MECHANICAL ARTHROPATHY:

MECHANICAL ARTHROPATHY:CARTILAGE PATHOPHYSIOLOGY AND OSTEOARTHRITIS

OBJECTIVES1.List the features of normal structure of cartilage, collagen, and proteoglycans.2.Describe the changes in cartilage, collagen and proteoglycans that occur in osteoarthritis.3.Recognize the clinical and radiographic changes in osteoarthritis.4.Describe the management of osteoarthritis.5.Know the clinical features, associated diseases, and management of diffuse idiopathic skeletal hyperostosis, osteochondritis dissecans, chondromalacia patellae, osteonecrosis, and neuropathic arthritis.3I. IntroductionA. Terminology1. Osteoarthritis (OA)2. Osteoarthrosis3. Degenerative Joint Disease (DJD)4. Hypertrophic Arthropathy

B. Definition - Osteoarthritis is characterized by:1. Progressive disintegration of articular cartilage2. Formation of new bone in the floor of the cartilage lesions (eburnation) and at the joint margins (osteophytes)

II. Normal Cartilage ReviewA. Physiology1. Cartilage is avascular2. Nutritiona. Subchondral boneb. Synovial fluid

B. Components1. 65-80% of cartilage is water2. Major matrix components- 90% of dry weighta. Proteoglycans (particularly aggrecan)b. Collagen3. Chondrocytes 1-2% of volume a. Biosynthetically active, but relatively quiescentb. Produce proteoglycans, but little collagenc. Source of enzymes and enzyme inhibitors4. Other important componentsa. Enzymes - Eg. Matrix metaloproteinases (MMPs) - e.g. collagenaseb. Enzyme inhibitors. E.g. Tissue inhibitors of metaloproteinases (TIMP)

C. Collagen - Type II in hyaline cartilage, Type II and Type I in fibrocartilage1. Vertical orientation in deep regions2. Horizontal orientation in superficial regionsD. Proteoglycans1. Propertiesa. Hydrophilicb. Polar2. Componentsa. Glycosaminoglycans (GAGs) - "acid mucopolysaccharides"(1) Chondroitins(2) Heparins(3) Keratan sulfates3. Core protein - binds GAGs to make proteoglycans4. Hyaluronic Acid - Non-covalent binding5. Most common cartilage proteoglycan is aggrecan

III. Pathology of OsteoarthritisA. Gross pathology1. Fibrillation and flaking of the cartilage surface2. Loss of cartilage3. Subchondral sclerosis (Eburnation)4. Osteophyte formation

B. Biochemical abnormalities1. Increase in water content2. Change in proteoglycans (PGs)a. Increased turnover and degradationb. Decrease in PG aggregation (smaller PGs)c. Increase in extractable PGsd. Decrease in chondroitin sulfate lengthe. Change in GAG composition

3. Collagena. Increase in collagen synthesis - a reflection of increased turnoverb. Production of some type I collagen4. Chondrocyte - damage and loss of chondrocytes is a late finding in OA5. Possible role of inflammation.a. Increase in cytokine levels (IL-1, IL-6. IL-8, and TNF-)b. Unclear what is the primary processIV. Risk FactorsA. Increasing ageB. Gender - More common in womenC. ObesityD. Trauma (Exercise on a normal joint has generally not been associated with more OA)E. Genetics1. Ethnic difference in populations - (e.g. Hip OA more common in Caucasians than in Chinese)2. Inherited genetic mutations of collagenF. Other causes of joint injury (e.g. inflammatory arthritis, congenital dislocations,etc)V. Clinical manifestationA. Symptoms1. Mechanical joint pain2. "Jelling" sensation3. Absence of morning stiffness

B. Physical Finding1. Local tenderness2. Bony swelling3. Crepitus

C. Laboratory1. Synovial Effusion - non-inflammatory (