Osteoarthritis Terminology PowerPoint Presentation

Slide 1 -

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

Slide 2 -

Osteoarthritis Terminology Osteoarthritis Osteoarthrosis Degenerative Joint Disease Hypertrophic Arthropathy

Slide 3 -

ppt slide no 3 content not found

Slide 4 -

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)

Slide 5 -

Osteoarthritis Normal Cartilage Review Nutrition Chondrocytes Collagen Proteoglycans Hyaluronic Acid

Slide 6 -

ppt slide no 6 content not found

Slide 7 -

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)

Slide 8 -

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

Slide 9 -

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

Slide 10 -

ppt slide no 10 content not found

Slide 11 -

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

Slide 12 -

ppt slide no 12 content not found

Slide 13 -

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

Slide 14 -

Osteoarthritis Normal Cartilage Review Nutrition Chondrocytes Collagen Proteoglycans Hyaluronic Acid

Slide 15 -

Pathology of Osteoarthritis Gross Pathology Biochemical Abnormalities

Slide 16 -

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

Slide 17 -

ppt slide no 17 content not found

Slide 18 -

ppt slide no 18 content not found

Slide 19 -

ppt slide no 19 content not found

Slide 20 -

ppt slide no 20 content not found

Slide 21 -

ppt slide no 21 content not found

Slide 22 -

ppt slide no 22 content not found

Slide 23 -

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

Slide 24 -

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.

Slide 25 -

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

Slide 26 -

ppt slide no 26 content not found

Slide 27 -

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

Slide 28 -

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

Slide 29 -

Pathology of Osteoarthritis Biochemical Abnormalities

Slide 30 -

Pathology of Osteoarthritis Biochemical Abnormalities

Slide 31 -

Pathology of Osteoarthritis Gross Pathology Biochemical Abnormalities

Slide 32 -

Osteoarthritis Risk Factors

Slide 33 -

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)

Slide 34 -

ppt slide no 34 content not found

Slide 35 -

Osteoarthritis Clinical Manifestation Symptoms Physical Finding Laboratory

Slide 36 -

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

Slide 37 -

Clinical Manifestation Physical Finding Local tenderness Bony swelling Crepitus

Slide 38 -

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

Slide 39 -

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

Slide 40 -

ppt slide no 40 content not found

Slide 41 -

ppt slide no 41 content not found

Slide 42 -

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

Slide 43 -

ppt slide no 43 content not found

Slide 44 -

ppt slide no 44 content not found

Slide 45 -

ppt slide no 45 content not found

Slide 46 -

ppt slide no 46 content not found

Slide 47 -

ppt slide no 47 content not found

Slide 48 -

ppt slide no 48 content not found

Slide 49 -

ppt slide no 49 content not found

Slide 50 -

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

Slide 51 -

Osteoarthritis Classification Primary Idiopathic Generalized osteoarthritis Erosive osteoarthritis

Slide 52 -

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

Slide 53 -

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

Slide 54 -

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

Slide 55 -

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.)

Slide 56 -

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

Slide 57 -

Osteoarthritis: Management Joint Injection Corticosteroids Hyaluronate preparations

Slide 58 -

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

Slide 59 -

Osteoarthritis: Management Surgery Osteotomy Total joint replacement Joint fusion

Slide 60 -

ppt slide no 60 content not found

Slide 61 -

ppt slide no 61 content not found

Slide 62 -

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

Slide 63 -

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

Slide 64 -

Normal Cervical Spine

Slide 65 -

ppt slide no 65 content not found

Slide 66 -

ppt slide no 66 content not found

Slide 67 -

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

Slide 68 -

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

Slide 69 -

ppt slide no 69 content not found

Slide 70 -

ppt slide no 70 content not found

Slide 71 -

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

Slide 72 -

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

Slide 73 -

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

Slide 74 -

Neuropathic Arthritis Clinical Features Diseases associated with Neuropathic arthritis Management

Slide 75 -

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.

Slide 76 -

ppt slide no 76 content not found

Slide 77 -

ppt slide no 77 content not found

Slide 78 -

ppt slide no 78 content not found

Slide 79 -

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

Slide 80 -

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

Slide 81 -

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

Slide 82 -

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

Slide 83 -

ppt slide no 83 content not found

Slide 84 -

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)

Slide 85 -

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

Slide 86 -

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

Slide 87 -

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

Slide 88 -

ppt slide no 88 content not found

Slide 89 -

ppt slide no 89 content not found

Slide 90 -

ppt slide no 90 content not found

Slide 91 -

ppt slide no 91 content not found

Slide 92 -

ppt slide no 92 content not found

Slide 93 -

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

Slide 94 -

MECHANICAL ARTHROPATHY: CARTILAGE PATHOPHYSIOLOGY AND OSTEOARTHRITIS Questions?