Cause:
Endogenous factors:
- Changes in articular cartilage like increased brittleness, decreased water binding, decreased chondroitin sulfate, perhaps increased protein/polysaccharide ratio
- Lubrication and viscosity failure
- Genetic defects in procollagen (Nejm 1990;322:526), which are autosomal dominant
Exogenous factors:
- Trauma, including injuries decades before (Ann IM 2000;133:321)
- Congenital anomalies
- Metabolic diseases like gout and ochronosis
- Endocrine diseases like acromegaly
- Inflammatory joint diseases
- Obesity, increases knee DJD esp (Am J Med 1999;107:542)
Pathophys:(rv of pathophys—New Eng J Med 1989;320:1322)
Figure 18.1 Pathophysiology of DJD.
Quadriceps weakness may precede and somehow cause knee arthritis (Ann IM 1997;127:97)
Pain due to adjacent marrow space edema (Ann IM 2001;134:541, 591)
Sx:Post-rest stiffness, pain on motion. Joints most frequently involved are great toe and thumb mcp’s, knee, hip, sacral and cervical spine
Si:Motion preserved but local tenderness. Bony enlargement at dip joints called Heberden’s nodes, or at pip joints called Bouchard’s nodes. Local inflammation occasionally, esp in erosive osteoarthritis variant with hot joints seen in middle-aged women
CNS sx’s from cord or vertebral artery compression (CERVICAL SPONDYLOSIS) occasionally causing paraplegia; but neck, head, and shoulder pain all common
r/o avascular necrosis: of femoral head, esp in patients on steroids, alcoholics, or those with sickle cell disease; of knee, medial femoral condyle, or tibia in elderly (Bull Rheum Dis 1985;35:42)
Lab:
Path:Synovial bx shows fibrous cartilaginous degeneration esp at points of stress
Biomarkers: V65 vitronectin, C3f distinguish OA patients from RA and healthy controls (Ann Rheum Dis 2011 [dio:10.1136/ard.2010.135541)
Xray: Hypertrophic changes, eg, osteophytes, sclerosis, and bone cysts without cortical bone changes unlike RA; MRI shows marrow edema (Ann IM 2003;139:330)
Rx: (Rheum Dis Clin N Am 2003;29:4; Ann IM 2000;133:726; knee—Nejm 2006;354:841)
Perhaps prevent with statin use: 57% reduction in incidence, 53% less progression among users (Clockaerts, et al.; presented in World Congress on Osteoarthritis 2010)
Braces, exercise (Ann IM 2000;132:173 vs 2003;138:613), weight reduction, SSRI or TCA rx, patellar (McConnell) taping (DBRCT—BMJ 2004;327:135)
Acupuncture by DBCT (Ann IM 2004;141:901)
NSAIDs of debatable efficacy (NSAIDs for OA of hip, 2003; Cochrane Library Issue 4); acetaminophen preferable? (Nejm 1991;325:87)
Glucosamine sulfate 500 mg po tid OTC dietary supplement, w chondroitin sulfate, no help for some (ACP J Club 2006;145:17), others benefit, need 2-mo trial before benefit, may worsen diabetic control, and variable purity of OTC products
Intra-articular:
- Steroid injection helps for usually up to 3 months as long as joint is stable; need fluoroscopic guidance in hip (Arth Rheum 2007;56:2278); shoulder glenohumeral joint
- Hyaluronic acid (Hyalgan, Synvisc), Synvisc One (ACP J Club 2003;138:20; Rheumatol 1999;38:602; Med Let 1998;40:69) weekly × 3-5; helpful esp in mild-moderate disease, but can cause allergic (pseudoseptic) reactions in contrast to low-molecular-weight, nonavian hyaluronic acids like Euflexxa or Orthovisc, but all of dubious benefit (ACP J Club 2008;148:42; Jama 2003;290:3115); $700
Surgical arthroplasties, joint replacements (hip—Nejm 1990;323:725; knee—Nejm 1990;323:801, shoulder (J Shoulder Elbow Surg 2011;20:77), arthroscopic lavage and/or debridement at least in knee no help by DBCT (Nejm 2008;359:1097); caution in young (<65 yr) patients due to breakdown of prosthesis and poor outcomes with replacement; complication rate 7.6%.
Experimental: leeches 4 at a time q3mos better than topical NSAIDs! (Ann IM 2003;139:724)