copolymer
with the D-form (poly-DLlactic
acid) is termed PDLLA. The
mechanical and degradation properties
of these two enantiomers differ
markedly, with PLLA being
highly crystalline and PDLLA being
more amorphous.1 The characteristics
of the copolymers are intermediate
between those of the two
monomers.
Polyglycolic acid is synthesized
by ring-opening polymerization
from glycolide. It is a hard, tough,
crystalline molecule that is more
hydrophilic in nature than PLA. Its
self-reinforced form is stiffer than
other clinically utilized polymers.2
Polyglycolic acid has been utilized
extensively in orthopaedic implants.
This polymer has more rapid degeneration
rates than PLA; there
have been more synovitic reactions
with this material, probably secondary
to its rapid degradation.9
Polydioxanone was first described
in 1981.3 This material is
manufactured by polymerizing the
monomer para-dioxanone. In its
natural state, PDS is a colorless crystalline
polymer; its purple hue is
obtained with the addition of violet
dye. The PDS suture is created by
the melt-extrusion of polymer granules
through the appropriate dyes.
The inherent stiffness of PDS suture
has made it invaluable in applications
in arthroscopic procedures, as
it goes easily through suture passers.
Degradation
The degradation of bioabsorbable
implants follows a predictable
pattern. The rate of degradation is
dependent on the starting molecular
weight of the polymer and its crys-
Table 1
Mechanical Properties of Various Bioabsorbable Implant Materials1-3
Bending Bending Shear
Diameter, Modulus, Strength, Strength,
Implant Material mm GPa MPa MPa
Stainless steel (for comparison) … 200 280 …
Self-reinforced polyglycolic acid 2 13 320 240
Injection-molded polyglycolic acid 2 7 218 95
Self-reinforced poly-L-lactic acid 1.3 10 300 220
Injection-molded poly-L-lactic acid 2 3 119 68
Polydioxanone (suture) … … … 48
Bioabsorbable Implants
tallinity, the composition and porosity
of the implant, and other factors,
such as loading conditions and local
vascularity. In the degradation process,
there is first a loss in molecular
weight, followed by loss of strength
and finally loss of mass. The early
phase of degradation is chemical in
nature. Biologic processing and removal
of the implant occur later.10-12
Because of this pattern of degradation,
these materials lose functional
strength long before they are completely
absorbed.
The initial phase of degradation
is one of hydrolysis. Water molecules
enter the implanted material,
causing cleavage of the monomeric
molecular bonds. This leads to the
scission of long polymer chains into
shorter chains, reducing the overall
molecular weight. This process is
affected by implant porosity.13,14
Low porosity enhances autocatalysis
of the implant because the slow
clearance of degradation products
from within the material leads to
increased acidity and more rapid
molecular scission. The molecular
weight plays an important role in
the internal friction within the implant,
and thus its mechanical properties;
hydrolysis of these long
chains leads to a loss in mechanical
strength. As a result, implants with
low porosity may have a shortened
functional life.
As the implant loses integrity and
fragments, biologic removal of the
implant takes place. The rapid degradation
of these implants has been
postulated to be the cause of marked
foreign-body reactions, synovitis,
and even activation of the complement
cascade.8,15-17 Studies evaluating
the tissue response to PGA and
PLLA implants have shown foreignbody
reactions to the degradation
products. The degradation of PLLA
has been associated with a foreignbody
reaction as late as 143 weeks
after implantation.12 A foreign-body
response reaction to PGA has been
seen as early as 3 to 6 weeks.11 Differences
in the timing of the cellular
response to these materials are
probably secondary to the different
rates of degradation of PGA and
PLLA. Clinically, most symptomatic
foreign-body reactions have
been associated with the more
rapidly degrading PGA,9,18 but reactions
to PLLA have also been described.
19 The rates of degradation
of these materials can be optimized
for biologic fixation by changing the
copolymer ratios of PGA and PLLA.5
The most common soft-tissue
complications related to use of these
materials are sterile sinus tract formation,
hypertrophic fibrous encapsulation,
and osteolysis. These inflammatory
responses occur in
fewer than 10% of patients, but may
be severe enough to require surgery
for resolution of the reaction.16
Biochemical Degradative Pathway
Alpha polyesters, such as PLA,
PGA, and PDS, primarily degrade
by hydrolysis, with the release of
their respective monomers. The
monomers are then incorporated
into normal cellular physiologic
processes for further degradation.
Lactic acid, glycolic acid, and paradioxanone
have well-defined biochemical
pathways that lead eventually
to their excretion in the form of
carbon dioxide and water7,20 (Fig. 1).
Lactic acid is produced by the
hydrolytic degradation of PLA.
Lactic acid is normally produced at
the end of the glycolytic pathway
from pyruvate when the amount of
oxygen is limiting. The oxidation of
lactate to form pyruvate is catalyzed
by lactate dehydrogenase. In aerobic
conditions, pyruvate undergoes
oxidative decarboxylation to produce
acetyl coenzyme A. This molecule
may then enter the citric acid
cycle for further oxidation to produce
carbon dioxide, water, and
adenosine triphosphate by oxidative
phosphorylation.
Degradation of PGA and PDS
follows nearly the same pathway.
Hydrolysis of PGA produces glycolic
acid, which is either excreted
directly in the urine or converted to
glyoxylate. The PDS degradation
products enter the pathway at glyoxylate.
The amino acid glycine can
be produced from glyoxylate by a
transamination reaction. Glycine, a
glucogenic amino acid, can be further
converted to pyruvate through
a serine intermediate. Pyruvate is
then converted to acetyl coenzyme
A to enter the citric acid cycle, as
previously discussed.
Mechanical Properties
The mechanical properties of
bioabsorbable orthopaedic implants
must be considered both at the time
of insertion and throughout degradation.
The implants are initially subjected
to considerable loads, which
gradually decrease with tissue healing.
The perfect implant will de-
Figure 1 Biochemical degradation pathways
for PLA, PDS, and PGA.
Acetyl coenzyme A
CO2
H2O
Glycine Urine
Serine
Glycolic
acid
PLA PDS PGA
Citric acid cycle
Pyruvate
Lactic acid Glyoxylate
William J. Ciccone II, MD, et al
Vol 9, No 5, September/October 2001 283
grade at a rate that gradually transfers
load to healing tissue and does
not outpace the healing response.
Factors that affect the mechanical
properties of an implant include the
type of material, its processing, and
the local testing environment.21
Bioabsorbable polymers differ from
common stainless steel implants in
that they are more viscoelastic in
nature. Therefore, they exhibit enhanced
properties of creep and
stress relaxation. Claes21 exhibited
the importance of this property by
demonstrating that when used in
the form of an interfragmentary
screw, bioabsorbable polymers lost
20% of their force 20 minutes after
application, due to stress relaxation.
Reinforcing techniques have been
developed to improve the mechanical
characteristics of bioabsorbable
implants. Self-reinforced absorbable
components are polymeric materials
in which the reinforcing elements
and matrix material have the same
chemical composition. The most
effective way to manufacture the
self-reinforced structure into the
polymer is by the mechanical deformation
of the nonreinforced material.
7 This deformation process leads
to the formation of oriented polymeric
chains, the self-reinforcing
structures.
The reported properties of these
implants vary, due mostly to differences
in processing and testing conditions.
Overall, the self-reinforced
materials show an improvement in
their initial mechanical values compared
with the nonreinforced polymers
(Table 1). The initial bending
strength of self-reinforced PGA
exceeds that of stainless steel; however,
with rapid rates of degradation,
this strength is not maintained. In
general, the mechanical properties of
these polymeric implants do not
approach those of standard stainless
steel implants. While rapid loss of
the mechanical properties might be
expected to allow excessive motion
between fracture fragments, these
materials have been used successfully
in specific clinical situations.
Mechanical degradation studies
have been performed in both in
vivo and in vitro conditions. The
most important determinant of the
rate of degradation is the material
itself, but the environment surrounding
the implantation site can
also be an influence. There is evidence
that degradation rates are
more rapid with in vivo testing secondary
to enzymatic contributions.1
Areas of high tissue metabolism and
blood flow facilitate material degradation.
Furthermore, implants under
load tend to degrade faster, possibly
secondary to microfracture.
The mechanical degradation rate
of PDS suture has been studied by
Ray et al.3 The breaking strength of
PDS suture was tested after being
implanted in the subcutaneous
tissue of rats. The PDS suture retained
74% of its nonimplanted
strength at 2 weeks, but by 6 and 8
weeks that value had dropped to
41% and 14%, respectively. The
authors also determined, with the
use of radioactive labeling, that the
material absorption was complete
by 182 days after implantation.
Likewise, PGA materials lose their
mechanical strength by 6 to 8
weeks. The loss of the mechanical
properties of this material occurs at
varying rates, with the loss of shear
strength being slower than loss of
bending strength. In self-reinforced
materials, the matrix material loses
its strength more rapidly than the reinforcing
elements. Therefore, these
materials may be more suited for
the fixation of fractures involving
periarticular cancellous bone, where
high shear loads are common.
Clinical Applications
The use of bioabsorbable fixation for
the attachment of soft tissue to bone
is being increasingly utilized by
orthopaedic surgeons, especially in
the treatment of soft-tissue lesions in
the shoulder. These implants have
facilitated the repair and reconstruction
of labral and rotator cuff lesions.
The development of bioabsorbable
tacks, suture anchors, and screwand-
washer implants has given surgeons
more treatment alternatives
(Fig. 2).
Bioabsorbable suture anchors are
useful as an alternative to metal staples
and screws, which may have a
high profile. They also eliminate the
need for passing sutures through
bone tunnels. Pullout strengths for
bioabsorbable suture anchors are
comparable to those of their metallic
counterparts.22 These implants have
sufficient strength that the point of
failure is the suture–soft-tissue interface.
23
The complications observed with
the use of bioabsorbable suture
anchors are similar to those seen
with metallic anchors. Improper
insertion of the anchor too deep in
the bone can cause suture fraying or
failure. Superficial insertion of the
anchor can lead to cartilage wear on
the opposing articular surface. The
anchor can also fail by pullout from
bone and become an intra-articular
loose body. As these implants are
radiolucent, this diagnosis can be
difficult to make postoperatively in
a persistently painful joint. Unique
to bioabsorbable anchors is the potential
for eyelet failure with secondary
suture cutout.
Bioabsorbable suture anchor fixation
has several advantages. The
anchor undergoes reabsorption and
therefore reduces the need for removal
of a prominent implant. Resorption
also makes revision surgery
less complicated, as hardware
removal is not necessary. The fixation
does not obscure the anatomy
as depicted on radiographs and is
compatible with magnetic resonance
imaging if further evaluation
of the affected joint is necessary.
Improperly placed anchors may
simply be drilled out rather than
Bioabsorbable Implants
284 Journal of the American Academy of Orthopaedic Surgeons
unscrewed or pushed through, as is
necessary with metallic anchors.
Finally, stress is gradually transferred
to the healing soft tissue as
the anchor degrades.
Repair of Shoulder Lesions
The effectiveness of bioabsorbable
anchors for use in Bankart repairs,
as well as in treatment of rotator
cuff tears and “SLAP” lesions
(i.e., anterior-to-posterior lesions of
the superior labrum), is currently
under investigation. Warme et al24
compared the usefulness of bioabsorbable
and nonabsorbable suture
anchors in a prospective randomized
study of open Bankart repairs. At
an average follow-up interval of 25
months, there was one failure in the
18 patients treated with nonabsorbable
anchors, compared with two
failures in 20 patients treated with
absorbable anchors. Radiographs
obtained at the 2-year follow-up in
the absorbable group demonstrated
near-complete implant degradation
and osseous replacement. At 6
months, the anchor holes used for
nonabsorbable implants demonstrated
a sclerotic rim but no increase
in size from the measurements
on the initial postoperative
radiographs. There was no subsequent
radiographic change after that.
It must be noted that no reports of
complications attributable to the bioabsorbable
nature of these suture
anchors have been published.
The use of bioabsorbable tacks for
the repair of labral lesions has made
arthroscopic management of these
injuries technically less complicated.
The development of labral tacks,
such as Suretac (Smith&Nephew,
Andover, Mass), TissueTack (Arthrex,
Naples, Fla), ConTack (Mitek,
Westwood, Mass), and the Contour
Labral Nail (Bionx Implants, Blue
Bell, Pa), has led to the ability to
treat more patients with Bankart and
SLAP injuries arthroscopically. These
tacks are cannulated for ease of
insertion and allow the labrum to be
reattached to the glenoid in an anatomic
position. These devices eliminate
the risks of metal around joint
surfaces, do not require transglenoid
drilling or an accessory posterior
incision, and avoid technically difficult
arthroscopic knot tying.
The first absorbable tack was
constructed of PGA, which rapidly
loses strength over the first 4 to 6
weeks. Complete reabsorption occurs
in approximately 6 months.
This implant has been implicated in
several cases of aseptic synovitis
secondary to a histiocytic or phagocytic
reaction to the rapidly degrading
polymer.9 Currently, most tacks
are composed of longer-absorbing
materials such as PDLA, PLLA, or
composites, which may reduce the
rate of synovitis.
Warner et al25 reported on a
cohort of 15 patients who underwent
“second look” arthroscopy for a
failed arthroscopic Bankart repair
performed with the Suretac device.
These patients were a subgroup of 96
patients initially treated for posttraumatic
recurrent anterior dislocation
or subluxation. The repeat procedure
was necessitated by recurrent
instability in 7 patients, pain in 6,
and pain with stiffness in 2. When
reevaluated, the failure in the patients
with instability was considered
to be secondary to inadequate reconstruction
of either the anterior glenohumeral
ligaments or the anterior
labral complex. The cause of failure
in the 8 patients with either pain or
pain and stiffness was less clear, although
an indolent inflammatory
response to the PGA polymer was
found in several. Six of the patients
eventually had complete or partial
pain relief after a second arthroscopy
and subacromial decompression, biceps
tenodesis, or a capsular release
or manipulation.
Bioabsorbable fixation devices
are now also being used for the
repair of rotator cuff tears. These
procedures were initially performed
with suture anchors, but more re-
Figure 2 Currently available bioabsorbable implants for fracture fixation, interference fixation,
and meniscal repair.
William J. Ciccone II, MD, et al
Vol 9, No 5, September/October 2001 285
cently screw-and-washer–type devices
have become available. The
rationale behind the use of these
soft-tissue screws is to repair the
tendon to bone without a suture,
reducing the incidence of complications
at the tendon-suture interface
and increasing the surface area of
tendon contact with bone. These
devices (Bio-Headed Corkscrew,
Arthrex; Biocuff Screw, Bionx; Biotwist,
Linvatec, Naples, Fla) all
employ a screw-in device with a
large head for soft-tissue compression.
The Biocuff screw has an independent
spiked washer to prevent
tendon damage and reduce pressure
necrosis. No clinical studies on the
use of these devices are yet available.
Meniscal Repair
The “all inside” technique of meniscal
repair described by Morgan
was developed to safely repair the
posterior and central peripheral
portions of the meniscus, a location
difficult to reach with traditional
arthroscopic techniques because of
the risk of neurovascular injury.
The use of bioabsorbable implants
for use in all-inside meniscal repair
has now been described.26 These
devices eliminate the need for a posterior
incision, reduce the risk of
neurovascular injury, and simplify
the fixation procedure.
The Bionx Meniscal Arrow is a
well-characterized bioabsorbable implant
that has been approved by the
US Food and Drug Administration
for meniscal repair. It is a T-shaped
device composed of self-reinforced
PLLA with a 1.1-mm-diameter barbed
stem. The stem penetrates the meniscus
and capsule, and the bar portion
approximates the torn meniscal leaf
to the periphery. The arrows remain
in the joint for approximately 1 year
and are gradually absorbed through
hydrolysis to carbon dioxide and
water.
Biomechanical data reported by
Boenisch et al27 compared the pullout
strength and linear stiffness of
meniscal repair performed with
bioabsorbable arrows and vertical
and horizontal looped sutures in bovine
menisci. The pullout strengths
in both suture groups were significantly
(P<0.05) higher than those in
the arrow-fixation group. Further,
vertical-suture fixation was significantly
stiffer than fixation with
either horizontal sutures or arrows.
However, more recent data from another
bovine study28 demonstrated
no difference between the pullout
strength of the arrow and that of a
vertical PDS suture when the arrow
was inserted with a mechanical “gun.”
In fact, significantly greater pullout
strength for arrow fixation was noted
at 12 and 24 weeks compared with
PDS-based implants. Technical considerations
of insertion, such as keeping
the arrow parallel to the joint surface
and maximizing the number of
barbs engaging beyond the tear, have
been demonstrated to be essential to
the integrity of the repair.
Albrecht-Olsen et al29 performed
a randomized prospective study
comparing meniscal repair utilizing
the bioabsorbable meniscal arrow
implant to inside-out repair with
horizontal meniscal sutures. Sixtyeight
patients were divided evenly
between the two groups. Repairs
were performed only in red-red or
red-white zones, and rehabilitation
protocols were standardized. In all,
65 patients (96%) underwent repeat
arthroscopy at 3 to 4 months. A
healed meniscus was observed in
91% of the arrow repair group but
in only 75% of those in the suture
group. There were no complications
reported in the group with
bioabsorbable fixation. The operative
time for the procedures averaged
30 minutes for repair with the
arrow and 60 minutes for suture repair.
The advantages of decreased
operative time, ease of insertion,
and improved meniscal healing
with an all-inside meniscal repair
with a bioabsorbable implant were
confirmed by this study.
Complications with the Bionx
Arrow have been published in several
case reports.30-34 These include
hematoma formation, subcutaneous
migration, foreign-body reaction,
and loss of fixation. The use of
these newly developed implants
appears to be simple. However,
attention to technical detail in terms
of placement, choice of length, and
orientation is required to avoid
complications and ensure optimal
fixation.
Anterior Cruciate Ligament
Reconstruction
Graft fixation devices for anterior
cruciate ligament reconstruction
have been manufactured in the past
from nonabsorbable materials such
as metal and plastic. These devices
are often difficult to remove or
avoid if revision anterior cruciate
ligament reconstruction is required.
Furthermore, the evaluation of softtissue
lesions with MR imaging
after the use of metal fixation is difficult.
Additionally, aperture fixation
(soft-tissue fixation at the joint
line), which provides a stiffer construct,
is hampered by concerns
about graft severance by metal
interference screws. Use of bioabsorbable
fixation devices, such as
interference screws, can potentially
eliminate some of these problems.
Several different types of screws,
which vary in polymeric composition,
are currently available. Graft
fixation strength in anterior cruciate
ligament reconstruction is critical in
the period from initial fixation to osseous
integration of the graft. This period
ranges from 6 weeks for bone–
patellar tendon–bone fixation to
approximately 12 to 16 weeks for
hamstring fixation. Therefore, the
bioabsorbable interference screw
must maintain virtually all of its
structural integrity during that
entire interval. The initial pullout
strengths of these implants should
exceed the estimated 500-N load for
activities of daily living. For this
Bioabsorbable Implants
286 Journal of the American Academy of Orthopaedic Surgeons
reason, most screws on the market
are manufactured from PLLA or a
variant copolymer with a longer
half-life (Fig. 3). This composition
can lead to delayed osseous integration,
thus negating the main benefit
of the bioabsorbable fixation.
No consensus is supported by
the results of recent biomechanical
studies. Pena et al35 published data
on the insertion torques and fixation
strengths of bone–patellar tendon–
bone grafts fixed with PLA interference
screws (Bioscrew, Linvatec,
Key Largo, Fla) and compared them
with metal interference screws in
cadaveric specimens from young
and middle-aged individuals. With
use of a correction factor for bonemineral
density, the pullout forces
were 730 N for the metal screws and
668 N for the PLA screws. The insertion
torque was 1.52 N for the
metal screws and 0.30 N for the bioabsorbable
screws. Both pullout
force and insertion torque were significantly
(P>0.05) higher for metal
interference fixation. The authors
noted that loss of tensile strength of
bioabsorbable screws is possible
with excessive time in storage due to
hydrolysis or wetting the implant
before insertion.
Caborn et al36 have published the
results of a biomechanical comparison
of metal and bioabsorbable interference
screw fixation of quadrupled
semitendinosus-gracilis grafts. No
statistically significant difference was
found in the maximum load at pullout,
nor did the screw insertional
torques correlate with the maximum
load at pullout. However, a followup
study in which the bone tunnels
were specifically sized within 5 mm
of the graft diameter showed that the
bioabsorbable screw-insertion torque
correlated directly with ultimate
graft failure strength.37 Therefore, it
appears that bioabsorbable interference
screw fixation is not appropriate
for all patients, especially those
with poor bone quality. Careful
graft preparation and sizing can,
however, result in interference fixation
capable of withstanding the
forces of accelerated rehabilitation.
A recent prospective, randomized
study by McGuire et al38 compared
the Linvatec Bioscrew with metal
interference screws in 204 patients.
A variety of graft sources were used,
including autogenous and allograft
bone and patellar tendon and allograft
Achilles tendon. The average
follow-up interval was 2.4 years,
and the mean age of patients was 30
years. A standardized rehabilitation
protocol was used. No statistically
significant difference was noted in
the Lysholm or Tegner score, pain,
thigh size, Lachman test result, pivot
shift, patellofemoral crepitus, or
joint effusion. There was no statistically
significant difference in mean
maximum manual side-to-side KT-
1000 rating between the 1.8-mm bioabsorbable
screw and the 1.6-mm
metal screw. Twelve PLLA screws
broke during insertion without adverse
effects. There were no reported
complications related to loss of fixation,
toxicity, allergenicity, or osteolysis.
Excellent clinical results are possible
with bioabsorbable interference
screws, although there is no
consensus opinion as to whether
biomechanical strength is the same
between metal and bioabsorbable
screw fixation. Disadvantages of
bioabsorbable interference screws
include concerns about sterile
drainage, cyst formation, lack of
complete osseous ingrowth into the
defect, early loss of pullout strength
secondary to hydrolysis, and intraoperative
breakage of the device.
The reported rate of these clinical
complications is low and has not
resulted in a clinically significant
difference in outcome studies published
to date.
Fracture Fixation
Although bioabsorbable fracturefixation
devices appear to have obvious
advantages over metal implants,
concerns about the initial fixation
strength of these materials have limited
their widespread acceptance.
These materials must have the initial
fixation strength necessary to maintain
the reduction of bone fragments
during the healing process. Manufacturing
techniques are critical, as
melt-molded polymers do not possess
the strength necessary for reliable
fixation, whereas self-reinforced
materials have the mechanical characteristics
more suitable for this use.
In a review of more than 2,500
fracture-fixation cases in which bioabsorbable
implants were used,
Rokkanen et al39 reported that the
incidence of bacterial wound infection
was 3.6%; nonspecific foreignbody
reaction, 2.3%; and failure of
fixation, 3.7%. Compared with
metallic fixation, absorbable fixation
has shown a lower incidence of
infection.40
Bucholz et al41 performed a prospective
randomized trial comparing
PLA screws with stainless steel
screws for fixation of displaced
medial malleolar fractures. They
found no statistically significant difference
in operative or postoperative
complications between the two
groups.
Figure 3 MR image obtained 24 months
after interference fixation of hamstring
autografts with bioabsorbable PLLA
screws shows minimal degradation.
William J. Ciccone II, MD, et al
Vol 9, No 5, September/October 2001 287
Foreign-body reactions to PGA
have been described,9,18,39 but neither
Rokannen et al39 nor Bucholz et
al41 reported late reactions to PLA
screws. However, a recent case report
described an osteolytic reaction
to an intraosseous PLA screw 52
months after the operative procedure.
19 Longer-term follow-up may
be necessary to determine the actual
clinical biocompatibility of intraosseous
PLA.
The use of bioabsorbable implants
for pediatric fracture fixation
is particularly appealing because it
obviates implant removal. In experimental
studies, the presence of
an absorbable implant does not
seem to interfere with the growth
plate any more than an empty drill
hole does.42 Biodegradable implants
have shown satisfactory results,
especially in the treatment of distal
humeral physeal fractures.43-45
Böstman et al43 evaluated the use
of absorbable self-reinforced PGA
pins in the treatment of 71 physeal
and nonphyseal fractures in skeletally
immature patients, with a mean
follow-up interval of 15.8 months.
Anatomic reduction was maintained
until union in 87% of the fractures,
but in only 8 of 14 supracondylar
humerus fractures. The authors felt
that the displacement forces encountered
in supracondylar fractures
overwhelmed the mechanical properties
of the absorbable pins, resulting
in displacement. They concluded
that the preliminary results of fracture
treatment with self-reinforced
PGA were satisfactory except for
supracondylar humerus fractures.
Long-term clinical studies are still
required to determine the effects of
these implants on the growth plate.
Summary
The use of bioabsorbable implants in
musculoskeletal procedures is gaining
acceptance. While most commonly
utilized in the field of sports
medicine for soft-tissue fixation,
these implants may have applications
in other aspects of orthopaedics.
Complications associated with
the use of these materials have diminished
with the development of
newer, self-reinforced polymers.
Until more long-term, peer-reviewed
research becomes available, the
appropriate clinical usage of these
implants remains a concern for the
practicing orthopaedist.
References
1. Daniels AU, Chang MKO, Andriano
KP: Mechanical properties of biodegradable
polymers and composites
proposed for internal fixation of bone.
J Appl Biomater 1990;1:57-78.
2. Törmälä P: Biodegradable self-reinforced
composite materials: Manufacturing
structure and mechanical properties.
Clin Mater 1992;10:29-34.
3. Ray JA, Doddi N, Regula D, Williams
JA, Melveger A: Polydioxanone (PDS),
a novel monofilament synthetic absorbable
suture. Surg Gynecol Obstet 1981;
153:497-507.
4. Pietrzak WS, Sarver DR, Verstynen ML:
Bioabsorbable polymer science for the
practicing surgeon. J Craniofac Surg
1997;8:87-91.
5. Miller RA, Brady JM, Cutright DE:
Degradation rates of oral resorbable
implants (polylactates and polyglycolates):
Rate modification with changes
in PLA/PGA copolymer ratios. J
Biomed Mater Res 1977;11:711-719.
6. Athanasiou KA, Agrawal CM, Barber
FA, Burkhart SS: Orthopaedic applications
for PLA-PGA biodegradable
polymers. Arthroscopy 1998;14:726-737.
7. Hollinger JO, Battistone GC: Biodegradable
bone repair materials: Synthetic
polymers and ceramics. Clin
Orthop 1986;207:290-305.
8. Bergsma JE, de Bruijn WC, Rozema FR,
Bos RRM, Boering G: Late degradation
tissue response to poly(L-lactide) bone
plates and screws. Biomaterials 1995;
16:25-31.
9. Burkart A, Imhoff AB, Roscher E:
Foreign-body reaction to the bioabsorbable
Suretac device. Arthroscopy
2000;16:91-95.
10. Päivärinta U, Böstman O, Majola A,
Toivonen T, Törmälä P, Rokkanen P:
Intraosseous cellular response to biodegradable
fracture fixation screws
made of polyglycolide or polylactide.
Arch Orthop Trauma Surg 1993;112:71-74.
11. Koskikare K, Toivonen T, Rokkanen P:
Tissue response to bioabsorbable selfreinforced
polylevolactide and polyglycolide
pins implanted intra-articularly
and directly into the bone on different
levels: An experimental study on rats.
Arch Orthop Trauma Surg 1998;118:
149-155.
12. Bos RRM, Rozema FR, Boering G, et al:
Degradation of and tissue reaction to
biodegradable poly(L-lactide) for use as
internal fixation of fractures: A study in
rats. Biomaterials 1991;12:32-36.
13. Vert M, Mauduit J, Li S: Biodegradation
of PLA/GA polymers: Increasing complexity.
Biomaterials 1994;15:1209-1213.
14. Athanasiou KA, Schmitz JP, Agrawal
CM: The effects of porosity on in vitro
degradation of polylactic acid–polyglycolic
acid implants used in repair of
articular cartilage. Tissue Eng 1998;4:
53-63.
15. Tegnander A, Engebretsen L, Bergh K,
Eide E, Holen KJ, Iversen OJ: Activation
of the complement system and
adverse effects of biodegradable pins
of polylactic acid (Biofix) in osteochondritis
dissecans. Acta Orthop Scand
1994;65:472-475.
16. Böstman O, Hirvensalo E, Mäkinen J,
Rokkanen P: Foreign-body reactions to
fracture fixation implants of biodegradable
synthetic polymers. J Bone Joint
Surg Br 1990;72:592-596.
17. Bergsma EJ, Rozema FR, Bos RRM, de
Bruijn WC: Foreign body reactions to
resorbable poly(L-lactide) bone plates
and screws used for the fixation of
unstable zygomatic fractures. J Oral
Maxillofac Surg 1993;51:666-670.
18. Böstman OM: Osteolytic changes
accompanying degradation of absorbable
fracture fixation implants. J Bone
Joint Surg Br 1991;73:679-682.
19. Böstman OM, Pihlajamäki HK: Late
foreign-body reaction to an intraosseous
bioabsorbable polylactic acid
screw: A case report. J Bone Joint Surg
Am 1998;80:1791-1794.
Bioabsorbable Implants
288 Journal of the American Academy of Orthopaedic Surgeons
20. Brady JM, Cutright DE, Miller RA,
Battistone GC, Hunsuck EE: Resorption
rate, route of elimination, and ultrastructure
of the implant site of polylactic
acid in the abdominal wall of the rat.
J Biomed Mater Res 1973;7:155-166.
21. Claes LE: Mechanical characterization
of biodegradable implants. Clin Mater
1992;10:41-46.
22. Barber FA, Herbert MA: Suture anchors:
Update 1999. Arthroscopy 1999;
15:719-725.
23. Burkhart SS, Diaz Pagàn JL, Wirth MA,
Athanasiou KA: Cyclic loading of
anchor-based rotator cuff repairs: Confirmation
of the tension overload phenomenon
and comparison of suture
anchor fixation with transosseous fixation.
Arthroscopy 1997;13:720-724.
24. Warme WJ, Arciero RA, Savoie FH III,
Uhorchak JM, Walton M: Nonabsorbable
versus absorbable suture anchors
for open Bankart repair: A prospective,
randomized comparison. Am J
Sports Med 1999;27:742-746.
25. Warner JJP, Miller MD, Marks P, Fu
FH: Arthroscopic Bankart repair with
the Suretac device: Part I. Clinical observations.
Arthroscopy 1995;11:2-13.
26. Cohen B, Tasto J: Meniscal arrow.
Tech Orthop 1998;13:164-169.
27. Boenisch UW, Faber KJ, Ciarelli M,
Steadman JR, Arnoczky SP: Pull-out
strength and stiffness of meniscal repair
using absorbable arrows or Ti-
Cron vertical and horizontal loop sutures.
Am J Sports Med 1999;27:626–631.
28. Arnoczky SP, Lavagnino M: Tensile fixation
strengths of absorbable meniscal
repair devices as a function of hydrolysis
time: An in vitro experimental study.
Am J Sports Med 2001;29:118-123
29. Albrecht-Olsen P, Kristensen G, Burgaard
P, Joergensen U, Toerholm C:
The arrow versus horizontal suture in
arthroscopic meniscus repair: A prospective
randomized study with arthroscopic
evaluation. Knee Surg Sports
Traumatol Arthrosc 1999;7:268-273.
30. Hutchinson MR, Ash SA: Failure of a
biodegradable meniscal arrow: A case
report. Am J Sports Med 1999;27:101-103.
31. Hechtman KS, Uribe JW: Cystic hematoma
formation following use of a
biodegradable arrow for meniscal repair.
Arthroscopy 1999;15:207-210.
32. Menche DS, Phillips GI, Pitman MI,
Steiner GC: Inflammatory foreignbody
reaction to an arthroscopic bioabsorbable
meniscal arrow repair.
Arthroscopy 1999;15:770-772.
33. Ganko A, Engebretsen L: Subcutaneous
migration of meniscal arrows after
failed meniscus repair: A report of two
cases. Am J Sports Med 2000;28:252-253.
34. Calder SJ, Myers PT: Broken arrow: A
complication of meniscal repair. Arthroscopy
1999;15:651-652.
35. Pena F, Grøntvedt T, Brown GA, Aune
AK, Engebretsen L: Comparison of
failure strength between metallic and
absorbable interference screws: Influence
of insertion torque, tunnel-bone
block gap, bone mineral density, and
interference. Am J Sports Med 1996;24:
329-334.
36. Caborn DNM, Coen M, Neef R, Hamilton
D, Nyland J, Johnson DL: Quadrupled
semitendinosus-gracilis autograft
fixation in the femoral tunnel: A
comparison between a metal and a bioabsorbable
interference screw. Arthroscopy
1998;14:241-245.
37. Brand JC Jr, Pienkowski D, Steenlage
E, Hamilton D, Johnson DL, Caborn
DNM: Interference screw fixation
strength of a quadrupled hamstring
tendon graft is directly related to bone
mineral density and insertion torque.
Am J Sports Med 2000;28:705-710.
38. McGuire DA, Barber FA, Elrod BF,
Paulos LE: Bioabsorbable interference
screws for graft fixation in anterior
cruciate ligament reconstruction.
Arthroscopy 1999;15:463-473.
39. Rokkanen P, Böstman O, Vainionpää
S, et al: Absorbable devices in the fixation
of fractures. J Trauma 1996;40(3
suppl):S123-S127.
40. Sinisaari L, Pätiälä H, Böstman O, et
al: Wound infections associated with
absorbable or metallic devices used in
the fixation of fractures, arthrodeses,
and osteotomies. Eur J Orthop Surg
Traumatol 1995;5:41-43.
41. Bucholz RW, Henry S, Henley MB:
Fixation with bioabsorbable screws for
the treatment of fractures of the ankle.
J Bone Joint Surg Am 1994;76:319-324.
42. Mäkelä EA, Vainionpää S, Vihtonen K,
et al: The effect of a penetrating biodegradable
implant on the growth
plate: An experimental study on growing
rabbits with special reference to
polydioxanone. Clin Orthop 1989;241:
300-308.
43. Böstman O, Mäkelä EA, Södergård J,
Hirvensalo E, Törmälä P, Rokkanen P:
Absorbable polyglycolide pins in
internal fixation of fractures in children.
J Pediatr Orthop 1993;13:242-245.
44. Mäkelä EA, Böstman O, Kekomäki M,
et al: Biodegradable fixation of distal
humeral physeal fractures. Clin
Orthop 1992;283:237-243.
45. Makela EA, Bostman O, Kekomaki M,
et al: Biodegradable fixation of distal
humeral physeal fractures. Clin
Orthop 1992;283:237-243.
surgery is not new, as gut suture
was described in the writings of
Galen in the second century. However,
recent improvements in polymer
science have led to the development
of new orthopaedic implants
made of bioabsorbable materials.
The chief advantage of these implants
is that there is initial stability
adequate for healing and then gradual
resorption after biologic fixation
has been established. In addition,
these materials limit stress shielding
of bone, gradually apply load as
they degrade, obviate hardware
removal procedures, and facilitate
postoperative radiologic imaging.
Polymers made from lactic acid,
glycolic acid, and dioxanone, as
well as copolymers of these materials,
have been studied and are readily
available for clinical use as implants
for both bone and soft-tissue
fixation.
Basic Science of
Bioabsorbable Implants
By definition, bioabsorbable implants
are degraded in a biologic
environment, and their breakdown
products are incorporated into normal
cellular physiologic and biochemical
processes. These materials
must also be biocompatible, with
degradation products that are well
tolerated by the host with no immunogenic
or mutagenic tendency. In
addition, for musculoskeletal applications,
these materials must maintain
adequate strength and not degrade
too rapidly, so that fixation is not lost
before adequate healing can occur.
The perfect bioabsorbable material
for orthopaedic use would initially
have mechanical characteristics
equal to those of standard stainless
steel implants. It would degrade
with the healing process so that load
is gradually transferred to the healing
tissue. The currently available
polymers still do not have mechanical
characteristics equal to those of
metal implants1-3 (Table 1), but
improvements continue to be made,
particularly with the use of reinforcing
techniques.
Polymer Science
Most research on the clinical applications
of bioabsorbable materials
has focused on the use of polymers
known as alpha-polyesters or poly-
(alpha-hydroxy) acids. These include
polylactic acid (PLA), polyglycolic
acid (PGA), and polydioxanone
(PDS). Combinations of these
materials allow optimization of
Dr. Ciccone is in private practice in Colorado
Springs, Colo. Dr. Motz is in private practice in
San Diego, Calif. Dr. Bentley is in private practice
in San Diego. Dr. Tasto is Associate Clinical
Professor of Orthopaedics, University of
California, San Diego.
One or more of the authors or the departments
with which they are affiliated have received
something of value from a commercial or other
party related directly or indirectly to the subject
of this article.
Reprint requests: Dr. Tasto, San Diego Sports
Medicine & Orthopaedic Center, #200, 6719
Alvarado Road, San Diego, CA 92120.
Abstract
The use of bioabsorbable implants in orthopaedic surgical procedures is becoming
more frequent. Advances in polymer science have allowed the production of
implants with the mechanical strength necessary for such procedures.
Bioabsorbable materials have been utilized for the fixation of fractures as well as
for soft-tissue fixation. These implants offer the advantages of gradual load
transfer to the healing tissue, reduced need for hardware removal, and radiolucency,
which facilitates postoperative radiographic evaluation. Reported complications
with the use of these materials include sterile sinus tract formation,
osteolysis, synovitis, and hypertrophic fibrous encapsulation. Further study is
required to determine the clinical situations in which these materials are of most
benefit.
J Am Acad Orthop Surg 2001;9:280-288
Bioabsorbable Implants in Orthopaedics:
New Developments and Clinical Applications
William J. Ciccone II, MD, Cary Motz, MD, Christian Bentley, MD, and James P. Tasto, MD
Perspectives on Modern Orthopaedics
William J. Ciccone II, MD, et al
Vol 9, No 5, September/October 2001 281
their biomechanical properties for
specific clinical uses.
Polymers are composed of covalently
bonded subunits that form
large macromolecules.4 These repeating
subunits are referred to as
monomers. A polymer made of a single
repeating monomer is a homopolymer.
A combination of two or
more different monomers results in a
copolymer. The various monomeric
units in a copolymer may be arranged
randomly (random copolymer)
or in long regions of one subunit
alternating with another (block
copolymer). The biomechanical
and biochemical properties of a
copolymer differ from those of its
constituent monomers.5
The polymer chains that constitute
the implant may be linear,
branched, or cross-linked to neighboring
chains. The microstructural
organization of the chains may be
amorphous or crystalline, as determined
by the orientation of the polymer
chains. The overall crystallinity
of a polymer affects its biomechanical
and degradation proerties. These
properties can be influenced by the
manufacturing technique, with elevated
temperatures and a slow rate
of cooling allowing the polymeric
chains to align themselves in an
ordered solid structure.6 Most bioabsorbable
implants are made of
“semicrystalline” materials containing
both amorphous and crystalline
regions, each of which plays a role in
strength and absorption rates.5,7,8
Many of the physical properties
of a polymer are dependent on the
chemical composition, the molecular
weight, and the arrangement of
the polymer chains. Polymers utilized
in orthopaedics are viscoelastic
in nature; therefore, their physical
properties change with the rate
of load application and are timedependent.
Increased molecular
weight implies an increased intrinsic
viscosity within the polymer,
leading to less deformability (i.e.,
less flow) with an applied load. In
general, high- to average-molecularweight
polymers that are highly viscous
will undergo slower biodegradation
than those of lesser molecular
weight and viscosity.
The mechanical properties of a
polymer are further influenced by
temperature. The glass-transition
temperature (Tg) is the temperature
below which the polymer is stiff and
hard and above which it is soft and
rubbery. The Tg will vary with the
chemical composition of the polymer,
the molecular weight, and the
percentage of the polymer involved
in amorphous domains. As a polymeric
implant is able to withstand
more load at temperatures below its
Tg, most polymers utilized clinically
have a Tg above body temperature.
Lactic acid is a small, hydrophobic
three-carbon molecule that
plays an important role in cellular
energy production. Due to the asymmetry
of the molecule, it has both a
dextrorotatory (D) and a levorotatory
(L) configuration. The D-form is
readily produced, but the L-isomer
is the biologically active form. Polymerized
L-lactic acid is referred to as
poly-L-lactic acid (PLLA). The copolymer
with the D-form (poly-DLlactic
acid) is termed PDLLA. The
mechanical and degradation properties
of these two enantiomers differ
markedly, with PLLA being
highly crystalline and PDLLA being
more amorphous.1 The characteristics
of the copolymers are intermediate
between those of the two
monomers.
Polyglycolic acid is synthesized
by ring-opening polymerization
from glycolide. It is a hard, tough,
crystalline molecule that is more
hydrophilic in nature than PLA. Its
self-reinforced form is stiffer than
other clinically utilized polymers.2
Polyglycolic acid has been utilized
extensively in orthopaedic implants.
This polymer has more rapid degeneration
rates than PLA; there
have been more synovitic reactions
with this material, probably secondary
to its rapid degradation.9
Polydioxanone was first described
in 1981.3 This material is
manufactured by polymerizing the
monomer para-dioxanone. In its
natural state, PDS is a colorless crystalline
polymer; its purple hue is
obtained with the addition of violet
dye. The PDS suture is created by
the melt-extrusion of polymer granules
through the appropriate dyes.
The inherent stiffness of PDS suture
has made it invaluable in applications
in arthroscopic procedures, as
it goes easily through suture passers.
Degradation
The degradation of bioabsorbable
implants follows a predictable
pattern. The rate of degradation is
dependent on the starting molecular
weight of the polymer and its crys-
Table 1
Mechanical Properties of Various Bioabsorbable Implant Materials1-3
Bending Bending Shear
Diameter, Modulus, Strength, Strength,
Implant Material mm GPa MPa MPa
Stainless steel (for comparison) … 200 280 …
Self-reinforced polyglycolic acid 2 13 320 240
Injection-molded polyglycolic acid 2 7 218 95
Self-reinforced poly-L-lactic acid 1.3 10 300 220
Injection-molded poly-L-lactic acid 2 3 119 68
Polydioxanone (suture) … … … 48
Bioabsorbable Implants
tallinity, the composition and porosity
of the implant, and other factors,
such as loading conditions and local
vascularity. In the degradation process,
there is first a loss in molecular
weight, followed by loss of strength
and finally loss of mass. The early
phase of degradation is chemical in
nature. Biologic processing and removal
of the implant occur later.10-12
Because of this pattern of degradation,
these materials lose functional
strength long before they are completely
absorbed.
The initial phase of degradation
is one of hydrolysis. Water molecules
enter the implanted material,
causing cleavage of the monomeric
molecular bonds. This leads to the
scission of long polymer chains into
shorter chains, reducing the overall
molecular weight. This process is
affected by implant porosity.13,14
Low porosity enhances autocatalysis
of the implant because the slow
clearance of degradation products
from within the material leads to
increased acidity and more rapid
molecular scission. The molecular
weight plays an important role in
the internal friction within the implant,
and thus its mechanical properties;
hydrolysis of these long
chains leads to a loss in mechanical
strength. As a result, implants with
low porosity may have a shortened
functional life.
As the implant loses integrity and
fragments, biologic removal of the
implant takes place. The rapid degradation
of these implants has been
postulated to be the cause of marked
foreign-body reactions, synovitis,
and even activation of the complement
cascade.8,15-17 Studies evaluating
the tissue response to PGA and
PLLA implants have shown foreignbody
reactions to the degradation
products. The degradation of PLLA
has been associated with a foreignbody
reaction as late as 143 weeks
after implantation.12 A foreign-body
response reaction to PGA has been
seen as early as 3 to 6 weeks.11 Differences
in the timing of the cellular
response to these materials are
probably secondary to the different
rates of degradation of PGA and
PLLA. Clinically, most symptomatic
foreign-body reactions have
been associated with the more
rapidly degrading PGA,9,18 but reactions
to PLLA have also been described.
19 The rates of degradation
of these materials can be optimized
for biologic fixation by changing the
copolymer ratios of PGA and PLLA.5
The most common soft-tissue
complications related to use of these
materials are sterile sinus tract formation,
hypertrophic fibrous encapsulation,
and osteolysis. These inflammatory
responses occur in
fewer than 10% of patients, but may
be severe enough to require surgery
for resolution of the reaction.16
Biochemical Degradative Pathway
Alpha polyesters, such as PLA,
PGA, and PDS, primarily degrade
by hydrolysis, with the release of
their respective monomers. The
monomers are then incorporated
into normal cellular physiologic
processes for further degradation.
Lactic acid, glycolic acid, and paradioxanone
have well-defined biochemical
pathways that lead eventually
to their excretion in the form of
carbon dioxide and water7,20 (Fig. 1).
Lactic acid is produced by the
hydrolytic degradation of PLA.
Lactic acid is normally produced at
the end of the glycolytic pathway
from pyruvate when the amount of
oxygen is limiting. The oxidation of
lactate to form pyruvate is catalyzed
by lactate dehydrogenase. In aerobic
conditions, pyruvate undergoes
oxidative decarboxylation to produce
acetyl coenzyme A. This molecule
may then enter the citric acid
cycle for further oxidation to produce
carbon dioxide, water, and
adenosine triphosphate by oxidative
phosphorylation.
Degradation of PGA and PDS
follows nearly the same pathway.
Hydrolysis of PGA produces glycolic
acid, which is either excreted
directly in the urine or converted to
glyoxylate. The PDS degradation
products enter the pathway at glyoxylate.
The amino acid glycine can
be produced from glyoxylate by a
transamination reaction. Glycine, a
glucogenic amino acid, can be further
converted to pyruvate through
a serine intermediate. Pyruvate is
then converted to acetyl coenzyme
A to enter the citric acid cycle, as
previously discussed.
Mechanical Properties
The mechanical properties of
bioabsorbable orthopaedic implants
must be considered both at the time
of insertion and throughout degradation.
The implants are initially subjected
to considerable loads, which
gradually decrease with tissue healing.
The perfect implant will de-
Figure 1 Biochemical degradation pathways
for PLA, PDS, and PGA.
Acetyl coenzyme A
CO2
H2O
Glycine Urine
Serine
Glycolic
acid
PLA PDS PGA
Citric acid cycle
Pyruvate
Lactic acid Glyoxylate
William J. Ciccone II, MD, et al
Vol 9, No 5, September/October 2001 283
grade at a rate that gradually transfers
load to healing tissue and does
not outpace the healing response.
Factors that affect the mechanical
properties of an implant include the
type of material, its processing, and
the local testing environment.21
Bioabsorbable polymers differ from
common stainless steel implants in
that they are more viscoelastic in
nature. Therefore, they exhibit enhanced
properties of creep and
stress relaxation. Claes21 exhibited
the importance of this property by
demonstrating that when used in
the form of an interfragmentary
screw, bioabsorbable polymers lost
20% of their force 20 minutes after
application, due to stress relaxation.
Reinforcing techniques have been
developed to improve the mechanical
characteristics of bioabsorbable
implants. Self-reinforced absorbable
components are polymeric materials
in which the reinforcing elements
and matrix material have the same
chemical composition. The most
effective way to manufacture the
self-reinforced structure into the
polymer is by the mechanical deformation
of the nonreinforced material.
7 This deformation process leads
to the formation of oriented polymeric
chains, the self-reinforcing
structures.
The reported properties of these
implants vary, due mostly to differences
in processing and testing conditions.
Overall, the self-reinforced
materials show an improvement in
their initial mechanical values compared
with the nonreinforced polymers
(Table 1). The initial bending
strength of self-reinforced PGA
exceeds that of stainless steel; however,
with rapid rates of degradation,
this strength is not maintained. In
general, the mechanical properties of
these polymeric implants do not
approach those of standard stainless
steel implants. While rapid loss of
the mechanical properties might be
expected to allow excessive motion
between fracture fragments, these
materials have been used successfully
in specific clinical situations.
Mechanical degradation studies
have been performed in both in
vivo and in vitro conditions. The
most important determinant of the
rate of degradation is the material
itself, but the environment surrounding
the implantation site can
also be an influence. There is evidence
that degradation rates are
more rapid with in vivo testing secondary
to enzymatic contributions.1
Areas of high tissue metabolism and
blood flow facilitate material degradation.
Furthermore, implants under
load tend to degrade faster, possibly
secondary to microfracture.
The mechanical degradation rate
of PDS suture has been studied by
Ray et al.3 The breaking strength of
PDS suture was tested after being
implanted in the subcutaneous
tissue of rats. The PDS suture retained
74% of its nonimplanted
strength at 2 weeks, but by 6 and 8
weeks that value had dropped to
41% and 14%, respectively. The
authors also determined, with the
use of radioactive labeling, that the
material absorption was complete
by 182 days after implantation.
Likewise, PGA materials lose their
mechanical strength by 6 to 8
weeks. The loss of the mechanical
properties of this material occurs at
varying rates, with the loss of shear
strength being slower than loss of
bending strength. In self-reinforced
materials, the matrix material loses
its strength more rapidly than the reinforcing
elements. Therefore, these
materials may be more suited for
the fixation of fractures involving
periarticular cancellous bone, where
high shear loads are common.
Clinical Applications
The use of bioabsorbable fixation for
the attachment of soft tissue to bone
is being increasingly utilized by
orthopaedic surgeons, especially in
the treatment of soft-tissue lesions in
the shoulder. These implants have
facilitated the repair and reconstruction
of labral and rotator cuff lesions.
The development of bioabsorbable
tacks, suture anchors, and screwand-
washer implants has given surgeons
more treatment alternatives
(Fig. 2).
Bioabsorbable suture anchors are
useful as an alternative to metal staples
and screws, which may have a
high profile. They also eliminate the
need for passing sutures through
bone tunnels. Pullout strengths for
bioabsorbable suture anchors are
comparable to those of their metallic
counterparts.22 These implants have
sufficient strength that the point of
failure is the suture–soft-tissue interface.
23
The complications observed with
the use of bioabsorbable suture
anchors are similar to those seen
with metallic anchors. Improper
insertion of the anchor too deep in
the bone can cause suture fraying or
failure. Superficial insertion of the
anchor can lead to cartilage wear on
the opposing articular surface. The
anchor can also fail by pullout from
bone and become an intra-articular
loose body. As these implants are
radiolucent, this diagnosis can be
difficult to make postoperatively in
a persistently painful joint. Unique
to bioabsorbable anchors is the potential
for eyelet failure with secondary
suture cutout.
Bioabsorbable suture anchor fixation
has several advantages. The
anchor undergoes reabsorption and
therefore reduces the need for removal
of a prominent implant. Resorption
also makes revision surgery
less complicated, as hardware
removal is not necessary. The fixation
does not obscure the anatomy
as depicted on radiographs and is
compatible with magnetic resonance
imaging if further evaluation
of the affected joint is necessary.
Improperly placed anchors may
simply be drilled out rather than
Bioabsorbable Implants
284 Journal of the American Academy of Orthopaedic Surgeons
unscrewed or pushed through, as is
necessary with metallic anchors.
Finally, stress is gradually transferred
to the healing soft tissue as
the anchor degrades.
Repair of Shoulder Lesions
The effectiveness of bioabsorbable
anchors for use in Bankart repairs,
as well as in treatment of rotator
cuff tears and “SLAP” lesions
(i.e., anterior-to-posterior lesions of
the superior labrum), is currently
under investigation. Warme et al24
compared the usefulness of bioabsorbable
and nonabsorbable suture
anchors in a prospective randomized
study of open Bankart repairs. At
an average follow-up interval of 25
months, there was one failure in the
18 patients treated with nonabsorbable
anchors, compared with two
failures in 20 patients treated with
absorbable anchors. Radiographs
obtained at the 2-year follow-up in
the absorbable group demonstrated
near-complete implant degradation
and osseous replacement. At 6
months, the anchor holes used for
nonabsorbable implants demonstrated
a sclerotic rim but no increase
in size from the measurements
on the initial postoperative
radiographs. There was no subsequent
radiographic change after that.
It must be noted that no reports of
complications attributable to the bioabsorbable
nature of these suture
anchors have been published.
The use of bioabsorbable tacks for
the repair of labral lesions has made
arthroscopic management of these
injuries technically less complicated.
The development of labral tacks,
such as Suretac (Smith&Nephew,
Andover, Mass), TissueTack (Arthrex,
Naples, Fla), ConTack (Mitek,
Westwood, Mass), and the Contour
Labral Nail (Bionx Implants, Blue
Bell, Pa), has led to the ability to
treat more patients with Bankart and
SLAP injuries arthroscopically. These
tacks are cannulated for ease of
insertion and allow the labrum to be
reattached to the glenoid in an anatomic
position. These devices eliminate
the risks of metal around joint
surfaces, do not require transglenoid
drilling or an accessory posterior
incision, and avoid technically difficult
arthroscopic knot tying.
The first absorbable tack was
constructed of PGA, which rapidly
loses strength over the first 4 to 6
weeks. Complete reabsorption occurs
in approximately 6 months.
This implant has been implicated in
several cases of aseptic synovitis
secondary to a histiocytic or phagocytic
reaction to the rapidly degrading
polymer.9 Currently, most tacks
are composed of longer-absorbing
materials such as PDLA, PLLA, or
composites, which may reduce the
rate of synovitis.
Warner et al25 reported on a
cohort of 15 patients who underwent
“second look” arthroscopy for a
failed arthroscopic Bankart repair
performed with the Suretac device.
These patients were a subgroup of 96
patients initially treated for posttraumatic
recurrent anterior dislocation
or subluxation. The repeat procedure
was necessitated by recurrent
instability in 7 patients, pain in 6,
and pain with stiffness in 2. When
reevaluated, the failure in the patients
with instability was considered
to be secondary to inadequate reconstruction
of either the anterior glenohumeral
ligaments or the anterior
labral complex. The cause of failure
in the 8 patients with either pain or
pain and stiffness was less clear, although
an indolent inflammatory
response to the PGA polymer was
found in several. Six of the patients
eventually had complete or partial
pain relief after a second arthroscopy
and subacromial decompression, biceps
tenodesis, or a capsular release
or manipulation.
Bioabsorbable fixation devices
are now also being used for the
repair of rotator cuff tears. These
procedures were initially performed
with suture anchors, but more re-
Figure 2 Currently available bioabsorbable implants for fracture fixation, interference fixation,
and meniscal repair.
William J. Ciccone II, MD, et al
Vol 9, No 5, September/October 2001 285
cently screw-and-washer–type devices
have become available. The
rationale behind the use of these
soft-tissue screws is to repair the
tendon to bone without a suture,
reducing the incidence of complications
at the tendon-suture interface
and increasing the surface area of
tendon contact with bone. These
devices (Bio-Headed Corkscrew,
Arthrex; Biocuff Screw, Bionx; Biotwist,
Linvatec, Naples, Fla) all
employ a screw-in device with a
large head for soft-tissue compression.
The Biocuff screw has an independent
spiked washer to prevent
tendon damage and reduce pressure
necrosis. No clinical studies on the
use of these devices are yet available.
Meniscal Repair
The “all inside” technique of meniscal
repair described by Morgan
was developed to safely repair the
posterior and central peripheral
portions of the meniscus, a location
difficult to reach with traditional
arthroscopic techniques because of
the risk of neurovascular injury.
The use of bioabsorbable implants
for use in all-inside meniscal repair
has now been described.26 These
devices eliminate the need for a posterior
incision, reduce the risk of
neurovascular injury, and simplify
the fixation procedure.
The Bionx Meniscal Arrow is a
well-characterized bioabsorbable implant
that has been approved by the
US Food and Drug Administration
for meniscal repair. It is a T-shaped
device composed of self-reinforced
PLLA with a 1.1-mm-diameter barbed
stem. The stem penetrates the meniscus
and capsule, and the bar portion
approximates the torn meniscal leaf
to the periphery. The arrows remain
in the joint for approximately 1 year
and are gradually absorbed through
hydrolysis to carbon dioxide and
water.
Biomechanical data reported by
Boenisch et al27 compared the pullout
strength and linear stiffness of
meniscal repair performed with
bioabsorbable arrows and vertical
and horizontal looped sutures in bovine
menisci. The pullout strengths
in both suture groups were significantly
(P<0.05) higher than those in
the arrow-fixation group. Further,
vertical-suture fixation was significantly
stiffer than fixation with
either horizontal sutures or arrows.
However, more recent data from another
bovine study28 demonstrated
no difference between the pullout
strength of the arrow and that of a
vertical PDS suture when the arrow
was inserted with a mechanical “gun.”
In fact, significantly greater pullout
strength for arrow fixation was noted
at 12 and 24 weeks compared with
PDS-based implants. Technical considerations
of insertion, such as keeping
the arrow parallel to the joint surface
and maximizing the number of
barbs engaging beyond the tear, have
been demonstrated to be essential to
the integrity of the repair.
Albrecht-Olsen et al29 performed
a randomized prospective study
comparing meniscal repair utilizing
the bioabsorbable meniscal arrow
implant to inside-out repair with
horizontal meniscal sutures. Sixtyeight
patients were divided evenly
between the two groups. Repairs
were performed only in red-red or
red-white zones, and rehabilitation
protocols were standardized. In all,
65 patients (96%) underwent repeat
arthroscopy at 3 to 4 months. A
healed meniscus was observed in
91% of the arrow repair group but
in only 75% of those in the suture
group. There were no complications
reported in the group with
bioabsorbable fixation. The operative
time for the procedures averaged
30 minutes for repair with the
arrow and 60 minutes for suture repair.
The advantages of decreased
operative time, ease of insertion,
and improved meniscal healing
with an all-inside meniscal repair
with a bioabsorbable implant were
confirmed by this study.
Complications with the Bionx
Arrow have been published in several
case reports.30-34 These include
hematoma formation, subcutaneous
migration, foreign-body reaction,
and loss of fixation. The use of
these newly developed implants
appears to be simple. However,
attention to technical detail in terms
of placement, choice of length, and
orientation is required to avoid
complications and ensure optimal
fixation.
Anterior Cruciate Ligament
Reconstruction
Graft fixation devices for anterior
cruciate ligament reconstruction
have been manufactured in the past
from nonabsorbable materials such
as metal and plastic. These devices
are often difficult to remove or
avoid if revision anterior cruciate
ligament reconstruction is required.
Furthermore, the evaluation of softtissue
lesions with MR imaging
after the use of metal fixation is difficult.
Additionally, aperture fixation
(soft-tissue fixation at the joint
line), which provides a stiffer construct,
is hampered by concerns
about graft severance by metal
interference screws. Use of bioabsorbable
fixation devices, such as
interference screws, can potentially
eliminate some of these problems.
Several different types of screws,
which vary in polymeric composition,
are currently available. Graft
fixation strength in anterior cruciate
ligament reconstruction is critical in
the period from initial fixation to osseous
integration of the graft. This period
ranges from 6 weeks for bone–
patellar tendon–bone fixation to
approximately 12 to 16 weeks for
hamstring fixation. Therefore, the
bioabsorbable interference screw
must maintain virtually all of its
structural integrity during that
entire interval. The initial pullout
strengths of these implants should
exceed the estimated 500-N load for
activities of daily living. For this
Bioabsorbable Implants
286 Journal of the American Academy of Orthopaedic Surgeons
reason, most screws on the market
are manufactured from PLLA or a
variant copolymer with a longer
half-life (Fig. 3). This composition
can lead to delayed osseous integration,
thus negating the main benefit
of the bioabsorbable fixation.
No consensus is supported by
the results of recent biomechanical
studies. Pena et al35 published data
on the insertion torques and fixation
strengths of bone–patellar tendon–
bone grafts fixed with PLA interference
screws (Bioscrew, Linvatec,
Key Largo, Fla) and compared them
with metal interference screws in
cadaveric specimens from young
and middle-aged individuals. With
use of a correction factor for bonemineral
density, the pullout forces
were 730 N for the metal screws and
668 N for the PLA screws. The insertion
torque was 1.52 N for the
metal screws and 0.30 N for the bioabsorbable
screws. Both pullout
force and insertion torque were significantly
(P>0.05) higher for metal
interference fixation. The authors
noted that loss of tensile strength of
bioabsorbable screws is possible
with excessive time in storage due to
hydrolysis or wetting the implant
before insertion.
Caborn et al36 have published the
results of a biomechanical comparison
of metal and bioabsorbable interference
screw fixation of quadrupled
semitendinosus-gracilis grafts. No
statistically significant difference was
found in the maximum load at pullout,
nor did the screw insertional
torques correlate with the maximum
load at pullout. However, a followup
study in which the bone tunnels
were specifically sized within 5 mm
of the graft diameter showed that the
bioabsorbable screw-insertion torque
correlated directly with ultimate
graft failure strength.37 Therefore, it
appears that bioabsorbable interference
screw fixation is not appropriate
for all patients, especially those
with poor bone quality. Careful
graft preparation and sizing can,
however, result in interference fixation
capable of withstanding the
forces of accelerated rehabilitation.
A recent prospective, randomized
study by McGuire et al38 compared
the Linvatec Bioscrew with metal
interference screws in 204 patients.
A variety of graft sources were used,
including autogenous and allograft
bone and patellar tendon and allograft
Achilles tendon. The average
follow-up interval was 2.4 years,
and the mean age of patients was 30
years. A standardized rehabilitation
protocol was used. No statistically
significant difference was noted in
the Lysholm or Tegner score, pain,
thigh size, Lachman test result, pivot
shift, patellofemoral crepitus, or
joint effusion. There was no statistically
significant difference in mean
maximum manual side-to-side KT-
1000 rating between the 1.8-mm bioabsorbable
screw and the 1.6-mm
metal screw. Twelve PLLA screws
broke during insertion without adverse
effects. There were no reported
complications related to loss of fixation,
toxicity, allergenicity, or osteolysis.
Excellent clinical results are possible
with bioabsorbable interference
screws, although there is no
consensus opinion as to whether
biomechanical strength is the same
between metal and bioabsorbable
screw fixation. Disadvantages of
bioabsorbable interference screws
include concerns about sterile
drainage, cyst formation, lack of
complete osseous ingrowth into the
defect, early loss of pullout strength
secondary to hydrolysis, and intraoperative
breakage of the device.
The reported rate of these clinical
complications is low and has not
resulted in a clinically significant
difference in outcome studies published
to date.
Fracture Fixation
Although bioabsorbable fracturefixation
devices appear to have obvious
advantages over metal implants,
concerns about the initial fixation
strength of these materials have limited
their widespread acceptance.
These materials must have the initial
fixation strength necessary to maintain
the reduction of bone fragments
during the healing process. Manufacturing
techniques are critical, as
melt-molded polymers do not possess
the strength necessary for reliable
fixation, whereas self-reinforced
materials have the mechanical characteristics
more suitable for this use.
In a review of more than 2,500
fracture-fixation cases in which bioabsorbable
implants were used,
Rokkanen et al39 reported that the
incidence of bacterial wound infection
was 3.6%; nonspecific foreignbody
reaction, 2.3%; and failure of
fixation, 3.7%. Compared with
metallic fixation, absorbable fixation
has shown a lower incidence of
infection.40
Bucholz et al41 performed a prospective
randomized trial comparing
PLA screws with stainless steel
screws for fixation of displaced
medial malleolar fractures. They
found no statistically significant difference
in operative or postoperative
complications between the two
groups.
Figure 3 MR image obtained 24 months
after interference fixation of hamstring
autografts with bioabsorbable PLLA
screws shows minimal degradation.
William J. Ciccone II, MD, et al
Vol 9, No 5, September/October 2001 287
Foreign-body reactions to PGA
have been described,9,18,39 but neither
Rokannen et al39 nor Bucholz et
al41 reported late reactions to PLA
screws. However, a recent case report
described an osteolytic reaction
to an intraosseous PLA screw 52
months after the operative procedure.
19 Longer-term follow-up may
be necessary to determine the actual
clinical biocompatibility of intraosseous
PLA.
The use of bioabsorbable implants
for pediatric fracture fixation
is particularly appealing because it
obviates implant removal. In experimental
studies, the presence of
an absorbable implant does not
seem to interfere with the growth
plate any more than an empty drill
hole does.42 Biodegradable implants
have shown satisfactory results,
especially in the treatment of distal
humeral physeal fractures.43-45
Böstman et al43 evaluated the use
of absorbable self-reinforced PGA
pins in the treatment of 71 physeal
and nonphyseal fractures in skeletally
immature patients, with a mean
follow-up interval of 15.8 months.
Anatomic reduction was maintained
until union in 87% of the fractures,
but in only 8 of 14 supracondylar
humerus fractures. The authors felt
that the displacement forces encountered
in supracondylar fractures
overwhelmed the mechanical properties
of the absorbable pins, resulting
in displacement. They concluded
that the preliminary results of fracture
treatment with self-reinforced
PGA were satisfactory except for
supracondylar humerus fractures.
Long-term clinical studies are still
required to determine the effects of
these implants on the growth plate.
Summary
The use of bioabsorbable implants in
musculoskeletal procedures is gaining
acceptance. While most commonly
utilized in the field of sports
medicine for soft-tissue fixation,
these implants may have applications
in other aspects of orthopaedics.
Complications associated with
the use of these materials have diminished
with the development of
newer, self-reinforced polymers.
Until more long-term, peer-reviewed
research becomes available, the
appropriate clinical usage of these
implants remains a concern for the
practicing orthopaedist.
References
1. Daniels AU, Chang MKO, Andriano
KP: Mechanical properties of biodegradable
polymers and composites
proposed for internal fixation of bone.
J Appl Biomater 1990;1:57-78.
2. Törmälä P: Biodegradable self-reinforced
composite materials: Manufacturing
structure and mechanical properties.
Clin Mater 1992;10:29-34.
3. Ray JA, Doddi N, Regula D, Williams
JA, Melveger A: Polydioxanone (PDS),
a novel monofilament synthetic absorbable
suture. Surg Gynecol Obstet 1981;
153:497-507.
4. Pietrzak WS, Sarver DR, Verstynen ML:
Bioabsorbable polymer science for the
practicing surgeon. J Craniofac Surg
1997;8:87-91.
5. Miller RA, Brady JM, Cutright DE:
Degradation rates of oral resorbable
implants (polylactates and polyglycolates):
Rate modification with changes
in PLA/PGA copolymer ratios. J
Biomed Mater Res 1977;11:711-719.
6. Athanasiou KA, Agrawal CM, Barber
FA, Burkhart SS: Orthopaedic applications
for PLA-PGA biodegradable
polymers. Arthroscopy 1998;14:726-737.
7. Hollinger JO, Battistone GC: Biodegradable
bone repair materials: Synthetic
polymers and ceramics. Clin
Orthop 1986;207:290-305.
8. Bergsma JE, de Bruijn WC, Rozema FR,
Bos RRM, Boering G: Late degradation
tissue response to poly(L-lactide) bone
plates and screws. Biomaterials 1995;
16:25-31.
9. Burkart A, Imhoff AB, Roscher E:
Foreign-body reaction to the bioabsorbable
Suretac device. Arthroscopy
2000;16:91-95.
10. Päivärinta U, Böstman O, Majola A,
Toivonen T, Törmälä P, Rokkanen P:
Intraosseous cellular response to biodegradable
fracture fixation screws
made of polyglycolide or polylactide.
Arch Orthop Trauma Surg 1993;112:71-74.
11. Koskikare K, Toivonen T, Rokkanen P:
Tissue response to bioabsorbable selfreinforced
polylevolactide and polyglycolide
pins implanted intra-articularly
and directly into the bone on different
levels: An experimental study on rats.
Arch Orthop Trauma Surg 1998;118:
149-155.
12. Bos RRM, Rozema FR, Boering G, et al:
Degradation of and tissue reaction to
biodegradable poly(L-lactide) for use as
internal fixation of fractures: A study in
rats. Biomaterials 1991;12:32-36.
13. Vert M, Mauduit J, Li S: Biodegradation
of PLA/GA polymers: Increasing complexity.
Biomaterials 1994;15:1209-1213.
14. Athanasiou KA, Schmitz JP, Agrawal
CM: The effects of porosity on in vitro
degradation of polylactic acid–polyglycolic
acid implants used in repair of
articular cartilage. Tissue Eng 1998;4:
53-63.
15. Tegnander A, Engebretsen L, Bergh K,
Eide E, Holen KJ, Iversen OJ: Activation
of the complement system and
adverse effects of biodegradable pins
of polylactic acid (Biofix) in osteochondritis
dissecans. Acta Orthop Scand
1994;65:472-475.
16. Böstman O, Hirvensalo E, Mäkinen J,
Rokkanen P: Foreign-body reactions to
fracture fixation implants of biodegradable
synthetic polymers. J Bone Joint
Surg Br 1990;72:592-596.
17. Bergsma EJ, Rozema FR, Bos RRM, de
Bruijn WC: Foreign body reactions to
resorbable poly(L-lactide) bone plates
and screws used for the fixation of
unstable zygomatic fractures. J Oral
Maxillofac Surg 1993;51:666-670.
18. Böstman OM: Osteolytic changes
accompanying degradation of absorbable
fracture fixation implants. J Bone
Joint Surg Br 1991;73:679-682.
19. Böstman OM, Pihlajamäki HK: Late
foreign-body reaction to an intraosseous
bioabsorbable polylactic acid
screw: A case report. J Bone Joint Surg
Am 1998;80:1791-1794.
Bioabsorbable Implants
288 Journal of the American Academy of Orthopaedic Surgeons
20. Brady JM, Cutright DE, Miller RA,
Battistone GC, Hunsuck EE: Resorption
rate, route of elimination, and ultrastructure
of the implant site of polylactic
acid in the abdominal wall of the rat.
J Biomed Mater Res 1973;7:155-166.
21. Claes LE: Mechanical characterization
of biodegradable implants. Clin Mater
1992;10:41-46.
22. Barber FA, Herbert MA: Suture anchors:
Update 1999. Arthroscopy 1999;
15:719-725.
23. Burkhart SS, Diaz Pagàn JL, Wirth MA,
Athanasiou KA: Cyclic loading of
anchor-based rotator cuff repairs: Confirmation
of the tension overload phenomenon
and comparison of suture
anchor fixation with transosseous fixation.
Arthroscopy 1997;13:720-724.
24. Warme WJ, Arciero RA, Savoie FH III,
Uhorchak JM, Walton M: Nonabsorbable
versus absorbable suture anchors
for open Bankart repair: A prospective,
randomized comparison. Am J
Sports Med 1999;27:742-746.
25. Warner JJP, Miller MD, Marks P, Fu
FH: Arthroscopic Bankart repair with
the Suretac device: Part I. Clinical observations.
Arthroscopy 1995;11:2-13.
26. Cohen B, Tasto J: Meniscal arrow.
Tech Orthop 1998;13:164-169.
27. Boenisch UW, Faber KJ, Ciarelli M,
Steadman JR, Arnoczky SP: Pull-out
strength and stiffness of meniscal repair
using absorbable arrows or Ti-
Cron vertical and horizontal loop sutures.
Am J Sports Med 1999;27:626–631.
28. Arnoczky SP, Lavagnino M: Tensile fixation
strengths of absorbable meniscal
repair devices as a function of hydrolysis
time: An in vitro experimental study.
Am J Sports Med 2001;29:118-123
29. Albrecht-Olsen P, Kristensen G, Burgaard
P, Joergensen U, Toerholm C:
The arrow versus horizontal suture in
arthroscopic meniscus repair: A prospective
randomized study with arthroscopic
evaluation. Knee Surg Sports
Traumatol Arthrosc 1999;7:268-273.
30. Hutchinson MR, Ash SA: Failure of a
biodegradable meniscal arrow: A case
report. Am J Sports Med 1999;27:101-103.
31. Hechtman KS, Uribe JW: Cystic hematoma
formation following use of a
biodegradable arrow for meniscal repair.
Arthroscopy 1999;15:207-210.
32. Menche DS, Phillips GI, Pitman MI,
Steiner GC: Inflammatory foreignbody
reaction to an arthroscopic bioabsorbable
meniscal arrow repair.
Arthroscopy 1999;15:770-772.
33. Ganko A, Engebretsen L: Subcutaneous
migration of meniscal arrows after
failed meniscus repair: A report of two
cases. Am J Sports Med 2000;28:252-253.
34. Calder SJ, Myers PT: Broken arrow: A
complication of meniscal repair. Arthroscopy
1999;15:651-652.
35. Pena F, Grøntvedt T, Brown GA, Aune
AK, Engebretsen L: Comparison of
failure strength between metallic and
absorbable interference screws: Influence
of insertion torque, tunnel-bone
block gap, bone mineral density, and
interference. Am J Sports Med 1996;24:
329-334.
36. Caborn DNM, Coen M, Neef R, Hamilton
D, Nyland J, Johnson DL: Quadrupled
semitendinosus-gracilis autograft
fixation in the femoral tunnel: A
comparison between a metal and a bioabsorbable
interference screw. Arthroscopy
1998;14:241-245.
37. Brand JC Jr, Pienkowski D, Steenlage
E, Hamilton D, Johnson DL, Caborn
DNM: Interference screw fixation
strength of a quadrupled hamstring
tendon graft is directly related to bone
mineral density and insertion torque.
Am J Sports Med 2000;28:705-710.
38. McGuire DA, Barber FA, Elrod BF,
Paulos LE: Bioabsorbable interference
screws for graft fixation in anterior
cruciate ligament reconstruction.
Arthroscopy 1999;15:463-473.
39. Rokkanen P, Böstman O, Vainionpää
S, et al: Absorbable devices in the fixation
of fractures. J Trauma 1996;40(3
suppl):S123-S127.
40. Sinisaari L, Pätiälä H, Böstman O, et
al: Wound infections associated with
absorbable or metallic devices used in
the fixation of fractures, arthrodeses,
and osteotomies. Eur J Orthop Surg
Traumatol 1995;5:41-43.
41. Bucholz RW, Henry S, Henley MB:
Fixation with bioabsorbable screws for
the treatment of fractures of the ankle.
J Bone Joint Surg Am 1994;76:319-324.
42. Mäkelä EA, Vainionpää S, Vihtonen K,
et al: The effect of a penetrating biodegradable
implant on the growth
plate: An experimental study on growing
rabbits with special reference to
polydioxanone. Clin Orthop 1989;241:
300-308.
43. Böstman O, Mäkelä EA, Södergård J,
Hirvensalo E, Törmälä P, Rokkanen P:
Absorbable polyglycolide pins in
internal fixation of fractures in children.
J Pediatr Orthop 1993;13:242-245.
44. Mäkelä EA, Böstman O, Kekomäki M,
et al: Biodegradable fixation of distal
humeral physeal fractures. Clin
Orthop 1992;283:237-243.
45. Makela EA, Bostman O, Kekomaki M,
et al: Biodegradable fixation of distal
humeral physeal fractures. Clin
Orthop 1992;283:237-243.
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