There is perhaps no disease that is as close to the human condition as arthritis, or joint pain.It is among the earliest diseases described in the ancient medical literature, and is clearly found throughout the anthropological record, such as in bone and fossil remains.Researchers from many fields tell us that it is a disease we share with a great many animals, including our fellow mammals, as well as birds, reptiles and fish.For all of us, the sad commonality is that it is apparently inevitable: a simple process of wear and tear to joints over a lifetime of use.Interestingly enough, some mammals that hang upside down such as bats and sloths don’t seem to experience this kind of joint damage, although mammals supported by water such as whales do (Berkow 1992).In yogic tradition this might be seen as evidence that inverse postures (asanas) such as headstands promote the proper flow of energy that overcomes stagnant energy… in the philosophical tradition of ancient India this is represented by Bodhi, or Enlightenment tree, which as it grows sends its branches back down into the earth…
Broken down, busted up and good ol’ fashioned deee-generating joint problems got a high falootin’ name in western medicine: osteoarthritis (OA).It nonetheless has a precise definition, to differentiate it from the other forms of arthritis such as the rheumatoid, gouty, or bacterial arthritides (plural of arthritis).OA is characterized as a mild inflammatory joint disease with a gradual loss of articular cartilage and the subsequent hypertrophy of bone producing osteophytes.Its prevalence increases with age, as does its severity, with a usual onset of it more symptomatic forms in the fourth to fifth decades of life (or usually earlier with sports injuries). Men typically have an earlier onset than women, but women get it at an increasing frequency with age. (Berkow 1992; Rubin and Farber 1990, 723)
OA is classified as either primary (idiopathic) or secondary to some identifiable cause. Primary OA involves the distal and proximal interphalangeal joints, the first carpometacarpal joint, the intervertebral disks and zygapophyseal joints in the cervical and lumbar vertebrae, the first metatarsophalangeal joint, the hip, and knee. Secondary OA may present as above, but has a known underlying cause, including congenital joint abnormalities, genetic defects, crystal deposits, infection, metabolic diseases, endocrinopathies, inflammatory disease (e.g. RA, gout), and trauma from fracture or simple “wear and tear.” (Berkow 1992; Rubin and Farber 1990, 723)
Joints are an amazing feature of anatomical mechanics.Cartilage is a spongy, dense tissue covering the articular surfaces of bones, comprised mostly of extracellular matrix managed by a small number of very long-lived chondrocytes.This spongy surface is bathed in an extremely slippery synovial fluid filled with nutrients to feed the chrondrocytes and support cartilage health. Surrounding the synovium is a series of tough fibrous tissues and muscles to unite the joint, and maintain stability. As the cartilage is compressed with movement, fluid is pumped out of it and into the joint space.In essence, this action squeezes the wastes from out of the spongy cartilage, to be absorbed by the capillaries and then venules of the muscosa.As the cartilage is released the cartilage expands, swelling back up with nutrient-rich, slippery synovial fluid.As a result, normal joint movement is essential to joint health, and because joints have a very coefficient of friction, they should maintain themselves almost indefinitely with normal activity.The primary pitfall with cartilage is that it is an avascular tissue, as well as both aneural and alymphatic: or in other words, a part of the body that we have an inherent capacity to take for granted (aneural), but can take a very long time heal (avascular, alymphatic). (Berkow 1992; Rubin and Farber 1990, 723)
The earliest changes of osteoarthritis are the loss of proteoglycans and type II collagen, which is the principal structural elements of cartilage, from the surface of the articular cartilage, followed by the death of the chondrocytes.This process may take several years.Overtime, the articular surface develops microfractures, and the synovial fluid works its way down into these fissures, extending the cracks deeper.Neovascularization from the epiphysis and subchondral bone extends into the areas of the fissures, inducing subchondral osteoclastic bone resorption.Adjacent osteoblastic activity occurs simultaneously, resulting in a thickening of the subchondral bone plate in the area of the crack. Fibrocartilage plugs then form as a substitute for the articular cartilage, and the subchondral bone becomes exposed as it grinds against the opposite joint surface, which is usually undergoing a similar process.These thick, shiny smooth areas or subchondral bone are described as eburnated, or “ivory-like .”This eburnated bone then cracks, allowing synovial fluid to extend into the subchondral bone marrow, leading to a subchondral bone cyst.An osteophyte or bone spur then develops, consisting of bone and a mixture of connective tissues with a coating of fibrocartilage and sometimes islands of hyaline cartilage within the osteophyte. The degree of formation of these spurs varies among the joints, in proportion to the underlying cause. Finally, bony cysts (pseudocysts) form in the marrow below the subchondral bone, resulting from extrusion of joint fluid through the hyaline cartilage into the marrow, with a fibroblastic and osteoblastic cellular reaction. The gross pathology includes a roughening, pitting, and irregularity of the hyaline cartilage surface, proceeding to gross ulceration with focal and then diffuse areas of complete loss of cartilage, leaving only eburnated bony surfaces. By the time symptoms appear, synovial proliferation and some mild synovitis are virtually always present. (Berkow 1992; Rubin and Farber 1990, 723)
The signs and symptoms of OA are insidious and gradual, usually involving one or only a few joints. Pain with movement and morning stiffness are among the earliest symptoms of OA.As the condition progresses joint movement is impaired, with crepitus, tenderness, grating sensations or muscle spasm. Overtime the joint can become edematous and swollen, with the proliferation of the various joint tissues.With improper treatment and repeated injury the chances for recovery become progressively less and less. (Berkow 1992; Rubin and Farber 1990, 723)
The primary focus in the medical treatment of osteoarthritis is upon eliminating risk factors and treating symptoms such as pain and immobility.Thus patient education, physical and occupational therapy, weight reduction, exercise, and corrective devices such as orthotics may be recommended.Initial medications include OTC analgesics such as ASA, acetaminophen and NSAIDs.Prescription NSAIDs may be recommended when OTC medications are ineffective, including the newer generation COX-2 inhibitors that include valdecoxib, celecoxib and rofecoxib. COX-2 inhibitors are believed to exert their anti-inflammatory effects by inhibiting the enzyme cyclooxygenase-2 (COX-2) and thus the synthesis of proinflammatory prostaglandins from arachidonic acid.The stated benefits of COX-2 inhibitors over other non-selective NSAIDs that inhibit both COX-1 and COX-2 is that they do not inhibit COX-1, which plays an important role in prostaglandin-dependent mucosal protective mechanisms.Clinical studies have shown that patients taking selective COX-2 inhibitors have a lower incidence of gastrointestinal irritation and inflammation than patients taking non-selective NSAIDs.Despite being heavily marketed as a safe and important alternative to manage pain in osteoarthritis however, recent research indicates that COX-2 inhibitors also inhibit angiogenesis through direct effects on endothelial cells, and interfere with normal healing (Jones et al 1999).Furthermore, a series of studies published in the New England Journal of Medicine (Mar 17, 2005) have shown an increased risk of cardiovascular complications in patients taking various COX-2 inhibitors, including celecoxib, parecoxib, valdecoxib and rofecoxib.These studies and others initially caused the US FDA to ban these drugs, although in what was seen as a politically motivated move they have been placed back on the market, albeit for more limited indications, and not for sustained periods of time.
Surgical procedures in OA include arthroplasty (joint surfaces are replaced with artificial materials, usually metal or plastic), chondroplasty (surgical repair of the damaged cartilage) and arthrodesis (surgical fusion of the articular surfaces, which prevents movement-induced pain).In some cases joint replacement is recommended, in which the diseased or damaged joints are replaced with an artificial joint composed of a combination of metal and plastic.Knee and hip replacement are among the most common joint replacement procedures, but some joints such those of the spine cannot be replaced with the present technology.
It is fairly well-established that osteoarthritis is better prevented than treated, as effective treatment is hampered by the relatively poor circulatory supply to cartilage.Thus proper attention to preventing joint injury is key to preventing the later development of OA. Nutritional status however is key in the pathogenesis of OA, and care should be taken to supply the body with an optimal volume of key vitamins, minerals, and accessory nutrients involved in joint repair. To control pain and inflammation medicinal plants are used along with essential fatty acids that can help to down-regulate the production of pro-inflammatory eicosanoids.
Both Ayurvedic and Chinese medicine view osteoarthritis as an evolution of chronically poor circulation, and thus treatments are undertaken to restablish the proper flow of blood to the affected area.In Ayurvedic medicine osteoarthritis is called Sandhigata vata, of which Vata and ama are the primary the pathogenic factors taken into account.
1. Ensure proper nutrition.See the Paleolithic diet listed under The Fire Within: Digestive function and Botanical medicine.Care should be taken to remove foods that are associated with inflammatory symptoms, including red meat (i.e. feed-lot beef, pork), grains, dairy, sugar, fried foods, transfatty acids and solanaceous foods (e.g. potatoes, tomatoes, eggplant etc.).The diet should be optimized to provide the body with all the nutrients needed for proper bone and joint health, including generous amounts of cartilage and bone soups that contain chondroitin and glucosamine sulfate.In particular, chondroitin andglucosamine promote an increase in the synthesis of collagen and proteoglycans that form joints, as well as exert antiinflammatory effect.
- Calcium citrate or malate, 800-1200 mg daily
- Magnesium citrate or malate, 400-600 mg daily
- Manganese, 15-30 mg daily
- Boron, 3 mg daily
- Zinc, 15-20 mg daily
- Copper, 1.5-3 mg daily
- Folic acid, 400-800 mcg daily
- Vitamin A, 20,000 IU daily
- Niacin, 250 mg up to six times daily (taken with a B complex formula, 100 mg daily)
- Vitamin C, to bowel tolerance
- Vitamin D3,1000-1200 IU daily, taken all year in temperate climates
- Vitamin E, 800 IU daily
- Vitamin K, 200 mcg daily
- Chondroitin, 0.5-3 g bid-tid
- Glucosamine sulfate,0.5-3 g bid-tid
2. Decrease pain and inflammation. The focus should be on restoring joint function and limiting the production of proinflammatory eicosanoids.
- antiinflammatory botanicals, e.g. Black Cohosh (Actaea racemosa), Wild Yam(Dioscorea villosa), Ash (Fraxinus excelsior), Licorice (Glycyrrhiza glabra), Lignum Vitae (Guaiacum officinale), Devil’s Claw (Harpagophytum procumbens), Buckbean (Menyanthes trifoliata), Trembling Aspen (Populus tremuloides), Salix, Yucca spp., Smilax spp., Tanacetum,, Huang Qin (Scutellaria baicalensis), Ashwagandha (Withania somnifera), Guggulu (Commiphora mukul), Amalaki (Emblica officinalis), Huang Bai Phellodendron amurense),Mandukaparni (Centella asiatica), Fang Feng (Ledebouriella divaricata), Kushta (Saussurea lappa)
- analgesic botanicals, e.g. Arnica, Hypericum, Populus, Salix, Lactuca, Gelsemium, Piscidia, Ashwagandha (Withania somnifera),Guggulu (Commiphora mukul), Han Fang Ji (Stephania tetrandra), Yan Hu Suo (Corydalis yanhusuo), Jatiphala (Myristica fragrans)
- EPA/DHA, 1000 mg each daily
- MSM, 2-3 g bid-tid; also MSM cream applied topically
- antioxidants, e.g. vitamins A, C, E; minerals such as zinc and selenium
3. Ensure proper digestion.
- Digestive enzymes, full spectrum, 2-3 capsules with each meal
- Bitters (e.g. Berberis, Gentian,etc.) to enhance gastric and hepatic secretions
- Dipanapachana dravyas, to enkindle agni, e.g. Yavani (Trachyspermum spp.),Shunthi (Zingiber officinalis), Pippali (piper longum), Hingu (Ferula foetida)
- Botanicals to relieve Food Stagnation and strengthen the Spleen Qi, e.g. Chen Pi (Citrus reticulata), Shan Zha (Crataegus pinnatifida),Huang Qi (Astragalus membranaceus), Dang Shen (Codonopsis pilosula)
- Probiotics and synbiotics to restore the ecology of the gut
4. Promote alterative changes and enhance elimination.Conduct a proper review of eliminative function, with particular attention paid to kidney, liver and bowel function.
- alteratives, e.g. Smilax, Apium, Rumex, Guaiacum, Galium, Chimaphila, Berberis, Trifolium, Haritaki (Terminalia chebula), Amritbhallataka (Semecarpus anacardium milk extract), Guduchi (Tinospora cordifolia), Haridra (Curcuma longa), Guggulu (Commiphora mukul), Manjishta (Rubia cordifolia)
- alkalizing diuretics, e.g. Celery seed or juice (Apium graveolens), Nettle (Urtica dioica), Cleaver (Galium aparine),Pipsissewa (Chimaphila umbellata)
- Triphala churna, 2-3 g bid-tid, with equal parts laxative herb, e.g. Trivrit (Operculina), Turkey Rhubarb (Rheum) in chronic constipation
5. Enhance systemic and local circulation.
- steam baths, sauna
- circulatory stimulants, e.g. Prickly Ash (Zanthoxylum), Ginger (Zingiber), Cayenne (Capsicum), Tvak (Cinnamomum cassia)
- rubefacients, applied topically, used as a poultice, medicated oil, or volatile oil in joint edema with pain, but little indication of active inflammation, e.g. Ginger (Zingiber), Cayenne (Capsicum),Mustard seed (Brassica spp.), Peppermint (Mentha piperita), Jimsonweed (Datura), Nirgundi (Vitex negundo), Yavani (Trachyspermum spp.), Pippali (Piper longum)
- low impact weight bearing exercise
- niacin, 250 mg up to six times daily
- massage therapy, e.g. with rubefacient medicated oils (see above), or Ayurvedic tailam such as Narayana taila, Balashvagandhalakshadi taila,Pinda taila, Balaguduchyadi taila
6. Joint trophorestoratives, to rebuild the integrity of the joint.Many of these botanicals are rasayanas in Ayurvedic medicine, and in Chinese medicine, function to support Kidney and Jing.
- Western botanicals, e.g. Milky Oats (Avena sativa), Horsetail (Equisetum arvense), Nettle (Urtica), Bladderwrack (Fucus spp),Hawthorn (Crataegus), Bilberry (Vaccinium), Comfrey (Symphytum), Irish Moss (Chondrus), Alfalfa (Medicago)
- Ayurvedic botanicals, e.g. Ashwagandha (Withania somnifera), Gokshura (Tribulus terrestris), Amalaki (Emblica officinalis), Brahmi (Bacopa monniera), Mandukaparni (Centella asiatica), Guggulu (Commiphora mukul), Bala (Sida spp.), Shilajitu, Shuktibhasma (purified oyster shell ash), Shringaputa (deer horn ash)
- Chinese botanicals, e.g. Ren Shen (Panax spp.), Shan Yao (Dioscorea opposita),Huang Jing (Polygonatum sibiricum), Shu Di Huang(Rehmannia glutinosa), He Shou Wu (Polygonum multiflorum),Gou Qi Zi (Lycium chinense), Sang Shen (Morus alba),Lu Rong (Deer or Elk velvet), Dong Chong Xia Cao (Cordyceps sinensis), Yin Yang Huo (Epimedium grandiflorum), Bai Ji Tian (Morinda officinalis), Bu Gu Zhi (Psoralea coryfolia), Du Zhong (Eucommia ulmoides)
- Bone and seaweed soups
7. Specific formulations.
- Yogaraja guggulu, 2-3 g bid-tid
- Kaishora guggulu,2-3 g bid-tid
- Feng Shih Xiao Tong Wan, 10 pills bid-tid
- Guan Jie Yan Wan, 8 pills bid-tid
- Feng Shi Pian, 2 pills bid
- Te Xiao Yao Tong Ling (Specific Lumbaglin), 2 caps bid-tid