Arthritis is a general term for conditions in which joints of the body become inflamed by various mechanisms usually accompanied by pain, frequently involving changes in joint structure with progressive deterioration¹. Remembering basic joint structure, virtually all joints are lined with tissues composed predominantly of proteins (collagen and elastin)² proteoglycans, and synovial fluid consisting of proteins, a few antibodies, enzymes and WBCs³. This intricate and complex structure operates flawlessly until some event or condition causes inflammation and begins the degenerative process called arthritis.

    Arthritis can be caused by injuries, infection, immune responses, mechanical abnormalities, genetic predispositions and other conditions⁴. We as clinicians regularly see patients with osteoarthritis, rheumatoid and post-traumatic arthritis; less commonly gout, AS, psoriatic arthritis, septic arthritis and rarely autoimmune (other than RA) or metabolic arthridities. Virtually all forms of arthritis demonstrate a sign of inflammation in and around the joint affected and is a major factor of treatment. Signs of inflammation include swelling, stiffness, tenderness, redness and warmth. Inflammation can begin suddenly (within minutes or hours) or gradually over months. Cartilage becomes eburnated from the inflammation, eroded or brittle and fragment. Synovial membranes can hypertrophy producing excess or viscous fluid with eventual intra-articular fibrin formation. Ligaments can become thin initially allowing joint instability then later hypertrophy adding to immobility. Juxta-articular and mechanically associated muscles will spasm then later atrophy. Articular bone can hypertrophy producing osteophytes or generalized joint enlargement or become osteoporotic further compromising joint integrity. Virtually all of these processes are the result of inflammation, either directly or indirectly, usually occurring in concert.

    The symptoms of OA usually begin gradually over long periods of months or years and are diverse in presentation. One may experience progressive joint stiffness with mild pain starting more as an annoyance with progressive loss of joint motion. Joint crepitation is a common feature with infrequent tenderness⁶. Pain is usually worse after exercise accompanied by some inflammation. There is usually no severe joint inflammation as there is with RA but may occur as the condition progresses. This inflammation is without the defined redness and is less symmetrical than that of RA. Heberden's nodes⁷ often appear at the DIP joints of both hands and feet. With progression the cartilage of the joint deteriorates exposing the subarticular bone to direct contact. The pain of osteoarthritis comes from loss of articular cartilage, damage to connective tissues, muscle strain from abnormal biomechanics, inflammation and bone swelling.

    A primary characteristic of OA is the osteophytes that form at the periphery of the affected joints. They occur as a consequence of proliferative chondrocyte reactions to the mechanical joint stresses and inflammation. Large osteophytes can obstruct movement severely and interfere with other body functions, especially in the spine. OA predominantly affects weight-bearing joints such as hips, knees, feet and spine but any joint can be affected. One common place is the carpometacarpal joint of the thumb and DIP of the fingers in individuals over 45 years of age. Also wrist involvement is rare with the exception of the variant known as erosive osteoarthritis⁸.

    The specific cause of OA is unknown but genetic, metabolic, endocrine, biomechanical and hydrolytic enzyme factors have been suggested as potential etiologies⁹. It is hypothesized that increased loss of proteoglycans from the cartilage matrix or "aggregation" of these substances by enzymatic action through various mechanisms is key¹⁰. There appears to be a familial predisposition towards OA¹¹ or at least unusual joint stress from genetically determined body type that allows its development. Excess body weight provides a basis for stresses upon the large weight bearing joints that potentiate OA development. Weight loss with appropriate muscle conditioning, even when arthritis is present, will reduce the severity of symptoms or slow the progression of the disease. Traumatic events to individual or groups of joints is also a common factor and a point where some authorities believe OA should be divided into two subsets. Some authorities use the term osteoarthrosis to differentiate the more systemic condition from the regional or monarticular trauma induced conditions¹². I tend to agree differentiating osteoarthritis from posttraumatic arthritis, although the nutraceutical intervention for both is very similar.

    Diagnosis is obtained by a careful history with observation as to onset, frequency, timing of painful episodes, joints involved and careful physical examination. Include in your history whether current or previous events of colitis, COPD, psoriasis and other systemic conditions have occurred as these may present migratory joint pain mimicking early OA. Laboratory tests can include an ESR that may be normal or only slightly elevated and a negative RF. X-rays reveal a decreased joint space, osteophytes, bone cysts and subarticular sclerosis¹³.

    RA may start gradually or with a sudden, severe attack including fever and fatigue. Common signs and symptoms are listed in the adjoining table and vary from person to person. They may be mild with asymptomatic intervals to exacerbations with severe pain and immobility. Some individuals will experience continuous pain with only gradual symptom change, progressive joint damage and disability¹⁶.