Osteoarthritis (OA) is the most common joint disorder. It is characterized by hyaline cartilage degeneration and subchondral bone hypertrophy within a joint but is a disease of the entire joint, involving cartilage, joint lining, ligaments, and bone. While once thought to be a “wear and tear” process, there is now evidence that a variety of factors, including proinflammatory mediators, underlie the clinical manifestations. OA exhibits a great variation in disease expression, as many individuals are completely asymptomatic, while others experience severe joint destruction with resultant pain and disability.

OA may be idiopathic or secondary, and multiple factors generally influence its development. Idiopathic OA may be genetically driven. Joint shape, mechanics, and joint trauma are also key contributing factors in the development of clinically apparent OA. Secondary forms may occur due to endocrine abnormalities (e.g., hypothyroidism, diabetes mellitus), other joint diseases (e.g., rheumatoid arthritis, gout, infection), and bone pathology (e.g., avascular necrosis, Paget’s disease).

OA begins with pain and joint stiffness that is typically worsened by joint use. Symptoms may or may not progress to include joint swelling and a limited range of motion. The condition most commonly 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, and temporomandibular joints.

Risk Factors

Obesity. Knee and hip joints are particularly vulnerable in obese individuals. Excess weight puts stress on the knee, hip, ankle, and feet joints, as well as the lower spine.

Age. The incidence and prevalence of OA increase with age.

Female sex. Hand and knee OA is more common in females.[1]

Occupation. Certain occupations, such as construction work and carpentry, increase the risk for osteoarthritis of the hands, hips, and knees.

Genetics. Twin studies indicate that up to 40% of OA risk may be due to genetic factors.[2] However, the increased risk does not seem to follow typical patterns of Mendelian inheritance and is probably related to alterations in gene expression.[3]

Trauma. Post-traumatic OA is common after a significant joint injury, such as knee meniscal or anterior cruciate ligament tear. Repetitive joint trauma presents a cumulative risk.

Congenital or acquired anatomical joint abnormality. Laxity of the knees or of other joints (e.g., being “double-jointed”), poor proprioception, and quadriceps weakness increase the risk of osteoarthritis of the knee. Osteoarthritis may also be more common in the context of some dysplasias (i.e., abnormal growths of bone and cartilage) and Paget's disease.

Diagnosis

The diagnosis is based on history, physical examination, laboratory studies, and imaging. An atypical presentation warrants inquiry into a secondary cause.

OA is usually asymmetrical, but it can be bilateral in small joints. The following findings may be present on physical exam:

  • Tender joint.
  • Crepitus during joint motion.
  • Bony enlargements, especially of the distal interphalangeal joints (Heberden nodes) and proximal interphalangeal joints (Bouchard nodes).
  • Flexion contracture or varus deformity of the knee.

Joint effusion, if present, is mild and is not typically associated with signs of inflammation. However, a variant of OA termed “inflammatory osteoarthritis” may present with joint effusion, redness, warmth, 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 a joint aspirate suggests that an inflammatory arthritis, rather than OA, should be considered.

Radiographic imaging of affected joints may reveal joint space narrowing, osteophytes, or subchondral bone sclerosis.

Treatment

The choice of treatment depends partly on whether inflammation is present. Options include a supervised exercise/muscle-strengthening program, medication, and surgical intervention. Arthroscopy and joint replacement are usually reserved for patients with severe, functionally limiting disease.

Nonpharmacologic treatments, including low-impact exercise and physical therapy, may be sufficient for mild cases. Exercise can improve muscle strength, decrease joint pain and stiffness, and reduce the likelihood of disability. A physical therapist or occupational therapist can assist in developing an appropriate exercise plan and can recommend arthritis assistive devices, when needed. Weight loss and shoe inserts, braces, or splints may be helpful as well.

If, at any point, an individual develops recurrent joint swelling or does not respond to appropriate medical therapy, he or she should be evaluated for crystal arthroplasty and treated accordingly.

The first choice of treatment for non-inflammatory OA is oral acetaminophen. If acetaminophen is contraindicated or ineffective, then nonsteroidal anti-inflammatory (NSAIDs) medications can be used. Blood pressure should be monitored if NSAIDs are used on a regular basis. If suboptimal analgesia is attained with one NSAID at maximal dose, different NSAIDs should be tried, as some individuals respond differently to various NSAID options. It is important to monitor for symptoms of gastric ulcer and renal disease if using NSAIDs chronically. Gastroprotective agents, such as type 2 histamine receptor antagonists or proton pump inhibitors, should be initiated in any patient on chronic NSAID therapy. All NSAIDs increase risk for cardiovascular events and their use should be limited or avoided in those with known cardiovascular disease or multiple risk factors for a cardiovascular event.

Topical NSAIDs (diclofenac gel), topical lidocaine, or capsaicin cream can significantly reduce pain. Topical agents are useful in individuals who cannot tolerate oral acetaminophen or oral NSAIDs, or in those who wish to avoid joint injections.

COX-2 inhibitors may be considered in patients at higher risk for a gastrointestinal bleed. Like all NSAIDs, this class of medications increases cardiovascular risk, especially in patients who have coronary artery disease or heart failure.

Tramadol, another type of analgesic, may be combined with the above drugs.

Narcotics should be reserved for patients with short-term severe pain, in those whom other medications are contraindicated, or those who are unresponsive to the above therapeutics.

Duloxetine (Cymbalta). In 2010, the U.S. Food and Drug Administration approved the use of duloxetine (Cymbalta) for chronic musculoskeletal pain including that caused by OA. This oral medication is also is in use for other conditions, such as mood disorders, nerve pain, and fibromyalgia.

Intra-articular steroid injections should be reserved for individuals who are unresponsive to acetaminophen or NSAIDs or for whom NSAIDs are contraindicated. Adequate evidence for efficacy exists for the knee and hip joint. Symptom relief tends to be limited (weeks to months), and long-term benefit has not been supported by current evidence.[4] 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 Synvisc) may be beneficial when noninvasive treatments or steroid injections achieve suboptimal results. Data is still lacking regarding the efficacy and safety of repeated courses and frequency of treatment course with these compounds.

Surgical therapy may be indicated for severe cases. Joint replacement (arthroplasty) should be reserved for refractory cases in which activities of daily living are limited. Significant improvement in symptoms and function may occur after surgery. Arthroscopic debridement and synovectomy for OA have not been proven effective. Other surgical techniques, such as autologous chondrocyte implantation, may be beneficial for select patients.

Nutritional Considerations

Excess body weight is the primary determinant of the development and course of OA. However, inflammatory processes[5] ,[6] and oxidative stress[7] also play key roles, although antioxidant nutrients do not appear to help. Nevertheless, possible roles have emerged for certain types of fats, vitamin D, and spices with anti-inflammatory effects, and the ability of glucosamine sulfate and chondroitin sulfate have become further clarified.

Here are key preventive and therapeutic steps:

Maintaining a healthy weight. For every 5 kg of weight gained over a body mass index (BMI) of 25, the risk for developing OA of the knee increases by 36%. Although OA is usually associated with aging, the link between obesity and knee OA starts early, at around 11 years of age in girls and 20 years of age in men. Losing as little as 5 kg significantly decreases a woman’s chances of developing symptomatic knee OA.[8]

Replacing animal products with a plant-based diet. Animal products typically contain significant amounts of saturated fat and advanced glycation end products (AGEs). Investigators who followed roughly 2,100 participants in the Osteoarthritis Initiative over four years found a dose-response relationship between saturated fat intake intakes and joint space width loss. Individuals consuming the most saturated fat had a 60% greater risk for OA progression, when compared to those eating the lowest amount. AGEs increase stiffness and brittleness in articular cartilage, making it more prone to mechanical damage.[9] ,[10]

In contrast to the effects of saturated fat, higher intakes of mono- and poly-unsaturated fatty acids are associated with a reduced loss of joint space width.[11] The ratio between the intake of omega-6 and omega-3 fatty acids is also important in OA,[12] and the Multicenter Osteoarthritis Study (MOST) found a positive relationship between omega-6 animal source fat arachidonic acid and synovitis. MOST also found a relationship between plasma levels of omega-3 fatty acids and patellofemoral cartilage loss.[13] However, clinical trials have not supported fish oil supplementation as an effective treatment for OA.[14]

Maintaining adequate vitamin D status. Low blood levels of vitamin Dare associated with OA and cartilage loss (evidenced as joint space narrowing and changes in cartilage volume).[15] However, another review reported no benefit for vitamin D supplementation and progression of knee OA.[16]

Several over-the-counter products have also been found effective for OA. These include glucosamine sulfate and chondroitin sulfate, avocado and soybean unsaponifiables, diacerein, curcumin, and ginger. These are reviewed below.

Glucosamine sulfate and chondroitin sulfate. Although studies on the benefit of these supplements have yielded mixed results, a Cochrane review concluded that overall benefits were moderate.[17] The European Society for Clinical and Economic Aspects of Osteoporosis and Osteoarthritis (ESCEO) has reviewed the data on symptomatic slow-acting drugs for Osteoarthritis (SYSADOAs). They recommend these as a first-line therapy for OA, concluding that a patented crystalline form of glucosamine in knee OA patients has been found to be the only type of glucosamine demonstrating a clear superiority in terms of pain, functional impairment, reduction of joint space narrowing, and number of patients requiring total joint replacement, when compared with placebo. Fewer studies have been done with prescription strength chondroitin sulfate, but these have revealed benefits similar to glucosamine.[18]

Avocado/soybean unsaponifiables (ASU) are avocado and soybean oil extracts that have been shown, in several human clinical trials, to reduce pain and stiffness while improving joint function. Although the active component(s) remains unknown, the sterol contents are believed to help prevent cartilage degradation, inhibit cholesterol absorption, and inhibit endogenous cholesterol biosynthesis, which mediate reactive oxygen species pathology in chondrocytes.[19]

Diacerein is an anthraquinone obtained from rhubarb that has anti-catabolic and pro-anabolic effects on cartilage and synovial membrane, as well as protective effects against subchondral bone remodeling. The ESCEO confirmed that the efficacy of diacerein is similar to that of NSAIDs.[20]

Curcumin and turmeric. A meta-analysis of studies using turmeric extract (roughly 1,000 mg/d of curcumin) found reductions on the Western Ontario and McMaster Universities (WOMAC) scale of over 15 points (roughly 23% of total score). Its effects are comparable to NSAIDs but without gastric side effects.[5] Newer formulation that include piperine (black pepper); that provide curcumin particles in submicron size; or bound to phosphatidylcholine or polysorbate 80 (among others) increase curcumin bioavailability and have been found to be of benefit in controlled clinical trials in OA patients.[21]

Ginger may provide significant pain relief for osteoarthritis patients by acting as an inhibitor of inflammation in synoviocytes. Its effects can be variable, however, depending on the species of ginger, the maturity of the plant, the climate in which it grows, when it is harvested, and the preparation method of the extract.[22] Effective doses range from 170 mg ginger extract 3 times per day to 250 mg 4 times per day.

Orders

See Basic Diet Orders Chapter

What to Tell the Family

Family members can help the patient with lifestyle changes that affect the joints. In some cases, OA may be preventable or treatable through maintenance of a healthy weight with diet changes and exercise. Muscle-strengthening and low-impact exercises are the best options to avoid exacerbating the disease.

References

  1. Johnson VL, Hunter DJ: The epidemiology of osteoarthritis. Best Pract Res Clin Rheumatol 28:5, 2014  [PMID:24792942]
  2. Valdes AM, Spector TD: Genetic epidemiology of hip and knee osteoarthritis. Nat Rev Rheumatol 7:23, 2011  [PMID:21079645]
  3. Fernández-Moreno M, Rego I, Carreira-Garcia V, Blanco FJ. Genetics in osteoarthritis. Curr Genomics . 2008;9:542–547.
  4. Foster ZJ et al: Corticosteroid Injections for Common Musculoskeletal Conditions. Am Fam Physician 92:694, 2015  [PMID:26554409]
  5. Daily JW, Yang M, Park S: Efficacy of Turmeric Extracts and Curcumin for Alleviating the Symptoms of Joint Arthritis: A Systematic Review and Meta-Analysis of Randomized Clinical Trials. J Med Food 19:717, 2016  [PMID:27533649]Daily JW, Yang M, Park S: Efficacy of Turmeric Extracts and Curcumin for Alleviating the Symptoms of Joint Arthritis: A Systematic Review and Meta-Analysis of Randomized Clinical Trials. J Med Food 19:717, 2016  [PMID:27533649]
  6. Grover AK, Samson SE: Benefits of antioxidant supplements for knee osteoarthritis: rationale and reality. Nutr J 15:, 2016  [PMID:26728196]
  7. Leong DJ et al: Nutraceuticals: potential for chondroprotection and molecular targeting of osteoarthritis. Int J Mol Sci 14:23063, 2013  [PMID:24284399]
  8. Bliddal H, Leeds AR, Christensen R: Osteoarthritis, obesity and weight loss: evidence, hypotheses and horizons - a scoping review. Obes Rev 15:578, 2014  [PMID:24751192]
  9. Palimeri S, Palioura E, Diamanti-Kandarakis E: Current perspectives on the health risks associated with the consumption of advanced glycation end products: recommendations for dietary management. Diabetes Metab Syndr Obes 8:415, 2015  [PMID:26366100]
  10. Vos PA et al: Skin and urine pentosidine weakly correlate with joint damage in a cohort of patients with early signs of osteoarthritis (CHECK). Osteoarthr Cartil 18:1329, 2010  [PMID:20673850]
  11. Lu B et al: Dietary Fat Intake and Radiographic Progression of Knee Osteoarthritis: Data From the Osteoarthritis Initiative. Arthritis Care Res (Hoboken) 69:368, 2017  [PMID:27273934]
  12. Boe C, Vangsness CT: Fish Oil and Osteoarthritis: Current Evidence. Am J Orthop 44:302, 2015  [PMID:26161757]
  13. Baker KR et al: Association of plasma n-6 and n-3 polyunsaturated fatty acids with synovitis in the knee: the MOST study. Osteoarthr Cartil 20:382, 2012  [PMID:22353693]
  14. Senftleber NK, Nielsen SM, Andersen JR, et al. Marine oil supplements for arthritis pain: a systematic review and meta-analysis of randomized trials. Nutrients . 2017;9:1-21.
  15. Cao Y et al: Association between serum levels of 25-hydroxyvitamin D and osteoarthritis: a systematic review. Rheumatology (Oxford) 52:1323, 2013  [PMID:23542678]
  16. Gallagher B et al: Chondroprotection and the prevention of osteoarthritis progression of the knee: a systematic review of treatment agents. Am J Sports Med 43:734, 2015  [PMID:24866892]
  17. Singh JA et al: Chondroitin for osteoarthritis. Cochrane Database Syst Rev 1:, 2015  [PMID:25629804]
  18. Bruyère O et al: A consensus statement on the European Society for Clinical and Economic Aspects of Osteoporosis and Osteoarthritis (ESCEO) algorithm for the management of knee osteoarthritis-From evidence-based medicine to the real-life setting. Semin Arthritis Rheum 45:S3, 2016  [PMID:26806188]
  19. Christiansen BA et al: Management of Osteoarthritis with Avocado/Soybean Unsaponifiables. Cartilage 6:30, 2015  [PMID:25621100]
  20. Pavelka K et al: Diacerein: Benefits, Risks and Place in the Management of Osteoarthritis. An Opinion-Based Report from the ESCEO. Drugs Aging 33:75, 2016  [PMID:26849131]
  21. Chin KY: The spice for joint inflammation: anti-inflammatory role of curcumin in treating osteoarthritis. Drug Des Devel Ther 10:3029, 2016  [PMID:27703331]
  22. Bartels EM et al: Efficacy and safety of ginger in osteoarthritis patients: a meta-analysis of randomized placebo-controlled trials. Osteoarthr Cartil 23:13, 2015  [PMID:25300574]

Last updated: November 28, 2017

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TY - ELEC T1 - Osteoarthritis ID - 1342023 Y1 - 2017/11/28/ PB - Nutrition Guide for Clinicians UR - https://nutritionguide.pcrm.org/nutritionguide/view/Nutrition_Guide_for_Clinicians/1342023/all/Osteoarthritis ER -