Overview and Risk Factors
Osteoarthritis (OA), also known as degenerative joint disease, is the most common joint disorder. It is characterized by hyaline cartilage degeneration and subchondral bone hypertrophy within a joint. Unlike rheumatoid arthritis, OA usually produces minimal inflammation. In severe cases, the articular joint surface may be destroyed, with resultant pain and disability.
OA may be idiopathic or secondary, and multiple factors generally influence its development. Secondary forms are due to endocrine abnormalities (eg, hypothyroid, diabetes mellitus), other joint diseases (rheumatoid arthritis, gout, infection), and bone pathology (avascular necrosis, Paget's disease).
OA begins with initial articular stiffness, typically lasting less than 15 minutes a day, and gradually progresses to pain with joint motion. The condition often affects weight-bearing joints (knee, hip, or vertebra).
When the hands are involved, the distal interphalangeal (DIP) and the first carpometacarpal (CMC) joints are most commonly affected.
OA rarely affects the elbow, wrist, ankle, shoulder, and temporomandibular joints.
- Obesity. Knee and hip joints are particularly vulnerable in obese individuals.
- Age. The condition is rare in young people, but common in middle-aged and older adults.1 One-third of people older than 65 years have radiographic evidence of osteoarthritis in the knee.
- Female gender. Females have adjusted relative risk equal to 2.6, compared with men, although the etiology is uncertain.2
- Occupation. Hands, hips, and knees are vulnerable.
- Genetics. An identical twin of an individual with hand or knee osteoarthritis has double the risk of having the same condition, compared with a fraternal twin.3
- Trauma. Repetitive acts involving any of the vulnerable joints present a cumulative risk.
- Pre-existing or anatomical joint abnormality.
- Poor proprioception and/or quadriceps weakness.
- Knee laxity.
Diagnosis and Treatment
The diagnosis of idiopathic OA is based on history, as well as physical, laboratory, and radiologic findings. An atypical presentation warrants inquiry into a secondary cause.
OA is usually asymmetrical, but can be bilateral in small joints. The following findings may be present on physical exam:
- Tender joint.
- Crepitus during flexion and extension.
- Bony enlargements, especially of the distal interphalangeal joints (Heberden's nodes), and proximal interphalangeal joints (Bouchard's nodes).
- Flexion contracture or varus deformity of the knee.
Joint effusion, if present, is mild and is not typically inflammatory; usually no other signs of inflammation are present. However, a variant of OA termed "inflammatory osteoarthritis" may present with effusion, redness, warmth to palpation, and morning stiffness.
No lab test is specific for osteoarthritis. The presence of an abnormal erythrocyte sedimentation rate, rheumatoid factor, or >2000 WBC/mm3 in joint aspirate suggests an inflammatory arthritis, such as rheumatoid or infectious arthritis.
The choice of treatment depends partly on whether inflammation is present. Options include a supervised exercise/muscle strengthening program, medication, or surgical intervention. In some cases, isometric exercises may be emphasized. Arthroscopy and joint replacement are usually reserved for patients with severe, functionally limiting disease.
Nonpharmacologic treatments should generally be attempted first in mild cases. Depending on the affected joint, treatments can include weight loss, exercise (low-impact, individualized programs), physical therapy; and shoe inserts/braces/splints.
Capsaicin cream significantly reduces pain, possibly by depleting substance P.4
Glucosamine and chondroitin sulfate are oral cartilage-enhancers and can be safely used with other treatments. Although such supplementation may improve symptoms, no convincing evidence has shown that the underlying disease process is ameliorated.
Acetaminophen dosing up to 4 grams per day is helpful in noninflammatory mild OA. However, chronic use may lead to renal or liver impairment.
Nonsteroidal anti-inflammatory drugs (NSAIDs) are the most effective treatment in inflammatory OA, moderate to severe noninflammatory OA, knee/hip OA, or after a failed acetaminophen trial. Careful monitoring of blood pressure is necessary when employing NSAIDs owing to the potential for aggravating or causing hypertension, and a 2 to 4 week trial should be completed before increasing the dose. If analgesia is suboptimal after 2 to 4 weeks at the maximum dose, a different NSAID or a nonacetylated salicylate should be used.
There is no preferred NSAID.
Chronic use may lead to gastrointestinal ulceration or kidney disease, especially if it is combined with aspirin. Some evidence suggests less toxicity occurs with salsalate and nabumetone (nonacetylated salicylates).
COX-2 inhibitors require further study to determine whether the benefits outweigh the potential cardiovascular risks.
Tramadol, another type of analgesic, may be combined with the above drugs.
Narcotics should be reserved for short-term severe pain or for nonsurgical candidates unresponsive to the above therapeutics.
Intra-articular glucocorticoid injection should be reserved for noninflammatory OA that is refractory to NSAID treatment, or inflammatory OA when NSAIDs are contraindicated. Adequate evidence for efficacy exists only for the knee joint, and injections should be limited to 3 or 4 times a year per joint. Infection should be ruled out prior to injection.
Injections of hyaluronic acid derivatives (hyalgan or hylan GF-20) may be beneficial when noninvasive treatments achieve suboptimal results.
Joint replacement (arthroplasty) should be reserved for severe refractory cases when the disease limits activities of daily living. However, significant improvement in symptoms and function may occur after surgery.
Arthroscopic debridement and synovectomy for OA have not yet gained acceptance.
The role of nutrition in OA is mainly related to the effects of diet on body weight. Obesity increases the risk for osteoarthritis of the hip5 and of the hand.6 Conversely, weight loss was found to significantly improve functional mobility and knee pain.7,8 Some evidence suggests that a reduction in body fat, independent of body weight, may help relieve OA symptoms.9 To the extent that a low-fat, high-fiber diet in combination with exercise prevents weight gain, a nutrition-based approach is likely to be useful in preventing and treating OA.
Once the disease process is established, the combination of glucosamine sulfate (1500 mg/day) and chondroitin sulfate (1200 mg/day) has been suggested for knee osteoarthritis, based on favorable early studies.10,11 Subsequent controlled trials, however, have been less favorable. Although older brands of glucosamine are made from shellfish, the possibility of allergic reactions led to the formulation of newer brands derived from corn.
Elevated serum cholesterol was independently associated with generalized OA in one study,12 and with osteoarthritis of the knee in another study.13 Persons with lower blood concentrations of vitamin D appear to show greater risk for progression, as evidenced in part by joint space narrowing and loss of cartilage.14,15
Ginger may provide significant pain relief for osteoarthritis patients. Its effects appear to be attributable to inhibition of both cyclooxygenase and lipoxygenase and to subsequent reductions of inflammatory mediators, such as prostaglandin E2 (PGE2), nitric oxide,16 and chemokines.17 Effective doses range from 170 mg ginger extract 3 times per day to 250 mg 4 times per day.
What to Tell the Family
In some cases, OA may be preventable through maintenance of a healthy weight with diet and exercise. Muscle-strengthening and low-impact exercises are the best options to avoid exacerbating the disease. Once diagnosed, OA may be improved in some patients through a combination of dietary changes for weight reduction, pain-relieving medications and/or botanical agents, and vitamin D. A dietitian can assist the patient and family with specific recommendations. In severe cases, replacement of the affected joint may be necessary to regain mobility and function.
1. Brandt, K. Osteoarthritis: Clinical patterns and pathology. In: Kelley WN, Harris ED Jr, Ruddy S, Sledge CE, eds. Textbook of Rheumatology. 5th ed. Philadelphia, Pa: WB Saunders; 1997:1383.
2. Davis MA, Ettinger WH, Neuhaus JM, Hauck WW. Sex differences in osteoarthritis of the knee: The role of obesity. Am J Epidemiol. 1988;127:1019-1030.
3. Spector TD, Cicuttini F, Baker J, Loughlin J, Hart D. Genetic influences on osteoarthritis in women: a twin study. BMJ. 1996;312:940-943.
4. Deal CL, Schnitzer TJ, Lipstein E, et al. Treatment of arthritis with topical capsaicin: a double-blind trial. Clin Ther. 1991;13:383-395.
5. Lievense AM, Bierma-Zeinstra SM, Verhagen AP, van Baar ME, Verhaar JA, Koes BW. Influence of obesity on the development of osteoarthritis of the hip: a systematic review. Rheumatology (Oxford). 2002;41:1155-1162.
6. Sayer AA, Poole J, Cox V, et al. Weight from birth to 53 years: a longitudinal study of the influence on clinical hand osteoarthritis. Arthritis Rheum. 2003;48:1030-1033.
7. Christensen R, Astrup A, Bliddal H. Weight loss: the treatment of choice for knee osteoarthritis? A randomized trial. Osteoarthritis Cartilage. 2005;13:20-27.
8. Messier SP, Loeser RF, Miller GD, et al. Exercise and dietary weight loss in overweight and obese older adults with knee osteoarthritis: the Arthritis, Diet, and Activity Promotion Trial. Arthritis Rheum. 2004;50:1501-1510.
9. Toda Y, Toda T, Takemura S, Wada T, Morimoto T, Ogawa R. Change in body fat, but not body weight or metabolic correlates of obesity, is related to symptomatic relief of obese patients with knee osteoarthritis after a weight control program. J Rheumatol. 1998;25:2181-2186.
10. Bruyere O, Pavelka K, Rovati LC, et al. Glucosamine sulfate reduces osteoarthritis progression in postmenopausal women with knee osteoarthritis: evidence from two 3-year studies. Menopause. 2004;11:138-143.
11. Richy F, Bruyere O, Ethgen O, Cucherat M, Henrotin Y, Reginster JY. Structural and symptomatic efficacy of glucosamine and chondroitin in knee osteoarthritis: a comprehensive meta-analysis. Arch Intern Med. 2003;163:1514-1522.
12. Sturmer T, Sun Y, Sauerland S, et al. Serum cholesterol and osteoarthritis. The baseline examination of the Ulm Osteoarthritis Study. J Rheumatol. 1998;25:1827-1832.
13. Hart DJ, Doyle DV, Spector TD. Association between metabolic factors and knee osteoarthritis in women: the Chingford Study. J Rheumatol. 1995;22:1118-1123.
14. Lane NE, Gore LR, Cummings SR, et al, for the Study of Osteoporotic Fractures Research Group. Serum vitamin D levels and incident changes of radiographic hip osteoarthritis: a longitudinal study. Arthritis Rheum. 1999;42:854-860.
15. McAlindon TE, Felson DT, Zhang Y, et al. Relation of dietary intake and serum levels of vitamin D to progression of osteoarthritis of the knee among participants in the Framingham Study. Ann Intern Med. 1996;125:353-359.
16. Shen CL, Hong KJ, Kim SW. Effects of ginger (Zingiber officinale Rosc.) on decreasing the production of inflammatory mediators in sow osteoarthrotic cartilage explants. J Med Food. 2003;6:323-328.
17. Phan PV, Sohrabi A, Polotsky A, Hungerford DS, Lindmark L, Frondoza CG. Ginger extract components suppress induction of chemokine expression in human synoviocytes. J Altern Complement Med. 2005;11:149-154.