What you Should Know About Arthritis & Rheumatism (Part 1)

Osteoarthritis, the most common chronic arthritis, accounts for half of all cases. Inflammation may occur, but OA is generally considered a non-inflammatory type of arthritis - referred to as degenerative joint disease or "wear-and-tear arthritis". Osteoarthritis (OA) is most prevalent in the aged and is probably related to the normal aging process (although it is seen occasionally in younger people and some forms have a genetic basis). The usual symptoms are deep aching pains localized to the joint(s) involved, stiffness after rest, joint swelling and tenderness, a grating sound when the joint is moved, and in later stages bone deformities. The pain is usually present with movement of the joint and relieved by rest. The pain arises in the joint capsule, ligaments, tendons, muscles and bone surrounding the damaged cartilage.

As the disease progresses, the exposed bone tissue thickens and forms bony spurs that enlarge the bone ends. The spurs encroach on the joint space and may restrict joint movement. Patients complain of stiffness on arising that lessens with activity. The affected joints may make a crunching noise as they move. This sound, called crepitus, results as the roughened articular surfaces rub together. The joints most often affected are those of the fingers, the base of the thumb, the big toe, the cervical and lumbar spine, and large weight-bearing joints of the lower limbs (knees and hips).

Current theory holds that normal joint use prompts the release of enzymes that break down cartilage. In healthy individuals, this damaged cartilage is replaced. In people with OA, more is destroyed than replaced. Although its specific cause is unknown, OA may reflect the cumulative effects of years of compression and abrasion acting at joint surfaces (accompanied by excessive amounts of the cartilage-destroying enzymes) which ultimately cause the once smooth articular cartilages to soften, roughen, fray, and erode - resulting in friction. The tendons, ligaments, and muscles holding the joint together become weaker, and the joint itself becomes painful and stiff. There is usually some pain, but little or no swelling.

Biochemically the disease can be initiated by excessive pressure being applied to the joint i.e. in sport or manual work. Inflammation of the cartilage may also be associated with infection, toxic irritation, or by poor nutritional status of bones and surrounding structures. Epidemiologists have also identified hereditary factors which predispose people to osteoarthritis. Other contributing factors include poor diet, obesity, diabetes, a sedentary lifestyle, hypertension, bowel toxicity, hyperuricaemia, hypothyroidism and other endocrine disorders, hyper-insulinaemia, and high estrogen levels. Allergies and chemical sensitivities may also predispose or aggravate osteoarthritis.

The primary chemical change observed is the loss of proteoglycans (a protein sugar or mucopolysaccharide) from the hyaluronic backbone, and is initiated by activation of degenerative enzymes associated with inflammation. These proteoglycans are responsible for cartilage resilience or bounce and their loss from the cartilage results in a stiffer material that is more easily damaged by "wear and tear". Proteoglycans account for 75-80% of normal cartilage, in osteoarthritis proteoglycans are reduced to 35-40%. The increased turnover and eventual loss of proteoglycans from osteoarthritic tissue is a consequence of an increase in chondrocyte metabolism.