For now, however, the only definitive treatment for OA is surgical. Such treatment on OA joints should be attempted only if all the non-operative options have been exhausted, and the goal should be to decrease pain and improve mobility. The least extensive treatment is tidal irrigation. It is mostly performed on knee and shoulder joint and involves washing the joint space with large amounts of saline to remove fibrin and debris (usually while performing arthroscopy of the joint). Other surgical options include osteotomy, which is used in mild cases of OA and mostly involves removing painful osteophytes. The most intensive procedure is total joint replacement, which is used in severe cases and is considered to be the definitive treatment. There also is the new and experimental technique of abrasion arthroplasty. This involves stripping the damaged cartilage off of the entire joint surface and allowing it to be replaced by new cartilage. However the new cartilage is weaker and immature. There is no concrete data yet to show that this procedure is effective and further studies are needed.

Read the rest of this entry »

The general complications of OA include loss of range of motion, extremity deformity due to asymmetric loss of joint space, subluxation, ankylosis or complete bony fusion of a joint, and intraarticular loose bodies related to subchondral fractures.

Read the rest of this entry »

The reasons for formation of the osteophytes, that are at least partially responsible for the joint deformity and pain in OA, are unclear. Some possibilities include increase in vascularity of the basal layers of the degenerating cartilage, improperly healing stress fractures in subchondral trabculae near subchondral margins, or venous congestion in the bone. In animal models, joint immobilization seems to prevent osteophyte formation, glucocorticoid administration decreases their size and prevalence, and biphosphonate therapy does not affect their formation.

Read the rest of this entry »

Risk factors for primary OA include increasing age, history of injury to the joint (trauma, repetitive stress, inflammation, etc.), and obesity. Secondary OA can develop as a result of any physical, metabolic, or chemical injury to the joint such as congenital or developmental bone malformations (Legg-Calve-Perthes disease or SCFE), metabolic diseases (alcaptonuria, hemochromatosis, Wilson’s disease), endocrine (acromegaly, hyperparathyroidism, DM, hypothyroidism), abnormal calcium deposition (calcium pyrophosphate dihydrate deposition, apatitie arthropathy), other bone/joint diseases (AVN, RA, gout, infection, osteoporosis), neuropathic (Charcot joints), and even such entities as frostbite, Caisson’s disease, and hemoglobinopathies.

Read the rest of this entry »

Osteoarthritis (OA) is a non-inflammatory disease characterized by progressive loss of joint articular cartilage that results in pain and deformity. The disease is also known as degenerative arthritis, degenerative joint disease (DJD), and osteoarthrosis. Epidemiologic data on OA varies depending on the source but the general consensus is that it is the most common joint disease affecting approximately 20-million Americans. Although people can be affected by OA at any age, is it most prevalent in the older population, with 65% of individuals over 65 years old having radiographic evidence of the disease in at least one joint. The disease will become even more prevalent as the cohort of baby boomers grows older in the near future.

Read the rest of this entry »