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) 분당스웨디시.
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.
At the same time there is some kind of matrix destabilization possibly the result of collagen fibers breaking. Collagen fibers provide the high tensile strength of cartilage. The physical properties are not unlike a mattress which can be compressed but not pulled apart sideways. The collagen/proteoglycan matrix provides the structural framework of the tissue and also forms a fluid compartment for the transport of nutrients, waste products, chemical messengers and hormones, to and from chondrocytes. Whether the breaking of the collagen fibers is a consequence of increased proteoglycan degradation is still not clear.
The degenerative enzymes can be modulated by Bromelain, Quercetin, Rutin, and EFA’s. Zinc, Manganese, Magnesium, Calcium, Vitamin D, C, B6, E, Glucosamine, and DLPA are all useful to help with inflammation. This combination of nutrients increases protein, proteoglycan and amino acid synthesis, facilitates repair of ligament and connective tissue, improves and restores bone growth and muscle action, increases blood vessel integrity and supports immune system function.
An acid environment around the joint will also activate these enzymes and thus precipitate the loss of proteoglycan. Chondrocytes are cells within the joint that produce these proteoglycans. Stimulation of these cells by particular nutrients can forestall some of the degenerative changes associated with arthritis. Thus, improving the chondrocytes healing potential is essential in the treatment of osteoarthritis. Bone cells, the osteocytes and osteoblasts, become metabolically very active in osteoarthritis and bone remodeling is evident.
According to allopathy – the course of osteoarthritis is usually slow and irreversible and is thought to be medically untreatable as it was a result of “wear and tear”. In most cases, you will be offered symptom control with a mild pain reliever like aspirin, along with moderate activity to keep the joints mobile. Osteoarthritis is rarely crippling, but it can be, particularly when the hip or knee joint are involved. Each year, thousands of people around the world die from the adverse effects of both the anti-inflammatory medications and steroids. To add insult to injury, some research suggests that there is mounting evidence that non-steroidal anti-inflammatory drugs actually cause certain features of osteoarthritis to progress faster – by inhibiting the synthesis of proteoglycans and thus damaging cartilage. Interestingly, Folic acid 6-6.4 mg and Vitamin B12 200ug reduces the need for NSAID’s with improvements in hand grip and reduced tenderness in joints.
Osteoarthritis is now understood to be a disease due to the disordered synthesis of proteoglycan and collagen. Both biosynthetic pathways can be regulated by nutritional means, and manipulation with nutritive substances has been shown to have significantly beneficial results in regulating cartilage metabolism and the progression of the disease is slowed or reversed.