It is increasingly accepted that most OA results, at least in part, from altered mechanics within the joint.

Certain metabolic conditions such as hemochromatosis and Gaucher disease involve a genetic defect in collagen/cartilage. Altered mechanics may occur from minor gait abnormalities or major traumas that, over a lifetime, result in repeated stress and damage to cartilage. Repeated trauma may result in microfracture of cartilage, with incomplete healing due to continuation of the altered mechanics. Disruption of the otherwise smooth cartilage surface allows differential pressure on remaining cartilage, as well as stress on the underlying bone. Debris from fractured cartilage acts as a foreign body, causing low-level inflammation within the synovial fluid. These multiple influences combine to alter intrinsic efforts at cartilage repair, leading to progressive cartilage destruction and bony joint change. Current thinking suggests that the process is not immutable, but any intervention would have to be made while the joint is still asymptomatic—an unlikely occurrence.

Symptomatic OA represents the culmination of damage to cartilage, usually over many years.

 

  • Degenerative changes in the knee, hip, shoulder, spine, or virtually any other joint.

  • Pain with movement that improves with rest.

  • Joint deformity and mechanical alteration.

  • Sclerosis, thickening, spur formation, warmth, and effusion in the joints.

    +++++++

Bouchard's nodes were named after a famous French pathologist, Charles-Joseph Bouchard, who studied arthritis

patients in the 19th century.

These nodes are actually bony enlargements of the middle joints of the fingers, also known as the PIP joints or proximal interphalangeal joints. The PIP joint is the joint that is the first one above where you would wear a ring, the one toughest to get a ring past when you slip it on or off.

You may have also heard of Heberden's nodes, which are similar bony swellings that develop at the distal interphalangeal joint, or DIP point, which is the joint closest to the fingertips. In general, Bouchard's nodes are considered less common than Heberden's nodes.

Cause of Bouchard's Nodes

Bouchard's nodes are a classic sign of hand osteoarthritis, or hand OA, and the hand is the third most commonly affected joint in OA, following the knee and hip. In OA of the hand, the articular cartilage in the joints is worn away. Since this cartilage normally provides a cushion between the bones of the joint, as the cartilage wears away, a person may start to experience pain and stiffness. 

In addition to wearing away, the cartilage becomes rough and is no longer a smooth surface for the bones to slip past each other. Once the cartilage is worn away enough, the bones rub against each other, which can be quite painful.

As this rubbing continues, the existing bone may be destroyed. Your body then attempts to repair this bone loss. But instead of making a smooth replacement, a bony node grows alongside the existing bone of the finger joint and this is how a Bouchard's node develops.

Significance of Bouchard's Nodes

Bouchard's nodes, like Heberden's nodes, may or may not be painful, but they are typically associated with a limited motion of the affected joint. The nodes are strongly familial (meaning they are inherited), and most researchers believe they are caused by osteophytes, although some disagree. Even so, genetics plays only one role in the formation of OA, as generally OA is considered to occur from the wear-and-tear with aging. OA may also follow an injury to the affected joint.

It's worthy to note that the characteristic appearance of Bouchard's nodes and Heberden's nodes in the hand are significantly helpful in diagnosing OA.

That said, by the time you see a new Bouchard's node, significant damage has happened to the finger joint. In other words, the osteoarthritis has progressed and taken its toll on the joint.

Treatment of Bouchard's Nodes

The treatment for Bouchard's nodes is similar for hand OA without nodes. This includes resting the joint, perhaps using a splint to keep from moving it too much, pain relievers like nonsteroidal anti-inflammatories (NSAIDs), and heat and ice therapy. These therapies are mostly done when the node is in the formation phase.

Once the node has formed, most people do not have any pain, although they usually report a restriction in motion and function, and the finger may appear crooked or deformed.

At this stage, due to affected joint stiffness and loss of range of motion, physical or occupational therapy may be needed. In severe cases, surgery can be done to replace or fuse the joint, but this is rare.

Lastly, it's important to note that while Bouchard's nodes may be unsightly, surgery isn't done for cosmetic purposes. The joint is already degraded by the time the node appears, and replacement or fusion is needed rather than removal of a bump.

A Word From Verywell

In the end, a Bouchard's node is considered a visible sign of osteoarthritis, which can help with diagnosis. This is unlike other types of arthritis, like gout or rheumatoidarthritis, that may rely more on laboratory tests for diagnosis.

That said, there are also visible signs in the hands of some people with rheumatoid arthritis and gout. For example, rubbery bumps (called rheumatoid nodules) may be seen on the thumbs and knuckles in people with rheumatoid arthritis. Likewise, people who develop frequent gout attacks for many years may develop tophi on the fingers (tophi are hard bumps filled with uric acid crystals that get deposited in the joint space). 

The good news is that a doctor can easily distinguish these signs from those seen in osteoarthritis. 

View Article Sources 
  • Doherty M, Abhishek A. (2017). Clinical manifestations and diagnosis of osteoarthritis. Hunter D, ed. UpToDate. Waltham, MA: UpToDate Inc.
  • Dunkin MA. (n.d.). Arthritis Foundation: "What Your Hands Say About Your Health".
  • Leung GJ, Rainsford KD, Kean WF. Osteoarthritis of the hand I: etiology and pathogenesis, risk factors, investigation and diagnosis.J Pharm Pharmacol. 2014 Mar;66(3):339-46.
  • Rees F et al. Distribution of finger nodes and their association with underlying radiographic features of osteoarthritis. Arthritis Care Res (Hoboken).2012 Apr;64(4):533-8.

 

 

 

 

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Typically, the early development of OA is silent. When pain occurs, and pain is almost always the presenting complaint, the osteoarthritic process has already likely progressed to joint damage. Cartilage is damaged, bone reaction occurs, and debris mixes with synovial fluid. Consequently, when a diagnosis of OA is established, goals of therapy become control of pain, restoration of function, and reduction of disease progression. Although control of the patient’s complaints is possible, and long periods of few or no symptoms may ensue, the patient permanently carries a diagnosis of OA.

Treatment of OA involves multiple modalities and is inadequate if only a prescription for anti-inflammatory drugs is written. Patient education, assessment for physical therapy and devices, and consideration of intraarticular injections are additional measures in the total management of the patient.

Hochberg  MC  et al. American College of Rheumatology 2012 recommendations for the use of nonpharmacologic and pharmacologic therapies for osteoarthritis of the hand, hip and knee. Arthritis Care Res. 2012; 64(4):465.

A. Patient Education

Patient education is a crucial step. Patients must be made aware of the role they play in successful therapy. Many resources are available to assist the provider in patient education. Patient education pamphlets are widely available from government organizations, physician organizations (eg, American College of Rheumatology, American Academy of Family Physicians), insurance companies, pharmaceutical companies, or patient advocacy groups (eg, the Arthritis Foundation). Many communities have self-help or support groups that are rich sources of information, advice, and encouragement.

One of the most effective long-term measures to both improve symptoms and slow progression of disease is weight loss. Less weight carried by the hip, knee, ankle, or foot reduces stress on the involved arthritic joint, decreases the destructive processes, and probably slows progression of disease. Unfortunately, because of the pain and occasional limited mobility of OA, exercise—an almost required component of weight loss regimens—is less likely to be utilized. On the other hand, exercise is a crucial modality that should not be overlooked. Evaluation for appropriate exercise focuses on two issues: overall fitness and correction of any joint-specific disuse atrophy. One must be flexible in the choice of exercise. Swimming is an excellent exercise that limits stress on the lower extremities. Many older persons are reluctant to learn to swim anew, yet they may be amenable to water aerobic exercises. These exercises encourage calorie expenditure, flexibility, and both upper and lower muscle strengthening in a supportive atmosphere. Stationary bicycle exercise is also accessible to most people, is easy to learn, and may be acceptable to those with arthritis of the hip, ankle, or foot. Advice from an occupational or recreational therapist can be most helpful.

B. Physical Therapy and Assistive Devices

The pain of OA can result in muscular disuse. The best example is quadriceps weakness resulting from OA of the knee. The patient who favors the involved joint loses quadriceps strength. This has two repercussions—both cushioning (shock-absorption) and stabilization are lost. The latter is usually the cause of the knee “giving way.” Sudden buckling at the knee, often when descending stairs, is rarely due to the destruction of cartilage or bone but rather to inadequate strength in the quadriceps to handle the load required at the joint. Physical therapy with quadriceps strengthening is highly efficacious, resulting in improved mobility, increased patient confidence, and reduction in pain.

The physical therapist or physiatrist should also be consulted for advice regarding assistive devices. Advanced OA of lower extremity joints may cause instability and fear of falls that can be addressed by canes of various types. Altered posture or joint malalignment can be corrected by orthotics, which has the advantage, when used early, of slowing progression of OA. Braces can protect the truly unstable joint and permit continued ambulation.

Fransen  M  et al. Land-based exercise for osteoarthritis of the knee: a metaanalysis of randomized controlled trials. J Rheumatol. 2009;36:1109.

C. Pharmacotherapy

The patient wants relief from pain. Despite the widespread promotion of nonsteroidal anti-inflammatory drugs (NSAIDs) for OA, there is no evidence that NSAIDs alter the course of the disease. Nevertheless, NSAIDs are used for their analgesic, rather than disease-modifying, effects. Although effective as analgesics, NSAIDs have significant side effects and are not necessarily first-line drugs.

Begin with adequate doses of acetaminophen. Acetaminophen should be prescribed in large doses, 3–4 g/d, and continued at this level until pain control is attained. Once pain is controlled, dosage can be reduced if possible. Maintenance of adequate blood levels is essential and because acetaminophen has a relatively short half-life, frequent dosing is necessary (3 or 4 times a day). High doses of acetaminophen are generally well tolerated, although caution is important in patients with liver disease or in whom alcohol ingestion is heavy.

Administration of NSAIDs mixed as a cream or gel and rubbed onto joints has long been advocated for small- and even large-joint arthritis. There undoubtedly is less GI upset when delivered in this manner, but well-designed studies demonstrating prolonged effectiveness are lacking. There are two FDA-approved products on the US market (diclofenac, ketoprofen), although some compounding pharmacies apparently have more NSAIDs available.

Two main classes of NSAIDs are available, differentiated largely by half-life. NSAIDs with shorter half-lives (eg, diclofenac,, ibuprofen) need more frequent dosing than longer-acting agents (eg, naproxen, meloxicam). Several NSAIDs are available in generic or over-the-counter (OTC) form, which reduces cost. Despite differing pharmacology, there is little difference in efficacy, so a choice of medication should be based on individual patient issues such as dosing intervals, tolerance, toxicity, and cost. As with acetaminophen, adequate doses must be used for maximal effectiveness. For example, ibuprofen at doses of ≤800 mg 3 or 4 times a day should be maintained (if tolerated) before concluding that a different agent is necessary. Examples of NSAID dosing are given in Table 24-2.

Table 24–2.Selected nonsteroidal anti-inflammatory drugs with usual and maximal doses.
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Since such a major thrust of OA management is pain control, one must acknowledge the role played by narcotics. Narcotics should be confined to the patient with severe disease incompletely controlled by nonpharmacologic and nonnarcotic analgesics, and in whom joint replacement is not indicated. The narcotic medication should be additive to all other measures; for instance, full-dose acetaminophen or NSAIDs should be continued. The patient must be reminded of the fluctuating nature of OA symptoms and not expect complete elimination of pain. Once narcotics are started (in any patient for any cause), most generalist practices institute monitoring measures such as a “drug contract” or referral to a specialist pain management clinic.

Zhang  W  et al. OARSI recommendations for the management of hip and knee arthritis, Part II: OARSI evidence-based, expert consensus guidelines. Osteoarthr Cartilage. 2008;16:137–162. 
[PubMed: 18279766] 

D. Intraarticular Injections

Hyaluronic acid (hyaluronan) is a constituent of both cartilage and synovial fluid. Injection of hyaluronic acid, usually in a series of several weekly intraarticular insertions, is purported to provide improvement in symptomatic OA for ≤6 months. It is unknown why hyaluronic acid helps; there is no evidence that hyaluronic acid is incorporated into cartilage, and it apparently does not slow the progression of OA. It is expensive, and the injection process is painful. Use of these agents (Synvisc, Artzal) is limited to patients who have failed other forms of OA therapy.

Intraarticular injection of corticosteroids has been both under- and overutilized in the past. There is little question that steroid injection rapidly reduces inflammation and eases symptoms. The best use is one in which the patient has an exacerbation of pain accompanied by signs of inflammation (warmth, effusion). The knee is most commonly implicated and is most easily approached. Most authorities recommend no more than two injections during one episode and limiting injections to no more than two or three episodes per year. Benefits of injection are often shorter in duration than similar injection for tendinitis or bursitis, but the symptomatic improvement buys time to reestablish therapy with oral agents, physical exercise, and assistive devices.

New therapeutic investigation and translational studies hold some promise for actual cartilage modification of damaged joints. Therapies involving strontium ranelate, platelet-rich plasma injections, and mesenchymal stem cells are currently in stages of development and may truly alter the otherwise somewhat relentless progression of this disease.

Arrich  J. Intra-articular hyaluronic acid for the treatment of osteoarthritis of the knee: systematic review and meta-analysis. Can Med Assoc J. 2005;172:1039. 
[PubMed: 15824412] 
Reginster  JY  et al. Efficacy and safety of strontium ranelate in the treatment of knee osteoarthritis: results of a double-blind, randomized placebo-controlled trial. Ann Rheum Dis. 2013;72:179.

E. Surgery

At one time, orthopedic surgeons performed arthroscopic surgery on osteoarthritic knees in an effort to remove accumulated debris and to polish or débride frayed cartilage. However, a clinical trial using a sham-procedure methodology demonstrated that benefit from this practice could be explained by the placebo effect. Numbers of these procedures have reduced rather significantly, although there still remain some indications for performing this operation.

Joint replacement is a well-established option for treatment of OA, especially of the knee and hip. Pain is reduced or eliminated altogether. Mobility is improved, although infrequently to premorbid levels. Expenditures for total joint replacement have been increasing dramatically as the baby boomer generation reaches the age at which OA of large joints is more common. Indications for joint replacement (which also apply to other joints, including shoulder, elbow, and fingers) include pain poorly controlled with maximal therapy, malalignment, and decreased mobility. Improvement in pain relief and quality of life should be realized in ~90% of patients undergoing the procedure. Because complications of both the surgery and rehabilitation are increased by obesity, few orthopedic surgeons will consider hip or knee replacement without at least an attempt by the obese patient to lose weight. Patients need to be in adequate medical condition to undergo the operation and even more so to endure the often lengthy rehabilitation process. Some surgeons refer patients for “prehabilitation” or physical training prior to the operation. Counseling of patients should include the fact that there often is a 4–6-month recovery period involving intensive rehabilitation.

Moseley  JB  et al. A controlled trial of arthroscopic surgery for osteoarthritis of the knee. N Engl J Med. 2002; 347:81. 
[PubMed: 12110735] 

F. Complementary and Alternative Therapies

Glucosamine, capsaicin, bee venom, acupuncture, and a host of other products have been promoted as alternative therapies for OA. Glucosamine and chondroitin sulfate are components of glycosaminoglycans, which make up cartilage; although some advocates might suggest otherwise, there is no evidence that orally ingested glucosamine or chondroitin sulfate is actually incorporated into cartilage. Studies suggest these agents are superior to placebo in symptomatic relief of mild OA. The onset of action is delayed, sometimes by weeks, but the effect may be prolonged after treatment is stopped. Glucosamine-chondroitin sulfate combinations are available over the counter and are generally well tolerated by patients.

Capsaicin, a topically applied extract of the chili pepper, relieves pain by depletion of substance P, a neuropeptide involved in pain sensation. Capsaicin is suggested for tendinitis or bursitis, but may be tried for OA of superficial joints such as the fingers. The cream should be applied 3 or 4 times a day for ≥2 weeks before reaching any conclusion regarding benefit.

Bee venom is promoted in complementary medicine circles. A mechanism for action in OA is unclear. Although anecdotal reports are available, comparison studies to other established treatments are difficult to find. Various vitamins (D, K) and minerals have been recommended for treatment of OA but are supported, if at all, by only poorly controlled studies.

Acupuncture can be useful in managing pain and improving function. There are more comparisons between acupuncture and conventional treatment for OA of the back and knee than for other joints. Generally, acupuncture is equivalent to oral treatments for mild symptoms at these two sites.

++++++++++++++++++++++++++++

An international task force of 19 clinicians, healthcare professionals, and patients from 10 European countries used their expertise in conjunction with the evidence to come up with 5 overarching principles and 10 recommendations.

The 5 overarching principles of managing hand OA are as follows:

  1. The primary goal is to control symptoms and optimize hand function so that patients can maximize activity, participation, and quality of life.
  2. Clinicians should offer patients information regarding the nature and course of hand OA as well as education on self-management principles and treatment options.
  3. Clinicians should individualize the management of hand OA after taking localization, severity, and comorbidities into account.
  4. Clinicians should base the management of hand OA on a shared decision by the patient and clinician.
  5. The optimal management of hand OA usually requires a multidisciplinary approach; clinicians should consider non-pharmacologic, pharmacologic, and surgical treatment options.

The 10 recommendations are:

  1. Clinicians should offer education and training in ergonomic principles, pacing of activity, and the use of assistive devices.
  2. Clinicians should consider exercises to improve function, improve muscle strength, and reduce pain.
  3. Clinicians should consider orthoses for symptom relief in patients with thumb base OA. Long-term orthoses use is recommended.
  4. Topical treatments should be used over systemic treatments due to safety reasons. The first choice of pharmacologic topical treatment is topical nonsteroidal anti-inflammatory drugs (NSAIDs).
  5. Clinicians should consider a limited duration of oral analgesics, especially NSAIDs, for relief of symptoms.
  6. Clinicians should consider chondroitin sulfate for pain relief and improvement in functioning in patients with hand OA.
  7. Generally, intra-articular injections of glucocorticoids should not be used in patients with hand OA. However, they may be considered in patients with painful interphalangeal joints.
  8. Clinicians should not use conventional or biologic disease-modifying antirheumatic drugs for the treatment of hand OA.
  9. Clinicians should consider surgery in patients with structural abnormalities if other treatment methods have not been sufficiently effective in relieving pain. Consider trapeziectomy in patients with thumb base OA and consider arthrodesis or arthroplasty in patients with interphalangeal OA.
  10. Clinicians should adapt long-term follow-up of patients with OA based on individual patient needs.

The task force also developed a research agenda for topics relating to hand OA. They recommend placebo-controlled trials for a variety of hand OA treatments, including orthoses, topical NSAIDs, paracetamol, tramadol, glucosamine, chondroitin sulfate, intra-articular glucocorticoids, methotrexate, and low-dose oral glucocorticoids. Additional trials should be performed to assess the most effective types of exercise and surgery for hand OA.

The task force predicts that an update to these new recommendations may happen in the near future. “Advances in research of OA pathophysiology as well as outcome measurement increase the likelihood of finding new therapeutic options,” the researchers wrote. “The next update should be undertaken when sufficient new data are available, either on the current treatment options, or on new therapies.”

Reference

Kloppenburg M, Kroon FPB, Blanco FJ, et al. 2018 update of the EULAR recommendations for the management of hand osteoarthritis [published online August 28, 2018]. Ann Rheum Dis. doi:10.1136/annrheumdis-2018-213826

 

 

 Here is what doctors recommend to reduce the risk of OA or delay its onset.

Maintain a Healthy Weight
Excess weight is one of the biggest risk factors for osteoarthritis – and for good reason. Extra pounds put additional pressure on weight-bearing joints, such as the hips and knees. Each pound you gain adds nearly four pounds of stress to your knees and increases pressure on your hips six-fold. Over time, the extra strain breaks down the cartilage that cushions these joints.

But mechanical stress is not the only problem. Fat tissue produces proteins called cytokines that promote inflammation throughout the body. In the joints, cytokines destroy tissue by altering the function of cartilage cells. When you gain weight, your body makes and releases more of these destructive proteins. Unless you are very overweight, losing even a few pounds can reduce joint stress and inflammation, cutting your risk of OA in half.

Control Blood Sugar
The latest research suggests that diabetes, which affects the body's ability to regulate blood sugar (glucose), may be a significant risk factor for osteoarthritis. That's because high glucose levels speed the formation of certain molecules that make cartilage stiffer and more sensitive to mechanical stress. Diabetes can also trigger systemic inflammation that leads to cartilage loss. The newly discovered connection between diabetes and joint damage may help explain why more than half of Americans diagnosed with diabetes also have arthritis.

Get Physical
Physical activity is the best available treatment for OA. It's also one of the best ways to keep joints healthy in the first place. As little as 30 minutes of moderately intense exercise five times a week helps joints stay limber and strengthens the muscles that support and stabilize your hips and knees. Exercise also strengthens the heart and lungs, lowers diabetes risk and is a key factor in weight control.

You don't have to join a gym or have a formal workout plan to benefit. Walking, gardening – even scrubbing floors – count. But the greatest results come with a consistent and progressive exercise program adjusted for your age, fitness level and the activities you enjoy most.

No matter what type of exercise you choose, listen to your body. If you have pain after a workout that persists more than an hour or two, do less next time and take more breaks. To avoid injury, go slow until you know how your body reacts to a new activity and don't repeat the same exercise every day. If you have a hard time starting or sticking with an exercise program, the Arthritis Foundation's Walk With Ease program can help you reach your goals.

Play it Safe
Because cartilage doesn't heal well, an injured joint is nearly seven times more likely to develop arthritis than one that was never injured. Fractures, dislocations – even ligament tears and strains – can significantly increase the risk of OA, which occurs in about 50 percent of people who experience a traumatic injury.  

Although injuries aren't always avoidable, it pays to protect your joints. If you play sports, wear protective gear, such as joint padding for soccer or hockey. And make sure any baseball field you use has break-away bases. At home or work, use your largest, strongest joints for lifting and carrying and take breaks when you need to. After an injury, maintaining a healthy weight can help guard against further joint damage.

Choose a Healthy Lifestyle
Some risk factors for OA cant be changed. For instance, OA becomes more common as people age, though why this occurs isn't clear. One idea is that the number of cartilage cells simply diminishes over time. Because more women than men develop OA, especially after age 50, lower estrogen levels after menopause may also play a role.

In addition, some people inherit genes that make them more susceptible to OA. In one study, variations in the gene for a cytokine associated with inflammation and cartilage loss doubled the risk of severe arthritis. It's important to remember, though, that arthritis is a multifactorial disorder and simply inheriting a gene doesn't mean you will develop it.

Ultimately, the best defense against any disease, including OA, is a healthy lifestyle. The way you eat, exercise, sleep, manage stress and interact with others, and whether you smoke or drink can have a tremendous influence not just on overall health, but also on the health of your joints.

 

Prognosis

Restoring and rebuilding damaged cartilage is theoretically intriguing but not possible at this time. Investigations into regeneration of cartilage are proceeding as suggested earlier. Even so, reversal of the pathophysiologic process in OA is unlikely to be readily available anytime soon. With application of all modalities of treatment—adequate pain control, weight loss, appropriate exercise, orthotics and devices, and surgery—the successful management of osteoarthritis should be realized in most patients.

 

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