Osteoarthritis is a type of arthritis that is caused by the breakdown and eventual loss of the cartilage of one or more joints. Cartilage is a protein substance that serves as a "cushion" between the bones of the joints.
Osteoarthritis is also known as degenerative arthritis. Osteoarthritis occurs more frequently as we age. Before age 45, osteoarthritis occurs more frequently in males. After age 55 years, it occurs more frequently in females. Osteoarthritis commonly affects the hands, feet, spine, and large weight-bearing joints, such as the hips and knees.
What causes osteoarthritis?
Primary osteoarthritis is mostly related to aging. With aging, the water content of the cartilage increases, and the protein makeup of cartilage degenerates. Eventually, cartilage begins to degenerate by flaking or forming tiny crevasses.
In advanced cases, there is a total loss of cartilage cushion between the bones of the joints. Repetitive use of the worn joints over the years can irritate and inflame the cartilage, causing joint pain and swelling. Loss of the cartilage cushion causes friction between the bones, leading to pain and limitation of joint mobility. Inflammation of the cartilage can also stimulate new bone outgrowths (spurs, also referred to as osteophytes) to form around the joints.
Osteoarthritis occasionally can develop in multiple members of the same family, implying a hereditary (genetic) basis for this condition.
Secondary osteoarthritis is caused by another disease or condition. Conditions that can lead to secondary osteoarthritis include obesity, repeated trauma or surgery to the joint structures, abnormal joints at birth (congenital abnormalities), gout, diabetes, and other hormone disorders.
Obesity causes osteoarthritis by increasing the mechanical stress on the cartilage. In fact, next to aging, obesity is the most powerful risk factor for osteoarthritis of the knees. The early development of osteoarthritis of the knees among weight lifters is believed to be in part due to their high body weight. Repeated trauma to joint tissues (ligaments, bones, and cartilage) is believed to lead to early osteoarthritis of the knees in soccer players. Interestingly, recent studies have not found an increased risk of osteoarthritis in long-distance runners.
Crystal deposits in the cartilage can cause cartilage degeneration and osteoarthritis. Uric acid crystals cause arthritis in gout, while calcium pyrophosphate crystals cause arthritis in pseudogout.
Which calcium crystals occur in the body?
A substance called 'apatite' (a mixture of various calcium phosphate crystals) forms the normal mineral in human bones. In healthy adults apatite occurs only in our bones and teeth and there are no calcium crystals elsewhere. Sometimes, however, calcium crystals form in other body tissues. For example, apatite can form in tendons (the fibrous cords that attach muscles to bones). This condition is called 'calcific tendinitis'. The usual site for this is the shoulder, in the tendon of the supraspinatus muscle that helps move the shoulder joint (see Figure 2). But tendons around the hip, hand, or occasionally other places in the body can also be affected.
Rather than forming in tendons, however, it is much more common for the abnormal formation of calcium crystals to be in the cartilage within joints. This is called 'cartilage calcification', or 'chondrocalcinosis'. This can affect the soft, slippery gristle attached to the bone ends (hyaline cartilage), or the tougher form of cartilage (fibrocartilage) which makes up the free 'spacers' (menisci) in some joints, such as the knee. (See Figure 3)
Iif the crystals move from their protected site within the cartilage or tendon they become exposed to the body's defence systems and can cause attacks of severe inflammation. This movement of crystals out of surrounding tissues into the joint cavity, or out of a tendon into the surrounding soft tissues, is called 'crystal shedding' spell of very noticeable inflammation caused by shedding of calcium pyrophosphate crystals into a joint is called 'pseudogout' or 'acute pyrophosphate arthritis'. The attack caused by shedding of apatite from a tendon is called 'acute calcific tendinitis'. It is also sometimes known as 'acute periarthritis', meaning inflammation not inside, but near a joint.
Why do people get calcium crystal deposits?
If a chemical is dissolved in water in a laboratory there is a certain concentration at which crystals start to develop. Even in healthy people, certain chemicals may be present in the blood, urine or soft tissues at levels which in other circumstances would be high enough for crystals to form. The reason crystals do not usually occur in body tissues and fluids is that there are other substances, mainly proteins, which prevent them developing. These are called 'inhibitors'. Other substances can actually increase the likelihood of crystals forming ; these are called 'promoters'.
This applies to the basic materials needed to make calcium crystals (calcium and pyrophosphate or phosphate). The most likely reason crystals form is because the balance between inhibitor and promoter substances changes. This balance tends to alter as part of normal ageing, but also because of osteoarthritis. The common form of chondrocalcinosis that is associated with ageing and osteoarthritis usually involves just a few joints, mainly the knees. Occasionally the tendency to develop chondrocalcinosis and pseudogout may run in families.
Far less commonly, chondrocalcinosis may be due to a metabolic disease which interferes with the regulation of calcium or pyrophosphate levels.
Examples are conditions such as
1. hyperparathyroidism (overactivity of the parathyroid glands)
2. haemochromatosis ('iron-storage disease')
3. hypomagnesaemia (magnesium deficiency)
Oxalates and Osteoarthritis?
Oxalates are naturally-occurring substances found in plants, animals, and in humans. In chemical terms, oxalates belong to a group of molecules called organic acids, and are routinely made by plants, animals, and humans. Our bodies contain oxalates, and our cells routinely convert other substances into oxalates. For example, vitamin C is one of the substances that our cells routinely convert into oxalates.
Certain foods contain oxalates Healthy individuals can safely consume such foods in moderation, but those with kidney disorders, gout, rheumatoid arthritis and potentially osteoarthritis with calcium deposits are advised to avoid excessive consumption foods high in oxalic acid or oxalates. The calcium oxalate crystals or precipitate (better known as kidney stones) obstruct the kidney tubules. An estimated 80% of kidney stones are formed from calcium oxalate.
Foods that contain oxalates
The following are some examples of the most common sources of oxalates, arranged by food group. It is important to note that the leaves of a plant contain higher oxalate levels than the roots, stems, and stalks.
Blackberries, blueberries, raspberries, strawberries, currants, kiwifruit, concord (purple) grapes, figs, tangerines, and plums
Spinach, Swiss chard, beet greens, collards, okra, parsley, leeks and quinoa are among the most oxalate-dense vegetables Celery, green beans, rutabagas, and summer squash would be considered moderately dense in oxalates
Nuts and seeds
Almonds, cashews, and peanuts
Soybeans, tofu and other soy products
Wheat bran, wheat germ, quinoa (a vegetable often used like a grain)
Cocoa, chocolate, and black tea
Is osteoarthritis with calcium crystals different from osteoarthritis without calcium crystals?
Many, but not all, people with osteoarthritis have calcium pyrophosphate crystals in their osteoarthritic joint cartilage. This is particularly common with osteoarthritis of the knee. Osteoarthritis with crystals is sometimes called 'chronic pyrophosphate arthritis'. The presence of calcium pyrophosphate crystals tends to cause the osteoarthritis to be more troublesome and severe.
There is equivocal evidence for gastrointestinal bleeding or renal (kidney) damage with long-term use of 4 g/day. NSAIDs appear to be more potent, but pose greater risk of side-effects.
Non-steroidal anti-inflammatory drugs
In more severe cases, non-steroidal anti-inflammatory drugs (NSAID) reduce both the pain and inflammation; they all act by inhibiting the formation of prostaglandins. Most prominent drugs in the class include diclofenac, ibuprofen, naproxen and ketoprofen Diclofenac has been found to cause damage to the articular cartilage. Another type of NSAID, COX-2 selective inhibitors (such as celecoxib, rofecoxib and valdecoxib) have often been used but are no more effective than the other NSAIDs. The latter two NSAIDs (rofecoxib and valdecoxib) carry an elevated risk for cardiovascular disease.
Oral steroids are not recommended in the treatment of OA because of their modest benefit and high rate of adverse effects. However intra - articular corticosteroid temporarily improve symptoms Opioid analgesics For moderate to severe pain a opioid analgesic such as morphine or codeine may be useful short term. Topical There are several NSAIDs available for topical use (e.g. diclofenac, ibuprofen and ketoprofen) with little, if any, systemic side-effects and at least some therapeutic effect. Creams and lotions, containing capsaicin, are effective in treating pain associated with OA if they are applied with sufficient frequency.
If the above management is ineffective, joint replacement surgery may be required. Arthroscopic surgical intervention for osteoarthritis of the knee has been found to be no better than placebo at relieving symptoms
The majority of patients with arthritis have tried alternative treatments for their pain. Some studies have reported benefits for these approaches, including acupuncture and some supplements.
A 2006 Cochrane review supported the use of acupuncture for pain management in osteoarthritis.
Oral glucosamine is marketed as a treatment of osteoarthritis. Commonly sold forms of glucosamine are glucosamine sulphate and glucosamine hydrochloride. Glucosamine is often sold in combination with other supplements such as chondroitin sulphate and methylsulfonylmethane Glucosamine may take weeks to months before improvements in symptoms are noticed. Restoration of cartilage A 2009 review concluded that "Little evidence suggests that glucosamine is superior to a placebo treatment in restoring articular cartilage."
A 2009 scientific review of available studies concluded that glucosamine sulphate, glucosamine hydrochloride, and chondroitin sulphate have individually shown inconsistent efficacy in decreasing OA pain, but many studies confirmed OA pain relief with glucosamine and chondroitin sulphate in combined use.
Since glucosamine is a precursor for glycosaminoglycans, and glycosaminoglycans are a major component of joint cartilage, supplemental glucosamine may help to prevent cartilage degeneration and treat arthritis. Chondroitin sulphate is sometimes used in conjunction, and animal studies suggest that chondroitin may increase its efficacy. Use A typical dosage of glucosamine salt is 1,500 mg per day.
Since glucosamine is usually derived from shellfish, those allergic to shellfish may wish to avoid it; however, since glucosamine is derived from the shells of these animals while the allergen is within the flesh of the animals, it is probably safe even for those with shellfish allergy. Alternative sources using fungal fermentation of corn are available.
S-Adenosyl methionine (SAMe) has been tested; a review of 10 studies found that it has an effect on pain relief similar to nonsteroidal anti-inflammatory drugs · Frankincense resin from Boswellia serrata trees—Indian frankincense is a traditional treatment for arthritis in Ayurvedic medicine
Bromelain protease enzymes extracted from the plant family Bromeliacea (pineapple), blocks some proinflammatory metabolites
Antioxidants including vitamins C and E in both foods and supplements, provide pain relief from OA.
Ginger (rhizome) extract - has improved knee symptoms moderately.
Selenium deficiency has been correlated with a higher risk and severity of OA.
Vitamin B9 (folate) and B12 (cobalamin) taken in large doses reduce OA pain.
Vitamin D deficiency has been reported in patients with OA, and supplementation with Vitamin D3 is recommended for pain relief.
Diet appears to be a factor in the aetiology of arthritis based on surveys of over 1400 volunteers during a 20-year period. Plants in the drug family, Solanaceae (nightshades) are an important causative factor in arthritis in sensitive people.
This family includes;
Potato (Solanum tuberosum L.)
Tomato (Lycopersicon esculentum L.)
Eggplant (Solanum melongena L.)
Tobacco (Nicotiana tabacum L.)
Peppers (Capsicum sp.) of all kinds except the black pepper (family, Piperaceae).
A buildup of cholinesterase inhibiting glycoalkaloids and steroids from consumption and/or use (tobacco) of the nightshades and from other sources such as caffeine and some pesticides (organophosphates and carbamates) may cause inflammation, muscle spasms, pain, and stiffness.
Osteoarthritis appears to be a result of long-term consumption and/or use of the Solanaceae which contain naturally the active metabolite, vitamin D3, which in excess causes crippling and early disability (as seen in livestock). Rigid omission of Solanaceae, with other minor diet adjustments, has resulted in positive to marked improvement in arthritis and general health.
It is recommended to eliminate the solinaceae family for two weeks to see if there is an improvement in symptoms. If there is an improvement, there is no need to avoid the suspect food altogether but rather, don’t eat these foods everyday. Substitute potatoes with pumpkin and sweet potato.