Osteoarthritis Clinical Trials, Diagnosis, and Treatment

Browse All Available Clinical Trials

Join Now to be Notified of New Clinical Trials

View Information and Clinical Trials for Other Conditions

Osteoarthritis

Osteoarthritis (OA, also known as degenerative arthritis or degenerative joint disease, and sometimes referred to as "arthrosis" or "osteoarthrosis" or in more colloquial terms "wear and tear"), is a condition in which low-grade inflammation results in pain in the joints, caused by wearing of the cartilage that covers and acts as a cushion inside joints. As the bone surfaces become less well protected by cartilage, the patient experiences pain upon weight bearing, including walking and standing. Due to decreased movement because of the pain, regional muscles may atrophy, and ligaments may become more lax. OA is the most common form of arthritis. The word is derived from the Greek word "osteo", meaning "of the bone", "arthro", meaning "joint", and "itis", meaning inflammation, although many sufferers have little or no inflammation.

OA affects nearly 21 million people in the United States, accounting for 25% of visits to primary care physicians, and half of all NSAID (Non-Steroidal Anti-Inflammatory Drugs) prescriptions. It is estimated that 80% of the population will have radiographic evidence of OA by age 65, although only 60% of those will be symptomatic (Green 2001). Treatment is with NSAIDs, local injections of glucocorticoid or hyaluronan, and in severe cases, with joint replacement surgery. There has been no cure for OA, as cartilage has not been induced to regenerate. However, if OA is caused by cartilage damage (for example as a result of an injury) Autologous Chondrocyte Implantation may be a possible treatment. Clinical trials employing tissue-engineering methods have demonstrated regeneration of cartilage in damaged knees, including those that had progressed to osteoarthritis. Further, in January 2007, Johns Hopkins University was offering to license a technology of this kind, listing several clinical competitors in its market analysis.

Current Research

For current research articles click - here

Signs and Symptoms

The main symptom is chronic pain, causing loss of mobility and often stiffness. "Pain" is generally described as a sharp ache, or a burning sensation in the associated muscles and tendons. OA can cause a crackling noise (called "crepitus") when the affected joint is moved or touched, and patients may experience muscle spasm and contractions in the tendons. Occasionally, the joints may also be filled with fluid. Humid weather increases the pain in many patients.

OA commonly affects the hand, feet, spine, and the large weight-bearing joints, such as the hips and knees, although in theory, any joint in the body can be affected. As OA progresses, the affected joints appear larger, are stiff and painful, and usually feel worse, the more they are used throughout the day, thus distinguishing it from rheumatoid arthritis.

In smaller joints, such as at the fingers, hard bony enlargements, called Heberden's nodes (on the distal interphalangeal joints) and/or Bouchard's nodes (on the proximal interphalangeal joints), may form, and though they are not necessarily painful, they do limit the movement of the fingers significantly. OA at the toes leads to the formation of bunions, rendering them red or swollen.

Causes of Osteoarthritis

Osteoarthritis often affects multiple members of the same family, suggesting that there is hereditary susceptiblity to this condition. A number of studies have shown that there is a greater prevalence of the disease between siblings and especially identical twins, indicating a hereditary basis. Up to 60% of OA cases are thought to result from genetic factors. Researchers are also investigating the possibility of allergies, infections, or fungi as a cause. There is some evidence that allergies, whether fungal, infectious or systemically induced, may be a significant contributing factor to the appearance of osteoarthritis in a synovial sac.

Two Types:

Primary Osteoarthritis

This type of OA is a chronic degenerative disorder related to but not caused by aging, as there are people well into their nineties who have no clinical or functional signs of the disease. As a person ages, the water content of the cartilage decreases due to a reduced proteoglycan content, thus causing the cartilage to be less resilient. Without the protective effects of the proteoglycans, the collagen fibers of the cartilage can become susceptible to degradation and thus exacerbate the degeneration. Inflammation of the surrounding joint capsule can also occur, though often mild (compared to that which occurs in rheumatoid arthritis). This can happen as breakdown products from the cartilage are released into the synovial space, and the cells lining the joint attempt to remove them. New bone outgrowths, called "spurs" or osteophytes, can form on the margins of the joints, possibly in an attempt to improve the congruence of the articular cartilage surfaces. These bone changes, together with the inflammation, can be both painful and debilitating.

Secondary Osteoarthritis

This type of OA is caused by other factors or diseases but the resulting pathology is the same as for primary OA:

Congenital disorders, such as:
- Congenital hip luxation
- People with abnormally-formed joints (e.g. hip dysplasia) are more vulnerable to OA, as added stress is specifically placed on the joints whenever they move. (However, recent studies have shown that double-jointedness may actually protect the fingers and hand from osteoarthritis).
Cracking joints—the evidence is weak at best that this has any connection to arthritis.
Diabetes
Inflammatory diseases (such as Perthes' disease), (Lyme disease), and all chronic forms of arthritis (e.g. costochondritis, gout, and rheumatoid arthritis). In gout, uric acid crystals cause the cartilage to degenerate at a faster pace.
Injury to joints, as a result of an accident.
Hormonal disorders.
Ligamentous deterioration or instability may be a factor.
Obesity puts added weight on the joints, especially the knees.
Osteoporosis (High bone density).
Sports injuries, from exercise, athletic activity, or work. For example, certain sports, such as weightlifting, running, or even football, put undue pressure on the knee joints. Injuries resulting in broken ligaments can lead to instability of the joint and over time wear of the cartilage and eventually osteoarthritis.
Surgery to the joint structures.

Diagnosis

Diagnosis is normally done through x-rays. This is possible because loss of cartilage, subchondral ("below cartilage") sclerosis, subchondral cysts, the narrowing of the joint space between adjacent bones, and bone spur formation (osteophytes) show up clearly in x-rays. Plain films, however, often do not correlate with the findings of a physical examination of the affected joints.

With or without other techniques, such as MRI (magnetic resonance imaging), arthrocentesis and arthroscopy, diagnosis can be made by a careful study of the duration, location, the character of the joint symptoms, and the appearance of the joints themselves.

As yet, there are no methods available to detect OA in its early and potentially treatable stages.

Treatment

Generally speaking, the process of clinically detectable osteoarthritis is irreversible, and typical treatment consists of medication or other interventions that can reduce the pain of OA and thereby improve the function of the joint.

Coping Skills and Lifestyle Changes

No matter what the severity, or where the OA lies, conservative measures, such as weight control, appropriate rest and exercise, and the use of mechanical support devices are usually beneficial to sufferers. In the case of OA of the knees, knee braces, a cane, or a walker can be a helpful aid for walking and support. Regular exercise, if possible, in the form of walking or swimming, is encouraged. Applying local heat before, and cold packs after exercise, can help relieve pain and inflammation, as can relaxation techniques. Weight loss can relieve joint stress and may delay progression. Proper advice and guidance by a health care provider is important in OA management, enabling people with this condition to improve their quality of life.

Dealing with chronic pain can be difficult and result in depression. Communicating with other patients and carers can be helpful, as can maintaining a positive attitude. People who take control of their treatment, communicate with their health care provider, and actively manage their arthritis experience can reduce pain and improve function.

Dietary

Supplements which may be useful for treating OA include:

Antioxidants, including vitamins C and E in both foods and supplements, provide pain relief from OA. (McAlindon TE, et al, 1996).
Chondroitin sulphate improves symptoms of OA, and delays its progression (Poolsup N et al, 2005).
Hydrolyzed collagen (hydrolysate) (a gelatin product) may also prove beneficial in the relief of OA symptoms, as substantiated in a German study by Beuker F. et. al. and Seeligmuller et. al. In their 6-month placebo-controlled study of 100 elderly patients, the verum group showed significant improvement in joint mobility.
Ginger (rhizome) extract - has improved knee symptoms moderately (Altman RD, 1991).
Glucosamine: A molecule derived from glucosamine is used by the body to make some of the components of cartilage and synovial fluid. Supplemental glucosamine may improve symptoms of OA and delay its progression (Poolsup N et al, 2005). However, a recent large study suggests that glucosamine is not effective in treating OA of the knee (McAlindon et al 2004).
Methylsulfonylmethane (MSM): A small study by Kim et al. suggested that MSM significantly reduced pain and improved physical functioning in OA patients without major adverse events (Kim et al). The authors cautioned that although this short pilot study did not address the long-term safety and usefulness of MSM, they suggest that physicians should consider its use for certain osteoarthritis patients.
S-adenosyl methionine: small scale studies have shown it to be as effective as NSAIDs in reducing pain, although it takes about four weeks for the effect to take place.
Selenium deficiency has been correlated with a higher risk and severity of OA, therefore selenium supplementation may reduce this risk.
vitamins B9 (folate) and B12 (cobalamin) taken in large doses significantly reduced OA hand pain, presumbably by reducing systemic inflammation (Flynn MA 1994).
Vitamin D deficiency has been reported in patients with OA, and supplementation with Vitamin D3 is recommended for pain relief (Arabelovic, 2005).

Other nutritional changes shown to aid in the treatment of OA include decreasing saturated fat intake (Wilhelmi G, 1993) and using a low energy diet to decrease body fat (Christensen R, 2005). Lifestyle change may be needed for effective symptomatic relief, especially for knee OA (De Filippis L, 2004). Reducing sugar, processed foods, fatty foods and nightshade vegetables have helped many. According to Dr. John McDougall, a low fat vegetarian diet can reduce arthritis symptoms. A macrobiotic diet has been known to reduce symptoms as well.

Systemic Treatment

Included in the medication regime for most cases, a mild pain reliever may be sufficiently efficacious. In more severe cases, NSAIDs are usually prescribed which can reduce both the pain and inflammation quite effectively. These include medications such as diclofenac, ibuprofen and naproxen. High doses are often required. All NSAIDs act by inhibiting the formation of prostaglandins, which play a central role in inflammation and pain. However, these drugs are rather taxing on the gastrointestinal tract, and may cause stomach upset, cramping diarrhoea, and peptic ulcer.

Another type of NSAID, COX-2 selective inhibitors (such as celecoxib, and the withdrawn rofecoxib and valdecoxib) reduce this risk substantially. These latter NSAIDs carry an elevated risk for cardiovascular disease, and some have now been withdrawn from the market. Another medication, acetaminophen (paracetamol), is commonly used to treat the pain from OA, although unlike NSAID's acetaminophen does not treat the inflammation. Application of heat — often moist heat — eases inflammation and swelling in the joints, and can help improve circulation, which has a healing effect on the local area.

Most doctors nowadays are loath to use steroids in the treatment of OA as their effect is modest and the adverse effects may outweigh the benefits. For severe pain, narcotic pain relievers such as tramadol, and eventually opioids (hydrocodone, oxycodone or morphine) may be necessary; these should be reserved for very severe cases, and are rarely medically necessary for chronic pain.

Topical

"Topical treatments" are treatments designed for local application and action. Some NSAIDs are available for topical use (e.g. ibuprofen and diclofenac) and may improve symptoms without having systemic side-effects.

Creams and lotions, containing capsaicin, are effective in treating pain associated with OA if they are applied with sufficient frequency.

Severe pain in specific joints can be treated with local lidocaine injections or similar local anaesthetics, and glucocorticoids (such as hydrocortisone). Corticosteroids (cortisone and similar agents) may temporarily reduce the pain.

Surgery

If the above management is ineffective, joint replacement surgery may be required. Individuals with very painful OA joints may require surgery such as fragment removal, repositioning bones, or fusing bone to increase stability and reduce pain.

Other Approaches

There are various other modalities in use for osteoarthritis:

Low level laser therapy ; this is a light wave based treatment that may reduce pain. The treatment is painless, inexpensive and without risks or side effects. Unfortunately, it may not actually have any real benefits.
Prolotherapy (proliferative therapy); this is the injection of an irritant substance (such as dextrose) to create an acute inflammatory reaction. It is claimed to strengthen and heal damaged tissues including ligaments, tendons and cartilage as part of this reaction. The injection is painful (like corticosteroids or hyaluronic acid) and may cause an increase in pain for a few days afterwards. The only other significant risk is the rare possibility of infection.
Radiosynoviorthesis: A radioactive isotope (a beta-ray emitter with a brief half-life) is injected into the joint to soften the tissue. Due to the involvement of radioactive material, this is an elaborate and costly procedure, but it has a success rate of around 80%.

Prognosis

The most common course of OA is an intermittent, progressive worsening of symptoms over time, although in some patients the disease stabilizes. Prognosis also varies depending on which joint is involved.

Factors associated with progression of OA:

Knees: High body mass index, varus or valgus knee deformity.
Hips: Night pain, presence of femoral osteophytes, and subchondral sclerosis in females.
Hands: Older age.

(adapted from Wikipedia, the free encyclopedia http://en.wikipedia.org/wiki/Osteoarthritis)

Findings From Current Research

Oxygen, Nitric Oxide and Articular Cartilage.

Authors: Fermor B, Christensen SE, Youn I, Cernanec JM, Davies CM, Weinberg JB.

Department of Surgery, Division of Orthopedic Surgery, Duke University Medical Center, Durham, NC 27710, USA. bfer@duke.edu

Molecular oxygen is required for the production of nitric oxide (NO), a pro-inflammatory mediator that is associated with osteoarthritis and rheumatoid arthritis. To date there has been little consideration of the role of oxygen tension in the regulation of nitric oxide production associated with arthritis. Oxygen tension may be particularly relevant to articular cartilage since it is avascular and therefore exists at a reduced oxygen tension. The superficial zone exists at approximately 6% O2, while the deep zone exists at less than 1% O2. Furthermore, oxygen tension can alter matrix synthesis, and the material properties of articular cartilage in vitro. The increase in nitric oxide associated with arthritis can be caused by pro-inflammatory cytokines and mechanical stress. Oxygen tension significantly alters endogenous NO production in articular cartilage, as well as the stimulation of NO in response to both mechanical loading and pro-inflammatory cytokines. Mechanical loading and pro-inflammatory cytokines also increase the production of prostaglandin E2 (PGE2). There is a complex interaction between NO and PGE2, and oxygen tension can alter this interaction. These findings suggest that the relatively low levels of oxygen within the joint may have significant influences on the metabolic activity, and inflammatory response of cartilage as compared to ambient levels. A better understanding of the role of oxygen in the production of inflammatory mediators in response to mechanical loading, or pro-inflammatory cytokines, may aid in the development of strategies for therapeutic intervention in arthritis.

Journal: Eur Cell Mater. 2007 Apr 11;13:56-65; discussion 65.
Adapted from PubMed; click here to access full journal article.

Cardiovascular Outcomes in High-Risk Patients with Osteoarthritis Treated with Ibuprofen, Naproxen, or Lumiracoxib.

Authors: Farkouh ME, Greenberg JD, Jeger RV, Ramanathan K, Verheugt FW, Cheseboro JH, Kirshner H, Hochman JS, Lay CL, Ruland S, Mellein B, Matchaba PT, Fuster V, Abramson SB.

Mount Sinai School of Medicine, United States.

BACKGROUND: Evidence suggests that both selective cyclooxygenase (COX)-2 inhibitors and non-selective NSAIDs increase the risk of cardiovascular (CV) events. However, evidence from prospective studies of currently available COX-2 inhibitors and non-selective NSAIDs is lacking in high CV risk patients taking aspirin. METHODS: The Therapeutic Arthritis Research and Gastrointestinal Event Trial (TARGET) of 18,325 osteoarthritis patients comprised 2 parallel sub- studies, comparing lumiracoxib (COX-2 inhibitor) to either ibuprofen or naproxen. We performed a post hoc analysis stratified by baseline cardiovascular risk, treatment assignment, and low-dose aspirin use. The primary composite endpoint was cardiovascular mortality, nonfatal myocardial infarction, and stroke at 1 year; a secondary endpoint was the development of congestive heart failure (CHF). RESULTS: In high risk patients among aspirin users, patients in the ibuprofen sub-study had more primary events with ibuprofen than lumiracoxib (2.14% vs. 0.25%, p=0.038), whereas in the naproxen sub-study rates were similar for naproxen and lumiracoxib (1.58% vs. 1.48%, p=0.899). High risk patients not taking aspirin had fewer primary events with naproxen versus lumiracoxib (0% vs. 1.57%, p=0.027), but not ibuprofen versus lumiracoxib (0.92% vs. 0.80%, p=0.920). Overall, CHF developed more often with ibuprofen than lumiracoxib (1.28% vs. 0.14%; p=0.031), whereas no difference existed between naproxen and lumiracoxib. CONCLUSIONS: These data suggest that ibuprofen may confer an increased risk of thrombotic and CHF events relative to lumiracoxib among aspirin users at high cardiovascular risk. Our study indicates that naproxen may be associated with lower risk relative to lumiracoxib among non-aspirin users. Our data should be interpreted as hypothesis-generating.

Journal: Ann Rheum Dis. 2007 Apr 5;
Adapted from PubMed; click here to access full journal article.

High Abundance Synovial Fluid Proteome: Distinct Profiles in Health and Osteoarthritis.

Authors: Gobezie R, Kho AT, Krastins B, Thornhill TS, Sarracino DA, Chase M, Millett PJ, Lee DM.

ABSTRACT: The development of increasingly high throughput and sensitive mass-spectroscopy based proteomic techniques provides new opportunities for examination of physiology and pathophysiology of many biologic fluids and tissues. The purpose of this study was to determine protein expression profiles of high abundance synovial fluid proteins in health and in the prevalent joint disease osteoarthritis (OA). A cross-sectional study of 62 human subjects with early OA (NEOA=21), late OA (NLOA=21) and control subjects (NCon=20), was performed. The synovial fluid proteins (SF) were separated by using one-dimensional polyacrylamide gel electropheresis and the in-gel digested proteins were analyzed by electrospray ionization tandem mass spectrometry. A total of 362 spots were examined and 135 high abundance synovial fluid proteins were identified as expressed across all three study cohorts. One hundred thirty five SF proteins were identified. Eighteen proteins were found to be significantly differentially expressed in control subjects and OA patients. Two subsets of OA that are not disease duration dependent were identified using unsupervised analysis of the data. Several novel SF proteins were also identified. Our analyses demonstrate no disease duration dependent differences in abundant protein composition of synovial fluid in OA and we clearly identify two previously unappreciated distinct subsets of protein profiles in this disease cohort. Additionally, our findings identify novel abundant protein species in healthy synovial fluid whose functional contribution to synovial fluid physiology was not previously recognized. Finally, our studies identify candidate biomarkers for OA with potential for use as highly sensitive and specific tests for diagnosis or therapeutic response.

Journal: Arthritis Res Ther. 2007 Apr 2;9(2):R36
Adapted from PubMed; click here to access full journal article.

Current Role of Glucosamine in the Treatment of Osteoarthritis.

Authors: Reginster JY, Bruyere O, Neuprez A.

WHO Collaborating Center, Department of Public Health, Epidemiology and Health Economics, University of Liege, Liege, Belgium.

Objectives. To evaluate the interest of using the various preparations of glucosamine for symptomatic and structural management of osteoarthritis (OA). Methods. A critical analysis of the literature based on an exhaustive search (Medline, PubMed and manual search within the bibliography of retrieved manuscripts) from 1980 to 2005. Results. Despite multiple controlled clinical trials of the use of glucosamine in OA (mainly of the knee), controversy on efficacy related to symptomatic improvement continues. Differences in results originate from the differences in products, study design and study populations. Symptomatic efficacy described in multiple studies performed with glucosamine sulphate (GS) support continued consideration in the OA therapeutic armamentarium. The most compelling evidence of a potential for inhibiting the progression of OA is also obtain with GS. Conclusions. GS has shown positive effects on symptomatic and structural outcomes of knee OA. These results should not be extrapolated to other glucosamine salts [hydrochloride or preparations (over-the-counter or food supplements)] in which no warranty exists about content, pharmacokinetics and pharmacodynamics of the tablets.

Journal: Rheumatology (Oxford). 2007 Mar 31;
Adapted from PubMed; click here to access full journal article.

Office Management of Chronic Pain in the Elderly.

Authors: Weiner DK.

Division of Geriatric Medicine, Department of Medicine, University of Pittsburgh, Pittsburgh, Penn, USA. dweiner@pitt.edu

Chronic pain plagues older adults more than any other age group; thus, practitioners must be able to approach this problem with confidence and skill. This article reviews the assessment and treatment of the most common chronic nonmalignant pain conditions that affect older adults--myofascial pain, generalized osteoarthritis, chronic low back pain (CLBP), fibromyalgia syndrome, and peripheral neuropathy. Specific topics include essential components of the physical examination; how and when to use basic and advanced imaging in older adults with CLBP; a stepped care approach to treating older adults with generalized osteoarthritis and CLBP, including noninvasive and invasive management techniques; how to diagnose and treat myofascial pain; strategies to identify the older adult with fibromyalgia syndrome and avoid unnecessary "diagnostic" testing; pharmacological treatment for the older adult with peripheral neuropathy; identification and treatment of other factors such as dementia and depression that may significantly influence response to pain treatment; and when to refer the patient to a pain specialist. While common, chronic pain is not a normal part of aging, and it should be treated with an emphasis on improved physical function and quality of life.

Journal: Am J Med. 2007 Apr;120(4):306-15.
Adapted from PubMed; click here to access full journal article.

Efficacy and Safety of Opioids for Osteoarthritis: A Meta-Analysis of Randomized Controlled Trials.

Authors: Avouac J, Gossec L, Dougados M.

Rene Descartes University, Medicine Faculty, APHP Cochin Hospital, Rheumatology B Department, Paris, France.

OBJECTIVES: To determine the analgesic effectiveness, the effect on physical function and the safety of opioids in patients with osteoarthritis (OA). SEARCH STRATEGY: A systematic literature search was performed in electronic databases up to October 2006. A hand search of references was also performed. SELECTION CRITERIA: All randomized controlled trials evaluating the efficacy and/or the safety of opioids vs placebo or non-opioid analgesics in patients with OA were selected. DATA COLLECTION AND ANALYSIS: Data were collected using a predetermined form. Statistical analysis determined in each trial the effect size to assess the magnitude of treatment effect and the number needed to harm (NNH) to evaluate opioids safety. MAIN RESULTS: Eighteen randomized placebo-controlled trials were analyzed, i.e., a total of 3244 participants who received opioids and 1612 who received placebo. The mean trial duration was 13+/-18 weeks. The pooled effect sizes of all opioids vs placebo for pain intensity and physical function were -0.79 (95% confidence interval, CI, -0.98 to -0.59) and -0.31 (95% CI -0.39 to -0.24), respectively. The NNH was calculated to be 5 vs placebo. The number of studies (n=4) that compared opioids with non-opioid analgesics (paracetamol and non-steroidal anti-inflammatory drugs) was too limited to provide robust data. CONCLUSIONS: Opioids significantly decrease pain intensity and have small benefits on function compared with placebo in patients with OA. Adverse events, although reversible and not life threatening, often cause participants to stop taking the medication and could limit opioid usefulness. Moreover, the long-term efficacy and safety of these drugs for OA is yet to be determined due to the short mean trial duration.

Journal: Osteoarthritis Cartilage. 2007 Mar 28;
Adapted from PubMed; click here to access full journal article.

Predictors of Depression in a Sample of 1,021 Primary Care Patients with Osteoarthritis.

Authors: Rosemann T, Backenstrass M, Joest K, Rosemann A, Szecsenyi J, Laux G.

University Hospital of Heidelberg, Heidelberg, Germany.

OBJECTIVE: Although there is a strong relationship between depression, chronic pain, and physical activity, there are few findings regarding the prevalence and predictors of depression in patients with osteoarthritis (OA). The goal of the present study was to assess the prevalence and severity of depression in a large sample of patients with OA and to reveal predictors of depression. METHODS: Patients were approached consecutively in 75 general practices. Of 1,250 distributed questionnaires, 1,021 were returned and analyzed. Besides sociodemographic data, medication and comorbidities, depression, and arthritis were assessed using the Patient Health Questionnaire (PHQ-9) and the Arthritis Impact Measurement Scale. A stepwise multiple linear regression analysis with the PHQ-9 score as the dependent variable was performed. RESULTS: On the PHQ-9, 19.76% of men and 19.16% of women achieved a score of >/=15, indicating at least a moderately severe depression. Significant sex differences could not be revealed. The strongest predictor for depression severity was perceived pain (beta = 0.243, P < 0.001) and few social contacts (beta = 0.218, P < 0.001). Further predictors were physical limitation of the lower body (beta = 0.157, P < 0.001) and upper body (beta = 0.163, P < 0.001), age (beta = -0.168, P < 0.001), and body mass index (beta = 0.080, P = 0.020). CONCLUSION: These findings suggest an increased prevalence of depression among patients with OA and emphasize the need for recognition and appropriate treatment. Most of the revealed predictors are influenceable and should be potential targets in a comprehensive treatment of OA to interrupt the vicious circle of pain, physical limitation, and depression.

Journal: Arthritis Rheum. 2007 Mar 29;57(3):415-422
Adapted from PubMed; click here to access full journal article.

A Randomized Crossover Trial of a Wedged Insole for Treatment of Knee Osteoarthritis.

Authors: Baker K, Goggins J, Xie H, Szumowski K, Lavalley M, Hunter DJ, Felson DT.

Veterans Affairs Boston Health Care System, Boston, Massachusetts.

OBJECTIVE: In uncontrolled studies, a lateral-wedge insole has reduced knee pain in patients with medial knee osteoarthritis (OA). The aim of this study was to test the efficacy of this simple, low-cost intervention for pain in patients with medial knee OA. METHODS: We conducted a double-blind, randomized, crossover trial designed to detect a small effect of treatment. Participants were at least 50 years of age and had medial joint space narrowing on posteroanterior semiflexed radiographs and scores indicating moderate pain for 2 of the 5 items on the Western Ontario and McMaster Universities Osteoarthritis Index (WOMAC) pain scale. Participants were randomized to receive a 5 degrees lateral-wedge insole or a neutral insole for 6 weeks. Following a 4-week washout period, participants crossed over to the other treatment for 6 weeks. Knee pain, the primary outcome, was assessed by the WOMAC pain scale (visual analog scale version). Secondary outcomes included the WOMAC disability subscale, overall knee pain, 50-feet walk time, chair-stand time, and use of medications for knee pain. RESULTS: Ninety patients were randomized. The mean difference in pain between the 2 treatments was 13.8 points on the WOMAC pain scale (95% confidence interval -3.9, 31.4 [P = 0.13]). We observed similar small effects for the secondary outcomes. CONCLUSION: The effect of treatment with a lateral-wedge insole for knee OA was neither statistically significant nor clinically important.

Journal: Arthritis Rheum. 2007 Mar 28;56(4):1198-1203
Adapted from PubMed; click here to access full journal article.

Join Now - Become a free member and get notified about studies in your area when they become available.

Browse Our Current Studies - Look over all of our current studies being conducted throughout the United States.

View Information and Clinical Trials for Other Conditions - Access all of our health-related content.