15 Feb

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.

The prevalent opinion on the cause of OA is that it results from progressive fatigue failure, or, in other words, prolonged wear and tear. This would explain geometric increase in incidence of OA with age, as well as prevalence of OA in joints that are most used, not necessarily weight bearing (ankle in ballet dancers, MCPs in boxers, elbow in baseball pitchers, etc). Some studies supporting this idea show that articular cartilage alone cannot handle the entire force load during the joint movement. Much of the force is transmitted to and absorbed by the subchondral bone and periartricular muscles. Some recent studies suggest that in OA the elasticity of the subchondral bone is decreased due to increase in its mineral density.

Several other studies suggest quadriceps strengthening is beneficial in prevention and treatment of knee OA.

Others argue that the cause is not the wear and tear itself but the decrease in reparative abilities with age. Some biochemical findings listed above point to this, namely elevation in IL-1 and decrease in TIMP and PAI leading to unopposed degradation of the cartilage matrix by metalloproteinases.

A third opinion is that osteoarthritis is not a single disease but separate entities with a common final pathway. They separate primary OA into knee OA and hip OA, explaining that they have different risk factors and, therefore, could be distinct diseases, generalized OA, which is more dependent on systemic factors (such as genetic predisposition) than on local (i.e. mechanical) factors. They further divide the hip OA into hypertrophic, associated with pyrophosphate crystal deposition and diffuse idiopathic skeletal hyperostosis, and atrophic, associated with basic calcium phosphate crystals.


The main feature of the clinical presentation of OA is joint pain. The pain is usually a deep ache localized to the joint. It is typically aggravated by joint use and relieved by rest (in advanced OA the pain might be constant). If stiffness of the involved joints after rest is present, it usually lasts less than 20 minutes. It should be noted that the articular cartilage has no nerve endings and the pain comes from such structures as nerve endings in periosteum of osteophytes, microfractures of the subchondral bone, stretching of the joint capsule, periartricular muscle spasm, or synovitis in advanced OA.
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While OA diagnosis is made clinically, the x-ray findings include asymmetric joint space narrowing, subchondral bony sclerosis in most loaded areas due to bones rubbing on each other (eburna-tion), and in advanced cases, subchondral bony cysts from leakage of synovial fluid into the subchondral bone. The laboratory findings in primary OA are usually normal except for possible mild leukocytosis in the synovial joint fluid (less than 2000 WBC/L, mostly mononuclear cells). The laboratory specimens are usually obtained to rule out other causes of joint pain.

OA can affect any movable, synovial-lined joint, but the location is mostly influenced by which joint has been overloaded in the past, as discussed above. Weight-bearing joints are considered the most important ones affected, but not the only ones. The DIP and PIP joints in the hand are common sites for primary (idiopathic) OA. It is characterized by development of bony enlargements over distal interphalangeal joints (Heberden’s nodes) and proximal interphalangeal joints (Bouchard’s nodes). These nodes can be painful, especially if they develop fast, but once present, they are usually non-tender and do not interfere with the range of motion in the joints. Absence of the nodes does not, however, rule out OA. kamagra soft tablets

The second most common site of OA in hand is the 1st CMC joint (thumb base). Patients usually complain of swelling, tenderness, and crepitus on movement. Osteophyte development may lead to “squared” thumb base. Pain on motion of this joint also can lead to contracture of the first web space and hyperextension of the first metacarpophalangeal joint, which is similar to the swan-neck deformity seen in rheumatoid arthritis.

OA in the hip is most commonly secondary to congenital or developmental malformations such as acetabular dysplasia, Legg-Calve-Perthes disease, and SCFE. The pain is usually referred to the inguinal area and is worse on internal rotation. Gradual capsular fibrosis and growth of osteophytes result in progressive decrease in the range of motion of the hip joint.

The knee joint has been found to be involved more frequently in females than in males. The osteoarthritic knee joint is usually tender to palpation, contains osteophytes, and has bony crepitus on movement. Depending on which compartment is involved, the knee could go into either valgus or varus deformity. If the patellofemoral compartment is involved, one can elicit positive “shrug” test (pain on manually pressing patella against femur). However, in this case the evaluating physician must rule out another disease—chondromala cia patellae, which is characterized by bilateral patellofemoral compartment pain in teenagers and young adults (more commonly women). It is usually non-progressive, caused by patellar misalignment, and is treated by NSAIDs, physical therapy, and corrective surgery.
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OA of the spine is characterized by involvement of apophyseal joint, localized pain, and stiffness. It can also involve intervertebral disks and paraspinous ligaments. Notably, the cervical spine involvement is more common in women. Possible neurologic complications include compression of nerve roots by osteophytes, disk prolapse, and subluxation of an apophyseal joint, resulting in radicular pain and motor weakness.