MECHANICAL ARTHROPATHY: CARTILAGE PATHOPHYSIOLOGY AND OSTEOARTHRITIS

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Presentation transcript:

MECHANICAL ARTHROPATHY: CARTILAGE PATHOPHYSIOLOGY AND OSTEOARTHRITIS Grant W. Cannon, M.D. Friday, November 18, 2005

Osteoarthritis Terminology Osteoarthrosis Degenerative Joint Disease Hypertrophic Arthropathy

Osteoarthritis Definition Progressive disintegration of articular cartilage Formation of new bone in the floor of the cartilage lesions (eburnation) and at the joint margins (osteophtyes)

Osteoarthritis Normal Cartilage Review Nutrition Chondrocytes Collagen Proteoglycans Hyaluronic Acid

Normal Cartilage Review Components Water - 65-80% of cartilage is water Major matrix components- 90% of dry weight Proteoglycans (particularly aggrecan) Collagen Chondrocytes 1-2% of volume Other important components Enzymes - E.g. Matrix metaloproteinases (MMPs) - e.g. collagenase Enzyme inhibitors. E.g. Tissue inhibitors of metaloproteinases (TIMP)

Normal Cartilage Review Chondrocytes Chondrocytes 1-2% of volume Biosynthetically active, but relatively quiescent Produce proteoglycans, but little collagen Source of enzymes and enzyme inhibitors

Normal Cartilage Review Collagen Types of collagen Type II in hyaline cartilage Type II and Type I in fibrocartilage Vertical orientation in deep regions Horizontal orientation in superficial regions

Normal Cartilage Review Proteoglycans - I Properties Hydrophilic Polar Components Glycosaminoglycans Core protein - binds GAGs to make proteoglycans Hyaluronic Acid - Non-covalent binding

Normal Cartilage Review Proteoglycans - Components Glycosaminoglycans (GAGs) - "acid mucopolysaccharides” Chondroitins Heparins Keratan sulfates Core protein - binds GAGs to make proteoglycans Hyaluronic Acid - Non-covalent binding Most common cartilage proteoglycan is aggrecan

Osteoarthritis Normal Cartilage Review Nutrition Chondrocytes Collagen Proteoglycans Hyaluronic Acid

Pathology of Osteoarthritis Gross Pathology Biochemical Abnormalities

Pathology of Osteoarthritis Gross Pathology Fibrillation and flaking of the cartilage surface Loss of cartilage Subchondral sclerosis (Eburnation) Osteophyte formation

Pathology of Osteoarthritis Gross Pathology Fibrillation and flaking of the cartilage surface Loss of cartilage Subchondral sclerosis (Eburnation) Osteophyte formation

Pathology of Osteoarthritis Biochemical Abnormalities Increase in water content Change in proteoglycans (PGs) Collagen Chondrocyte - damage and loss of chondrocytes is a late finding in OA Possible role of inflammation.

Pathology of Osteoarthritis Biochemical Abnormalities Change in proteoglycans (PGs) Increased turnover and degradation Decrease in PG aggregation (smaller PGs) Increase in extractable PGs Decrease in chondroitin sulfate length Change in GAG composition

Pathology of Osteoarthritis Biochemical Abnormalities Collagen Increase in collagen synthesis - a reflection of increased turnover Production of some type I collagen

Pathology of Osteoarthritis Biochemical Abnormalities Chondrocyte - damage and loss of chondrocytes is a late finding in OA Possible role of inflammation Increase in cytokine levels (IL-1 and TNF-") Unclear what represent the primary process

Pathology of Osteoarthritis Biochemical Abnormalities

Pathology of Osteoarthritis Biochemical Abnormalities

Pathology of Osteoarthritis Gross Pathology Biochemical Abnormalities

Osteoarthritis Risk Factors

Osteoarthritis Risk Factors Increasing age Women Obesity Trauma (Heavy exercise on a normal joint has not generally not been associated with increased OA) Inherited genetic mutations of collagen Other causes of joint injury (e.g. inflammatory arthritis, congenital dislocations, etc)

Osteoarthritis Clinical Manifestation Symptoms Physical Finding Laboratory

Clinical Manifestation Symptoms Mechanical joint pain "Jelling" sensation Absence of morning stiffness

Clinical Manifestation Physical Finding Local tenderness Bony swelling Crepitus

Clinical Manifestation Laboratory Synovial Effusion - non-inflammatory (<2,000 WBCs/mm3) Other test normal

Osteoarthritis Joint Distribution Large joints of the lower extremities (Hips and Knees) Distal interphalangeal joints (DIPs) - Heberdon's Nodes Proximal interphalangeal joints (PIPs) - Bouchard's Nodes Shoulder involvement is rare

Osteoarthritis Radiographic Manifestations Joint space narrowing (cartilage loss) Subchondral sclerosis (Eburnation) Osteophyte formation Subchondral cysts

Osteoarthritis Radiographic Manifestations Joint space narrowing (cartilage loss) Subchondral sclerosis (Eburnation) Osteophyte formation Subchondral cysts

Osteoarthritis Classification Primary Idiopathic Generalized osteoarthritis Erosive osteoarthritis

Osteoarthritis Classification Secondary Congenital or developmental defects Post-traumatic Due to prior inflammatory joint disease Metabolic disorders Endocrinopathies Familial genetic disorders Neuropathic disorders/Charcot joints Miscellaneous

Osteoarthritis: Management Goals Non-medical therapy Medical therapy Joint injection Alternative therapies under investigation Surgery

Osteoarthritis: Management Goals Pain relief Minimize disability Stopping or delaying the destructive process

Osteoarthritis: Management Non-Medical Therapy Weight reduction Physical therapy Maintenance of muscle function Maintenance of range of motion Avoid weight bearing exercises (e.g. jogging) Appliances (bathtub bars, crutches, walkers, elevated toilet seat, etc.)

Osteoarthritis: Management Medical Therapy Non-narcotic analgesia (e.g. acetaminophen) Non-steroidal anti-inflammatory drugs (NSAIDs) Specific COX-2 inhibitors

Osteoarthritis: Management Joint Injection Corticosteroids Hyaluronate preparations

Osteoarthritis: Management Alternative Therapies Chondroitin sulfate Glucosamine Recent data No benefit over placebo in most patients No adverse events

Osteoarthritis: Management Surgery Osteotomy Total joint replacement Joint fusion

Diffuse Idiopathic Skeletal Hyperostosis Nomenclature DISH Forrestier's Disease Characteristics Variable clinical symptoms No specific treatment program

Diffuse Idiopathic Skeletal Hyperostosis Characteristics Calcification of the anterior spinal ligament Flowing osteophytes Involvement of at least four contiguous vertebral bodies Sparing of posterior elements Maintenance of disc height

Normal Cervical Spine

Diffuse Idiopathic Skeletal Hyperostosis Nomenclature Characteristics Variable clinical symptoms - often asymptotic No specific treatment program

Osteochondritis Dessicans Clinical Features Articular cartilage and underlying bone loose in the joint. Frequently associated with minor trauma Often a familial tendency Often seen in young adults

Osteochondritis Dessicans Management Surgical Repair Some cases may be observed and fragments removed

Chondromalacia Patellae Clinical Characteristics Thinning and damage of cartilage of patellofemoral joint More common in women May be associated with subluxation

Chondromalacia Patellae Management Quadriceps muscle strengthening exercises Patellar taping Non steroidal anti-inflammatory drugs (NSAIDs) Surgery Lateral release Avoid major surgery (e.g. patellectomy)

Neuropathic Arthritis Clinical Features Diseases associated with Neuropathic arthritis Management

Neuropathic Arthritis Clinical features Sensory neurologic deficit Joint deformity and destruction out of proportion to the severity of pain. Painless in the face of marked deformity Less painful than expected in view of the degree of deformity. Characteristically, there is significant Hypertrophic bone formation, Subchondral sclerosis, Severe cartilage degeneration Loose bone fragments.

Neuropathic Arthritis Diseases Associated with Neuropathic Arthritis Diabetes mellitus Syringomyelia Syphilis with tabes dorsalis Any peripheral neuropathy

Neuropathic Arthritis Management Education Reduce joint trauma DO NOT replace with artificial joints

Osteonecrosis (Avascular Necrosis/Aseptic necrosis) Pathophysiology Diseases associated with osteonecrosis Clinical Stages - In all stages joint space (cartilage) is maintained. Diagnosis Management

Osteonecrosis Pathophysiology Compromise of the blood supply to bone May in some cases be the result of increase in marrow fat and an increase in pressure within the bone May involve many sites - Hip is the most common site

Osteonecrosis Diseases associated with osteonecrosis Corticosteroids Glucocorticoid treatment (e.g. prednisone) Cushing’s disease Trauma Inflammatory arthritis Systematic lupus erythematosus Rheumatoid arthritis Hematologic disorders Hypercoagulability (antiphospholipid syndrome) Hemoglobinophathies (e.g. Sickle cell disease)

Osteonecrosis Diseases associated with osteonecrosis Infiltrative disorders Gaucher’s disease Decompression sickness (e.g. deep sea divers) Alcoholism Cirrhosis Malignancies Idiopathic

Osteonecrosis Clinical Stages Stage 0 - No symptoms, normal radiographs, abnormal MRI Stage 1 - Symptoms, normal radiographs, abnormal MRI Stage 2 - Patchy mottled sclerosis Stage 3 - Early bone collapse - Subcortical band immediately under the articular cartilage (crescent sign) Stage 4 - Late bone collapse - flattening of femoral head

Osteonecrosis Diagnosis Plan radiographs Magnetic Resonance Imaging (MRI) - EARLY Bone Scans May initially appear "cold" (decrease uptake) showing decreased blood flow. Later the affected area may appear "not' (increased uptake) showing revascularization and appositional new bone formation. Bone marrow pressure measurement and venography Bone biopsy

Osteonecrosis Management No proven effective treatment Some preliminary results with early lesions Vascular bone grafts Core decompression Surgery with joint replacement in advanced cases.

MECHANICAL ARTHROPATHY: CARTILAGE PATHOPHYSIOLOGY AND OSTEOARTHRITIS Questions?