Given the aging of the population and the increased prevalence of arthritis, this author discusses key considerations in detecting and treating common rheumatologic conditions in elderly patients.

      Treating musculoskeletal disorders in the elderly can be extremely challenging. As the proportion of elderly in the population continues to rise, the prevalence of chronic conditions such as arthritis is expected to increase as well. By the year 2020, the prevalence of arthritis is expected to reach 18.2 percent, affecting approximately 59.4 million people. Arthritis is reportedly one of the most common chronic conditions among community dwelling adults, affecting 49 percent of those over the age of 65.

       The National Arthritis Data Work Group demonstrated that arthritis affects 45 percent of people between the age of 65 to 74; 55.2 percent of those between the ages of 75 to 82 years old; and 57 percent of people over the age of 85.^1-3
       The impact of arthritis is significant. It has an obvious affect on activity limitation with approximately 78 percent of people over the age of 65 reporting limitation in one physical activity while 34 percent report limitation in five or more activities.^4-5 More recent data from the Longitudinal Canadian National Population Health Survey supports a relationship between arthritis onset, pain intensity, the development of activity limitation and poor self-rated health.⁶
       Arthritis also has an impact on a person’s psychological and social well being. It can create psychological distress, depression and anxiety resulting in diminished quality of life, mood disorders, limited independence as well as increased health care utilization.^3-7
       Although pain may be the most common initial complaint of a musculoskeletal condition, it may also be underreported in the elderly. Cognitively impaired patients may not be able to report pain but instead present with confusion or a decline in their ability to perform activities of daily living (ADL) or instrumental activities of daily (IADL).⁸ Elderly patients may also have a delay in diagnosis because they may have atypical disease presentations, false positive serologies and/or multiple coexisting conditions that can confound the presentation and diagnosis.⁹ Other obstacles that may delay diagnosis and treatment include the difficulty for many patients to obtain radiographs, laboratory studies, physical and occupational therapy and medications due to a lack of finances, family and social supports as well as an inability to access reliable transportation.
       These complexities often delay an accurate diagnosis and implementation of a treatment regimen.

Understanding The Impact Of Polypharmacy And Physiologic Changes With Aging
When prescribing pharmacologic therapy for older patients, one should choose a regimen based on the patient’s underlying comorbidities and drug regimen as well as the efficacy and safety profile of the drug one is considering.

Here one can see osteoarthritis which reveals Heberden’s and Bouchard’s nodes. Note the bony enlargement of the distal and proximal interphalangeal joints. (Photo courtesy of the American College of Rheumatology)

       Polypharmacy is a significant problem among the elderly as they may be visiting many doctors and receiving treatment for numerous coexisting conditions. One cannot understate the importance of careful drug surveillance when starting a new agent for an older patient. As the number of prescribed medications increase, there is an increased likelihood that either drug noncompliance or adverse drug reactions will occur. Adverse reactions may arise from inappropriate medication prescribing and/or administration, inappropriate monitoring, drug-drug interactions and/or altered pharmacodynamic and pharmacokinetic changes that occur with aging.
       An understanding of the physiologic changes that occur with aging may help prevent these complications. These physiologic changes include altered total body composition. With reduced free body water and increased total body fat, there is an associated increase in the plasma concentration of water-soluble drugs and a lowered plasma concentration of lipid soluble drugs.
       Reduced serum albumin increases the availability of the free fraction of medications that are normally protein bound.^10-11 Decreased hepatic flow and liver mass decreases hepatic metabolism yet Phase I reactions appeared unaltered.¹² There is often diminished renal clearance due to decreased renal blood flow, glomerular filtration, active tubular secretion and reabsorption. This may not be reflected in an elevated blood urea nitrogen or serum creatinine level since many elderly patients have decreased muscle mass.

The usual presentation of gout is an acute, extremely painful monoarticular attack that most frequently affects the first metatarsophalangeal joint (great toe). Note the podagra involving the swollen and red big toe and ankle. (Photo courtesy of the American College of Rheumatology)

       When treating elderly patients, one should be aware that end organ receptor sensitivity is augmented in many agents, especially psychoactive and analgesic agents.^11,12 These changes warrant the close monitoring of patients for adverse drug effects even at low or therapeutic doses.¹⁰

Emphasizing An Interdisciplinary Approach
In order to approach and overcome the frequent challenges in treating elderly patients, one should facilitate a collaborative effort via an interdisciplinary team of nurses, nurse practitioners, pharmacists, social workers, physical and occupational therapists and psychiatrists. The skills and knowledge provided by these individuals can be helpful in navigating through a complex health care system to meet the challenges facing the older adult. Ideally, it would be best to identify musculoskeletal problems and initiate nonpharmacologic and pharmacologic treatment regimens early so clinicians can preserve independence, reduce pain and enhance the overall quality of life for these patients.
       With these points in mind, let us consider the diagnosis and treatment of common rheumatic conditions among adults over the age of 50. As the proportion of elderly patients continues to increase, there will be a greater need for primary care providers to identify these disorders and key risk factors, and implement appropriate treatment interventions.

Assessing The Impact And Clinical Features Of Osteoarthritis
Osteoarthritis (OA) is one of the most common and disabling rheumatic disorders in people over the age of 55. It affects 12 percent of the population and more than 65 percent of people over the age of 65.¹³ The functional impact of osteoarthritis is determined by the affected joints. When patients have lower extremity joints that are affected by OA, there may be impaired ambulation, stair climbing, balance, transfers and ADL activity while upper extremity disease often impacts basic ADLs.¹³
       Several risk factors contribute to the development of OA. These risk factors include age, female sex, menopausal status, ethnic/racial background, genetic predisposition, chondrocalcinosis, obesity, mechanical factors, such as occupational knee bending and physical labor, and endogenous factors such as type II collagen mutation and dysplastic conditions.^14-16 Researchers have also identified quadriceps weakness as a risk factor contributing to the pathogenesis of the disease.^17-19 However, Sharma, et. al., recently questioned whether quadriceps strengthening is detrimental to patients with knee malalignment.²⁰

Here is a tophi involving the interphalangeal joints and metacarpophalangeal joints. (Photo courtesy of the American College of Rheumatology)

       Women are most frequently affected by generalized osteoarthritis, which involves distal interphalangeal joints (Heberden’s nodes), proximal interphalangeal joints (Bouchard’s nodes), first carpometacarpal joints, knees, the cervical and lumbar spine, first metatarsophalangeal joint and possibly the hip.^21-23 However, localized disease is prevalent in both sexes and most commonly affects weightbearing joints such as the knees, hips and spine.
       The most common symptoms associated with osteoarthritis are pain and stiffness that typically become worse with weightbearing and physical activity, and improve with rest. Affected individuals describe early morning stiffness that lasts between 20 to 30 minutes and increases after periods of inactivity. Patients may report joint buckling or instability as well as loss of function. Physical findings include joint swelling and tenderness with palpation, bony enlargement, deformity or malalignment, instability, crepitus and pain with motion or diminished range of motion. Inflammation is usually mild and involves the affected joint.24,25
       One would diagnose OA via the clinical examination and radiographic features. Radiographs do not always correlate with symptoms but characteristic features include joint space narrowing, osteophyte formation, subchondral bone sclerosis and cyst formation, and abnormalities of bony contour.
       By the time people reach the ages of 45 to 50, more than 50 percent of this population has radiographic evidence of osteoarthirits involving the hands, spine and feet. When patients reach the age of 80, both men and women almost universally have radiographic evidence of osteoarthritis involving the hands and feet. However, only 30 to 50 percent of these people have joint symptoms.26

Tophus involving the helix of the ear have a whitish appearance due to urate deposition. (Photo courtesy of the American College of Rheumatology)

       Currently, one can monitor the disease progression in affected individuals via clinical symptoms. In clinical trials, one may monitor disease progression via radiographs (an insensitive measure) or MRI and arthroscopy. Recent studies have demonstrated an association with biologic markers and disease progression of OA inflammation and synovitis. These markers include cartilage oligomeric matrix protein (COMP), serum level of C-reaction protein (CRP) and level of hyaluronic acid (HA). High disease activity suggests a rapid progression of disease.16

Key Risk Factors For Osteoarthritis

- Age Physical labor Sex and menopausal status Congenital abnormalities Ethnic/racial background Abnormal biomechanics Genetic predisposition Increased physical loading Obesity conditions Knee injury Quadriceps weakness Neuropathic arthropathy Metabolic disorders Chondrocalcinosis Septic arthritis

Pertinent Pointers On Nonpharmacologic Therapy For OA
When it comes to managing OA, one should emphasize disease prevention, alleviating symptoms of pain and disability, maximizing function and limiting progression of the disease. Preventive strategies include identifying risk factors such as obesity and emphasizing behavioral modification for weight loss. Clinicians should also educate patients about how to prevent injuries during exercise and alter job demands in order to reduce the potential for repetitive joint injury.14,21,27
       One may utilize nonpharmacologic and pharmacologic regimens to improve function and treat pain. Clinicians should always initiate nonpharmacologic regimens that include patient education, joint protection, relaxation techniques, bracing, the use of appropriate footwear, psychological counseling, aerobic and aquatic exercise.28 Obtaining a consult with a physical and/or occupational therapist should also be part of the cornerstone of therapy. The therapist can assist in developing an exercise program geared toward strengthening affected muscles surrounding the affected joint. They can also educate patients about the use of assistive devices to enable mobility and decrease joint load.15,27-29

Pharmacologic Therapy For OA: What You Should Know
When pain persists despite conservative treatment efforts, clinicians can usually initiate pharmacologic therapy. When choosing an appropriate regimen for a patient, practitioners should always consider the side effect profile of an agent, patient comorbidities and possible alterations in drug metabolism that occur with aging.
       One should also review the patient’s current drug regimen in order to avoid drug–drug interactions. Pharmacologic regimens including non-narcotic analgesics such as acetaminophen show similar efficacy and fewer side effects than traditional nonsteroidal anti-inflammatory regimens (NSAIDs) in patients with mild to moderate pain.28,30-32 Clinicians should monitor liver and renal function in long term users, especially patients who have known liver disease or alcoholic cirrhosis, due to the potential for toxicity.
       Nonsteroidal antiinflammatory agents are the most commonly prescribed agents for OA when acetaminophen fails to alleviate pain. However, one should only initiate NSAIDs for patients who are at low risk for gastrointestinal or renal side effects. Clinicians should first attempt a trial of non-acetylated salicylates and then consider more potent NSAIDs if treatment fails.21,33 The elderly are more likely to experience side effects due to NSAIDs. These side effects include gastrointestinal toxicity (inflammation, ulceration, bleeding, perforation), nephrotoxicity, hepatotoxicity, cardiovascular effects such as volume overload, central nervous system (CNS) effects, including dizziness, confusion, cognitive impairment, and hematological abnormalities.24 Risk factors associated with gastrointestinal complications include increasing age, a history of peptic ulcer disease, concomitant use of corticosteroids, anticoagulant use, cigarette smoking or alcohol use, and ingestion of multiple NSAIDs. Risk factors for developing renal failure include being older than 65, the presence of hypertension and/ or congestive heart failure and concomitant use of diuretics and angiotensin converting enzyme inhibitors.28

Using a polarizing microscope, one can make the diagnosis of gout when synovial fluid analysis from the affected joint reveals negatively birefringent needle shaped crystals. (Photo courtesy of the American College of Rheumatology)

       When prescribing NSAIDs, one should start with the lowest analgesic dose and titrate to the lowest effective dose necessary. Clinicians should also prescribe a gastroprotective agent such as misoprostol, a prostaglandin E2 inhibitor, or an H2 blocker or proton pump inhibitors such as omeprazole in order to decrease the incidence of gastric and duodenal ulcerations.24 The current cardiovascular safety concerns with cyclooxygenase 2 (COX-2) inhibitors and the recent removal of rofecoxib and valdecoxib from the market has limited their usefulness.
       One may consider using opiods to treat pain and they include agents such as codeine and oxycodone. Clinicians often utilize these agents when other measures have failed or when contraindications or side effects have been reported with more conservative regimens. Researchers have also found Tramadol, another centrally acting agent, useful in controlling symptoms. When prescribing all these agents, any dose adjustment should follow recommended guidelines and one must monitor for side effects. The provider should be aware of potential drug-drug interactions as well as altered drug distribution, clearance and enhanced sensitivity in the elderly. When using opiods, one must also prescribe a concurrent agent to prevent constipation. Other side effects that require close monitoring include delirium, dizziness, and somnolence, especially when these patients are using other CNS-acting agents.24,27

A Primer On Pharmacologic Treatment For Acute Gout

       Topical analgesic creams, such as methylsalicylate and capsaicin, have also been helpful in alleviating pain. Side effects reported with capsaicin include burning at the site of application or rash.27,28 Performing intraarticular injections with triamcinolone acetonide often provides up to four weeks of relief following the injection.34,35 Viscosupplementation with hyaluronan preparations alleviates symptoms and recent evidence suggests it may modify the disease.36,37
       The mechanism of action of these agents remains unclear although several theories suggest they inhibit inflammatory mediators. These agents produce an antiinflammatory and analgesic effect as well as a short-term lubricating effect. Symptom relief usually lasts longer with hyaluronan injections than with corticosteroids. The principal side effects reported include a local reaction at the injection site (reported in 10 percent of patients) as well as a few reports of increased pain and the development of joint effusions following injection. One should consider employing this regimen for patients when conservative measures have failed.27

In another diagnostic view of gout, one can see bilateral erosions of the head of the proximal phalanx, which are described as “overhanging edges.” (Photo courtesy of the American College of Rheumatology)

       Studies using alternative agents, such as glucosamine sulfate and chondroiten sulfate, have suggested improved symptom control and less radiographic progression.38 Disease modifying agents that alter the progression of OA are presently being investigated.28 Invasive therapies such as joint lavage, arthroscopic debridement and joint replacement may be indicated when severe pain, limited mobility and function affect the patient’s quality of life.

An Overview Of Crystal Diseases
Crystal diseases are common in the elderly and increase in prevalence as the population ages. The major categories of crystal disease include gout, calcium pyrophosphate dihydrate deposition disease, basic calcium phosphate associated syndromes (calcium hydroxyapatite disease) and calcium oxalate arthritis.39 These diseases may coexist with other joint abnormalities including OA.
       Clinical presentations of these crystal diseases may include monoarticular and oligoarticular arthritis as well as polyarticular arthritis and periathritis that primarily affect large joints. Microscopy helps to distinguish these crystals and make a diagnosis. Erosive changes or chondrocalcinosis may be present radiographically or pathologically in both hyaline and fibrocartilage. This calcification may take the form of calcium pyrophosphate dihydrate disease, dicalcium phosphate dihydrate or calcium hydroxyapatite disease.40

Reviewing The Prevalence And Risk Factors Of Gout
Gout is one of the most common types of inflammatory arthritis encountered by primary care providers. It is more prevalent in men and frequently occurs during one’s 40s and 50s.41 In patients over the age of 60 years old, it is more common in women as 85 percent of new cases are being reported in women. Less than 15 percent of premenopausal women present with gout.42
       The prevalence of gout increases with age.43 Prevalence rates reported by the U.S. National Health Interview Survey indicate that gout was reported among 2.24 percent of people between the ages of 45 and 64 and in 3.17 percent of people between the ages of 65 to 74.42 The rise in the elderly may be due to the increased prevalence of hypertension, hyperlipidemia, congestive heart failure, insulin resistance, renal insufficiency, low dose salicylate use and diuretic use.43 Normal uric acid levels range around 7 mg/dl in men and post-menopausal women, and hover around 6 mg/dl in premenopausal women.
       The Normative Aging Study demonstrated that hyperuricemia contributed to the development of gout. Researchers reported an incidence rate of 4.9 percent at levels greater than 9 mg/dl, an incidence of 0.5 percent among those with serum uric acid between 7 to 8.9 mg/dl and an 0.1 percent incidence among men with serum uric acid levels less than 7mg/dl.42 In addition to acute gouty arthritis, hyperuricemia can lead to uric acid nephropathy and calcium oxalate urolithiasis.41

Pseudogout is another crystal disease, also known as calcium pyrophosphate dihydrate deposition disease, which is commonly associated with aging. Note the calcium pyrophosphate dihydrate crystal shown above. (Photo courtesy of the American College of Rheumatology)

       Gout has frequently been associated with a diet rich in purines and protein, especially meat and seafood, and a decreased consumption of dairy products.43 Most recently, a study by Choi demonstrated that a diet rich in purines such as meats (beef, pork, lamb) and seafood was strongly associated with gouty attacks while ingestion of animal and vegetable protein or purine-rich vegetables was not correlated with frequent flares.        Choi’s study demonstrated a strong inverse association with gout and ingestion of a high dairy diet (i.e. low fat yogurt and low fat milk due to a uricosuric affect of milk proteins (casein and lactalbumin)). Other risk factors for hyperuricemia and gout include hypertension, high body mass index (BMI), high alcohol intake, the use of thiazide and loop diuretics, low dose ASA, insulin resistance, menopausal status and renal insufficiency.42,44-46 Beer is high in purines and has been associated with an increased risk of gout.43
       Gout rarely occurs in women prior to menopause due to the uricosuric effect of estrogen.42 The prevalence of gout is increasing among postmenopausal women as a result of diuretic use, low-dose aspirin prophylaxis for cardiovascular disease and renal insufficiency. In women, the initial presentation of gout may be more atypical. One may see polyarticular flares resembling rheumatoid arthritis or flares that are more subacutely superimposed on joints that have deformities consistent with nodal osteoarthritis.41,45

Key Insights On The Pathophysiology And Diagnosis Of Gout
The usual presentation of gout is an acute, extremely painful monoarticular attack that most frequently affects the first metatarsophalangeal joint (great toe). This is referred to as podogra. This occurs in 50 percent of people with gout and clinicians will see podogra more frequently in younger patients. Acute attacks as well as a subacute and chronic smoldering arthritis can also occur in both oligoarticular and polyarticular distributions affecting the ankle, tarsal bones, knees and elbows. Clinicians will observe these more atypical attacks more frequently in the elderly.43,45 Interestingly, serum urate levels are often normal during these attacks.41
       Chronic tophaceous gout is a form of polyarticular gout associated with deposits of urate crystals in cartilage, synovium, tendons and joints. It usually develops over many years in the setting of increased uric acid concentration.
       Uric acid crystal deposits usually occur in the setting of hyperuricemia but can also occur with a normal uric acid level. Hyperuricemia may be due to overproduction of uric acid or under excretion by the kidneys. Eighty to ninety percent of gouty patients are underexcretors.47 As the level of uric acid increases above 9 mg/dl, the incidence of gouty arthritis and urolithiasis increases.
       In older patients, gout usually occurs in the setting of renal insufficiency, diuretic use or low dose aspirin use while flares can also occur in patients who have myeloproliferative disorders resulting from an overproduction of uric acid. In the setting of insulin resistance syndrome, the disease may occur as a result of insulin directly stimulating urate reabsorption.45 Alcohol products such as beer have a greater effect on the development of gout compared to products such as wine and liquor.45,48

Here one can see chondrocalcinosis involving the menisci of the knee. (Photo courtesy of the American College of Rheumatology)

       One can diagnose gout when synovial fluid analysis from the affected joint reveals negatively birefringent needle shaped crystals that clinicians may see with a polarizing microscope.45 Radiographs can also be helpful when there are classic erosive changes commonly described as “overhanging edges.” Gouty complications include tophus formation causing deformities, joint destruction, as well as chronic and persistent pain. Gout has also been associated with urolithiasis and uric acid nephropathy has been reported in 10 to 15 percent of people with gout.42

Key Considerations For Treating Gout In Elderly Patients
Gouty flares are often self-limiting but the pain and disability they cause warrant treatment. One would usually implement pharmacologic treatment for both acute and chronic disease but concomitant behavorial modification is equally important. Clinicians should ensure that all patients with gout receive education on weight loss, dietary modification (decreasing intake of meats, seafood, carbohydrates and fats), increasing dairy intake, decreasing alcohol intake and maintaining hydration.28,41 One should also discuss with patients the possibility of avoiding medications such as low dose aspirin, thiazides and loop diuretics as they decrease uric acid excretion.
       When it comes to treating the initial gouty flare, NSAIDs are the most commonly recommended treatment. These agents provide symptomatic relief within the first 24 hours for patients who do not have contraindications such as hypersensitivity, peptic ulcer disease or renal insufficiency. Most NSAIDs are equivalent in efficacy. However, one should proceed with caution when considering the use of NSAIDs in elderly patients and in patients with hepatic disease, renal insufficiency, a history of gastropathy or congestive heart failure. Risk factors for GI toxicity include increasing age, a history of peptic ulcer disease, cigarette smoking, steroid use and the use of anticoagulants and antiplatelet agents. When initiating NSAID treatment for elderly patients, one should also prescribe misoprostol, a PGE 2 inhibitor, or omeprazole, a proton pump inhibitor, simulataneously for gastroprotection.23
       Alternative agents used to treat acute gout include corticotrophin, which induces the release of adrenal corticosteroids and systemic corticosteroids. One may utilize oral colchicine for the acute flare. The most common regimen is 0.6 mg every one to two hours (not to exceed 4 mg) until there is symptomatic relief or GI symptoms occur or 0.6 mg every hour for three doses.41,48 Clinicians should start either regimen within the first 24 hours of a flare but gastrointestinal side effects often limit the medication’s usefulness. Keep in mind that colchicine is usually ineffective if one uses it after 48 hours of the onset of a flare.49 Clinicians also need to adjust the dose for creatinine clearance less than 50 cc/min. One should avoid using colchicine in transplant patients and in patients on hemodialysis due to the potential for neuromyopathy and other toxicities.48 Intravenous colchicine has been associated with serious adverse events including extravasation, bone marrow suppression and death.
       Intraarticular steroids are very useful in patients with a monoarticular flare or those who have contraindications to systemic therapy.41,42 Prophylactic regimens usually consist of NSAIDs or dose-adjusted colchicine and one can initiate these regimens to prevent future attacks, especially when initiating uric acid lowering regimens.
       When frequent gouty flares (more than three or four) occur, when there is evidence of urate nephropathy or when an overproduction of uric acid manifests as tophi or erosive changes on radiographs, clinicians should consider chronic suppressive therapy either with a xanthine oxidase inhibitor such as allopurinol or an uricosuric agent such as probenicid or sulfinpyrazone. When treating elderly patients, one does need to lower the dose of all these agents due to the frequent presence of renal insufficiency and drug-drug interactions.
Uricosurics are ineffective when the glomerular filtration rate (GFR) is less than 60 cc/min. In addition to determining the GFR, the choice of a regimen usually depends on establishing whether someone is an overproducer (a 24 hour urine urate excretion greater than 800 mg to 1000 mg) or an underexcretor. In the elderly, uricosuric agents are often ineffective because the presence of renal insufficiency limits their usefulness.41
       When starting allopurinol, one should titrate the dose slowly to avoid toxicity, especially hypersensitivity reactions.43 Clinicians should start treatment a minimum of two weeks following a flare.48 One should also initiate a prophylactic antiinflammatory agent in the absence of contraindications in order to help prevent rebound gouty flares that may occur following the initiation of a urate lowering agent.49 Identifying precipitating factors as well as emphasizing dietary modification can help to diminish the frequency of flares.41,43
       The goal of therapy is to lower the uric acid load and one should aim for serum uric acid levels below 6 mg/dl.42,48 In patients with hypertension or hyperlipidemia, one may consider using agents such as losartan or irbesartan that also have a mild uricosuric effect, angiotensin II receptor blockers, which are used for hypertension and diabetic nephropathy, and fenofibrate, a lipid lowering agent which may lower uric acid levels by 8 percent.41-43,45,48
       Although there is increasing experimental data which suggest a relationship between hyperuricemia and the development of hypertension, athlerosclerotic disease and renal dysfunction, there presently is no recommendation for the treatment of asymptomatic hyperuricemia. In the absence of gouty flares or uric acid nephropathy, there is no indication for initiating therapy.43,49 Presently, researchers are investigating new agents to lower uric acid. These agents include the nonpurine xanthine oxidase inhibitor febuxostat. In clinical trials, researchers have shown that this agent decreases uric acid levels.48

How To Detect And Treat Pseudogout
Pseudogout is another crystal disease that is also known as calcium pyrophosphate dihydrate deposition disease. It is commonly associated with aging. Using a polarizing microscope, one would diagnose this condition via synovial fluid analysis, which demonstrates a weak positively birefringent crystal shaped as a rhomboid.
       Radiographs frequently demonstrate intraarticular calcification, which is referred to as chondrocalcinosis. This finding may be asymptomatic. When viewing radiographs, one might also note uniform joint space narrowing, which is common with inflammatory disorders.40 The most frequently involved sites include the fibrocartilage of the knee, the triangular ligament of the wrist, elbow, patellofemoral joint in the knee, symphysis pubis and hyaline cartilage of the hips and shoulders. One will frequently note the involvement of non-weightbearing joints and osteophytes are often absent.
       Clinicians may detect chondrocalcinosis in more the 40 percent of persons over the age of 80 and this condition may also be associated with OA. Other radiographic findings include periarticular calcification at the tendon insertion sites, bursae or joint capsule and involvement of the patellofemoral, radiocarpal and talocalcaneonavicular articulations. Chondrocalcinosis usually affects women and men equally, and can result in a chronic, smoldering arthritis.45
       Pseudogout can also resemble gout by presenting as an acute monoarticular, oligoarticular or polyarticular flare that frequently affects larger joints such as knee, wrist, shoulder or ankle. It may also affect small joints and present as a polyarticular flare resembling rheumatoid arthritis. It may occur as a primary diagnosis or has been associated with secondary causes such as osteoarthritis, gout, hemachromatosis, hypothyroidism, hyperparathyroidism, Wilson’s disease, hypomagnesemia and hypophosphatemia.39 Treatment of the metabolic abnormality often does not affect the course of the disease.45
       Similar to gout, acute attacks are treated with nonsteroidal antiinflammatory drugs, colchicine or corticosteroids. The choice of treatment depends on patient-specific contraindications including a history of peptic ulcer disease, renal and hepatic impairment as well as patient comorbidities and drug-drug interactions. When dosing these medications, one needs to consider altered pharmacokinetic and pharmacodynamic changes occurring with aging.23,39,45

What You Should Know About Other Crystal Diseases
The “Milwaukee Shoulder” is an aggressive form of destructive arthritis that frequently affects the shoulder. It is caused by the deposit of calcium hydroxyapatite crystals in articular cartilage, and one often finds this in conjunction with osteoarthritis.50
       Radiographic features demonstrate joint space loss, subchondral sclerosis, erosions and rotator cuff tears.40 Hydroxyapatite disease usually affects periarticular structures such as tendons and bursae, and are associated with a periarthritis that causes severe pain at sites of deposition.
       Treatment regimens used for apatite disease are similar to those one would use for calcium pyrophosphate dihydrate (CPPD). These treatments include colchicine, NSAIDs and intraarticular or systemic steroids. Both CPPD and hydroxyapatite disease can deposit in the spine within the intervertebral disc. One may also detect CPPD deposits in the ligamentum flava. If these deposits become too large, they may result in symptoms due to inflammation or nerve compression.40

In Conclusion
In addition to recognizing these common disorders and implementing both behavioral and pharmacologic treatment strategies, primary care providers need to remain vigilant to the unique challenges in treating elderly patients so they can help preserve the patients’ independence, reduce pain and enhance their quality of life.

       Dr. Schwab is an Assistant Professor of Clinical Medicine within the Division of Geriatric Medicine at the University of Pennsylvania.

       Editor’s Note: For a related article, see “NSAIDs: Where Do We Go From Here?” in the May/June issue of Arthritis Practitioner or check out the archives at www.arthritispractitioner.com.