Showing posts with label Osteoarthritis. Show all posts
Showing posts with label Osteoarthritis. Show all posts

Friday, September 18, 2009

Summarized Epidemiology

Self-reported prevalence

In the 2001 NHS, about 75 out of 1,000 Australians reported osteoarthritis. This equates to around
1.4 million people. This estimate is based on the NHS question: whether the survey respondent ‘currently has osteoarthritis’.

The NHS survey assumes all reported cases of osteoarthritis to be long term (i.e. conditions that
have lasted at least six months, or that are likely to last six months or more). The prevalence of osteoarthritis increases with age: relatively few people at younger ages report having it. By age 55, however, the prevalence rises sharply (ABS 2002).

Osteoarthritis is reported more frequently by females than males (92 compared with 57 per 1,000 persons in 2001). The difference persists across all ages.
In 2001,
• the prevalence was 331 per 1,000, among females aged 65–74.
• 374 per 1,000 among those aged 75 and over.
• Comparable rates among males that year were 186 and 236 per 1,000, respectively


• Several studies have reported a crossover in osteoarthritis prevalence between the two sexes around the age of 45.
• Males are affected more commonly below age 45, whereas above age 45 females are affected not only more frequently but also more severely .

• In an omnibus survey of the South Australian population, Hill et al. (1999) estimated the prevalence of osteoarthritis among those aged 15 and above to be around 86 per 1,000 persons (51 per 1,000 males and 111 per 1,000 females). The prevalence increased with age, rising above 261 per 1,000 among those aged
70 and above.
• A study in North Sydney estimated the prevalence of osteoarthritis to be around 79 per 1,000 persons

• Symptomatic osteoarthritis was also reported by more than one-quarter of persons aged 60 and above in the Dubbo Osteoporosis Study (Jones et al. 1995).

• The NHS indicates that the prevalence of osteoarthritis has risen from 69 per 1,000 persons in 1995 to 75 per 1,000 persons in 2001.

Thursday, September 17, 2009

Prevalence and Incidence

Prevalence and incidence
The proportion of people in the general population who experience osteoarthritis is a useful measure of its
impact. For an intermittent episodic problem such as osteoarthritis, prevalence needs to be measured across
a defined period of time. Regular national data, based on self-reports, are now available about its prevalence
through the National Health Surveys conducted by the Australian Bureau of Statistics. However, no national data
based on case definition by physical examination or radiological evidence are available.
The incidence of osteoarthritis can be modelled using the prevalence data and other epidemiological parameters
(AIHW: Mathers & Penm 1999). There are no direct sources for this information.
Self-reported prevalence
In the 2001 NHS, about 75 out of 1,000 Australians reported osteoarthritis. This equates to around
1.4 million people. This estimate is based on the NHS question: whether the survey respondent ‘currently has
osteoarthritis’. The NHS survey assumes all reported cases of osteoarthritis to be long term (i.e. conditions that
have lasted at least six months, or that are likely to last six months or more). The prevalence of osteoarthritis
increases with age: relatively few people at younger ages report having it. By age 55, however, the prevalence
rises sharply (ABS 2002).
Osteoarthritis is reported more frequently by females than males (92 compared with 57 per 1,000 persons in
2001). The difference persists across all ages. In 2001, the prevalence was 331 per 1,000, among females
aged 65–74, rising to 374 per 1,000 among those aged 75 and over. Comparable rates among males that year
were 186 and 236 per 1,000, respectively (Figure 3.2).
Several studies have reported a crossover in osteoarthritis prevalence between the two sexes around the
age of 45. Males are affected more commonly below age 45, whereas above age 45 females are affected not
only more frequently but also more severely (Kelsey & Hochberg 1988). No such crossover was noted in the
NHS self-reports.
Other regional/jurisdictional sources confirm the high prevalence of osteoarthritis in Australia.
• In an omnibus survey of the South Australian population, Hill et al. (1999) estimated the prevalence of
osteoarthritis among those aged 15 and above to be around 86 per 1,000 persons (51 per 1,000 males and
111 per 1,000 females). The prevalence increased with age, rising above 261 per 1,000 among those aged
70 and above.
• A study in North Sydney estimated the prevalence of osteoarthritis to be around 79 per 1,000 persons
(March et al. 1998).
• Symptomatic osteoarthritis was also reported by more than one-quarter of persons aged 60 and above in the Dubbo Osteoporosis Study (Jones et al. 1995).
There is no regular time series available on the prevalence of osteoarthritis in Australia. The NHS indicates
that the prevalence of osteoarthritis has risen from 69 per 1,000 persons in 1995 to 75 per 1,000 persons in
2001. The Survey of Disability, Ageing and Carers (SDAC) categorises osteoarthritis together with other forms of
arthritis. No comparative information on that account is therefore available.
Radiological evidence
The radiological evidence suggests much higher prevalence of osteoarthritis than the self-reports. Osteoarthritisrelated
changes were noted on x-ray in more than 50% of persons over the age of 65, and almost universally in
those after age 85 in North Sydney (March 1997).
The radiographic evidence is based on the presence of osteophytes, joint space narrowing, subchondral cysts
and bone remodelling, with the severity of the condition, graded from none (0) through doubtful (1), minimal (2)
and moderate (3) to severe (4). One of the problems with this case definition is that many people with positive
x-ray findings report no pain or disability (Lawrence et al. 1966). Conversely, some individuals report pain but
show no radiological evidence. In addition, primary sources of data on osteoarthritis are based on radiographs of
only a few joints in each person (McDuffie et al. 1987).
Incidence
Direct estimation of the incidence of osteoarthritis is difficult. The Australian Burden of Disease Study, using
DISMOD software to model epidemiological parameters, estimated the incidence of radiological osteoarthritis in
Australia to be 2.9 per 1,000 females and 1.7 per 1,000 males (AIHW: Mathers & Penm 1999). This translates
to some 27,000 new cases annually. The incidence increases with age. It is highest among females between the
ages of 65 and 74 (14 per 1,000) and among males aged 75 and over (9 per 1,000).
To date, no prospective population-based study has been undertaken in Australia to estimate the incidence of
osteoarthritis. More recent longitudinal surveys in the United Kingdom suggest that the incidence may be higher,
with 20–30 per 1,000 females aged 50 to 60 developing new radiological knee, hip and spinal osteoarthritis
each year.
Estimating the prevalence and incidence of osteoarthritis is complicated by a variety of factors. The estimates
may vary depending upon the number of joints studied, the age and sex of the respondents, and the reporting
method used (physical examination, x-ray, self-report). The correspondence between the radiological evidence,
clinical features and self-assessment is also variable.

Tuesday, September 15, 2009

Management and Prevention of Osteoarthritis

MANAGEMENT OF OSTEOARTHRITIS
Non-pharmacological management

Education and behavioural intervention
Education of patients with OA can reduce their pain and improve their quality of life.The aim is to provide patients with an understanding of the disease process, its prognosis and the rationale and implications of managing their condition. Patients can be educated during the consultation with a doctor, through consumer groups or by being provided with written material.

Weight Loss
Obesity is a risk factor for the development of OA, and is associated with radiological progression of the disease, and disability.When people walk, three to six times their body weight is transferred across the knee joint; any excess weight should be multiplied by this factor to estimate the excess force across the knee joint of overweight people.Small studies of overweight patients with knee OA have shown that modest weight loss (< 5 kg) has significant short-term and long-term reduction in symptoms of OA.
In managing OA, weight reduction should be a key goal. Exercise plays a role, but pain and disability can make it difficult for patients to exercise sufficiently to lose weight. Weight loss can be achieved with regular sessions with a dietitian who can provide instruction on reducing caloric intake and the use of food diaries, and cognitive-behavioural modification to change dietary habits.

Exercise
The aim of exercise is to reduce pain and disability by strengthening muscle, improving joint stability, increasing the range of movement and improving aerobic fitness. Other, theoretical benefits include better self-esteem, weight reduction and improved general health.
Systematic reviews of short-term exercise programs show a small to moderate reduction of pain and disability, with similar benefits seen regardless of the type of exercise.Many such programs have involved intensive supervision and sophisticated equipment, with their sustainability over time unknown. A simple, largely unsupervised, home-based exercise program has been shown to reduce knee pain and disability, with its effects sustained over two years.Although hydrotherapy is widely used, no trials have shown any advantage over land-based exercise. Anecdotally, patients enjoy hydrotherapy and it may be a gentle start in encouraging exercise.
Osteoarthritis at different sites requires different approaches. Range-of-motion exercises may exacerbate pain in OA of the hip, and extension exercises can worsen the pain in patellofemoral OA. Thus, an individual exercise program should be formulated with the patient in consultation with a doctor, physiotherapist or qualified fitness instructor.

Mechanical aids
Although there is no evidence available from well-designed trials to support the efficacy of walking sticks in OA, they are widely recommended.Patients should be encouraged to wear shock-absorbing footwear with good mediolateral support, adequate arch support and calcaneal cushion. Short-term studies have shown biomechanical aids are effective in reducing OA-related pain. Lateral heel wedges may reduce pain related to OA of the medial tibiofemoral compartment,and applying adhesive tape to the patella can provide relief in patellofemoral OA.In patients with significant varus deformity, use of a tube-like knee support made of neoprene or an unloader brace both reduced pain over 6 months, with the brace being slightly more effective.Both may be uncomfortable to wear and the brace is expensive. Physiotherapy and occupational therapy assessment are recommended if there is functional limitation secondary to OA.


Pharmacological management

Pharmacological management should be considered an adjunct to non-pharmacological measures. Drug therapy should be individualised after a careful assessment of symptom severity, comorbid conditions, concomitant therapy, side effects, cost of therapy and patient preferences.

Systemic drugs
Paracetamol
It is widely accepted that paracetamol is the oral analgesic of first choice and, if successful, should be taken long term.Although some patients prefer non-steroidal anti-inflammatory drugs (NSAIDs), paracetamol should be used as initial therapy based on relative cost and safety. It should be taken in divided doses, at regular intervals, with the total daily dose not exceeding 4 g. Although it is one of the safest analgesics, paracetamol can be associated with clinically important adverse events. Paracetamol may prolong the half-life of warfarin, so patients taking warfarin must have their INR (international normalised ratio) monitored closely and their warfarin dose adjusted if necessary.Paracetamol should be used with caution in patients who have liver disease and those with a history of excessive alcohol consumption.

NSAIDs and cyclo-oxygenase-2-specific inhibitors
NSAIDs should be considered only for patients who do not obtain adequate pain relief with paracetamol. Clinicians now have a choice between conventional NSAIDs and cyclo-oxygenase-2-specific (COX-2) inhibitors. COX-2 inhibitors have similar analgesic effects to those of non-selective NSAIDs, with a gastrointestinal (GI) side-effect profile and incidence of endoscopic ulceration similar to placebo.Both NSAIDs and COX-2 inhibitors may cause acute deterioration in renal function, fluid retention and hypertension. The newer COX-2 inhibitors are considerably more expensive than NSAIDs, and uncertainty remains about potential increased risk of cardiovascular events. Cardiovascular risk factors should be considered and patients should be counselled before prescribing rofecoxib (Box 4).

The choice between NSAIDs and COX-2 inhibitors should be made after carefully assessing the risk of serious upper-GI complications and discussing with patients the risk of serious thrombotic cardiovascular events. Patients with no risk factors should use conventional NSAIDs, commencing at a low dose, with dose titration against effect. NSAIDs should be used on an as-required basis, although this often means continuous use. All NSAIDs have similar efficacy, so those with the lowest risk profile for upper-GI haemorrhage (ibuprofen and diclofenac) are recommended. COX-2 inhibitors are recommended for patients with any GI risk factors.Rofecoxib should be avoided in patients with known risk factors for cardiovascular disease. All patients prescribed NSAIDs and COX-2 inhibitors should be counselled about the symptoms of upper-GI haemorrhage and monitored for new or severe upper-GI symptoms. NSAIDs should never be used in combination, except with low-dose aspirin for cardioprotection.
For patients with any risk factors for deterioration in renal function, NSAIDs and COX-2 inhibitors should only be prescribed after very careful consideration of all other options. Plasma sodium, potassium and creatinine levels, blood pressure and the presence of oedema should be checked at baseline and regular intervals.

Glucosamine and chondroitin
Glucosamine sulfate (GS) and chondroitin sulfate (CS) are derivatives of glycosaminoglycans found in articular cartilage, and are available without prescription from pharmacies and supermarkets.Oral GS is able to reduce pain from
20%-25% in patients with mild to moderate primary knee OA.GS is contraindicated in seafood allergy, but is otherwise well tolerated and causes no major side effects. GS should be used at a dose of 1500 mg per day as a divided dose for at least 3 months to determine whether it is therapeutic in any given patient. Topical application of GS and CS may be effective in reducing pain from knee OA.

Opioids
The combination of codeine and paracetamol provides better analgesia than paracetamol alone. However, nausea, vomiting, dizziness and constipation lead to discontinuation of this combination in up to a third of patients.Some patients with intractable pain, who are unsuitable for arthroplasty, may require stronger opiate analgesia. Tramadol is a centrally acting synthetic opioid which inhibits the reuptake of serotonin and noradrenaline. It is generally well tolerated, but is contraindicated in seizure disorders, as it lowers the seizure threshold, and in combination with selective serotonin reuptake inhibitors because of the risk of serotoninergic syndrome.


Topical analgesia
Topical treatment is appropriate for patients as an adjunct to simple analgesia, monotherapy for a single symptomatic joint, or for patients who cannot tolerate systemic therapy. Topical capsaicin has a modest analgesic effect.A local burning sensation is common, but decreases with continued use. Patients must avoid inadvertently transferring the capsaicin to eyes or mucous membranes.

For optimal results, management of OA requires multiple therapies and an individualised approach. Patients need to be involved in formulating and executing the management plan. As the disease progresses, or as comorbid conditions develop, management may need to be revised. The doctor’s role is to coordinate non-pharmacological approaches, supervise pharmacological management with the aim of minimising toxicity, and empower patients to manage their chronic condition.


PREVENTION OF OSTEOARTHRITIS
Weight control. Maintaining a healthy weight may be the single most important thing you can do to prevent osteoarthritis.Being overweight puts extra strain on the joints, particularly the large weight-bearing joints such as the knees, the hips, and the balls of the feet. It is estimated that every 1lb of body weight means at least 3lb of stress at the knee joint, and even more at the hip joint. That would mean that losing just 5lb would take at least 15lb of stress off your knees. Extra weight may also alter the normal structure of the joint and increase the risk for osteoarthritis. Maintain a healthy weight to prevent or reduce joint damage and lower the stress on osteoarthritic joints.

Injury prevention. Protect your joints from serious injury or repeated minor injuries to decrease your risk of damaging cartilage. Repeated minor injuries include those from job-related activities such as frequent or constant kneeling, squatting, or other postures that place stress on the knee joint.

Exercise. Exercise can help reduce joint pain and stiffness. Light- to moderate-intensity physical activity may prevent a decline in, and may even restore, health and function.But some people with osteoarthritis may be reluctant to exercise because of joint pain after activity. You can take various steps to help relieve pain, such as heat and cold therapy or taking pain relievers, which may make it easier for you to exercise and stay active. Choose partial– or non–weight-bearing exercise, such as bicycling, swimming, or water exercise. You can also try light weight-lifting exercises, with supervision.

Research shows that even modest weight loss combined with exercise is more effective in decreasing pain and restoring function than either weight loss or exercise alone.

Young adults who have significant knee injuries have an increased risk of future osteoarthritis. Prevention of joint injuries during youth depends in good part on the use of proper sports equipment and on playing under safe playing conditions. A young person who has a serious knee injury can limit further damage by using a brace to stabilize the knee joint and by changing the way he or she does high-impact exercise.

Heat and cold therapy for osteoarthritis
For moderate to severe pain from osteoarthritis, try applying heat and cold to the affected joints as appropriate. Experiment with these heat and cold techniques until you find what helps you most.
-Apply heat 2 or 3 times a day for 20 to 30 minutes, using a heating pad, hot shower, or hot pack. Heat seems to be effective for pain and stiffness related to inactivity of a joint.
-Try putting cold packs on a painful joint for 10 to 20 minutes. Do not apply a cold pack directly to bare skin. Put a thin towel or pillowcase between the ice and your skin.
-Try ice massage. A small study showed that ice massage for 20 minutes, 5 days per week, improved range of motion and function, although its effect on pain was less clear.
-Try alternating between heat and cold.
-After a heat or cold treatment, try some gentle massage for relaxation and pain relief.
-Paraffin wax is a form of moist heat that may help if you have pain and stiffness in your hands or feet. It is especially useful before exercise. Your physical therapist can teach you to use paraffin at home.

Sunday, September 13, 2009

Pathological Basis Of Osteoarthritis

From Robbins & Cotran,

Osteoarthritis

††† Degenerative joint disease.
††† Most common type of joint disease.
††† One of the most disabling conditions in developed nations.
††† Secondary only to cardiovascular disease in causing long-term disability.
††† Characterized by progressive erosion of articular cartilage.
††† Considered to be an intrinsic disease of articular cartilage in which biochemical & metabolic alterations result in its breakdown, irregardless of presence of inflammatory cells.

Classification
††† Primary osteoarthritis appears to be idiopathic as an aging phenomenon.
††† Usually oligoarticular but may be generalized.

††† Secondary osteoarthritis appears in younger individuals with some predisposing conditions - e.g. previous macrotraumatic/repeated microtraumatic injuries to a joint, a congenital development deformity of a joint(s), some underlying systemic disease (diabetes, ochronosis, hemochromatosis, marked obesity) etc.
††† Often involves one or several predisposed joints.

††† Gender has some influence on distribution.
††† The knees & hands are more commonly affected in women.
††† The hips are more commonly affected in men.

Pathogenesis
††† Normal articular cartilage is located at the ends of the bones - bathed in synovial fluid, in ensures virtually friction-free movements within the joint; in weight-bearing joints, it spreads the load across the joint surface in a manner that allows the underlying bones to absorb shock & weight without being crushed.
††† These functions require the cartilage to be elastic & possess high tensile strength - these attributes are provided by type-II collagen & proteoglycans, both secreted by chondrocytes as major components of the cartilage.
††† In adult bones, turnover of cartilage is maintained by chondrocytes (both synthesis & degradation) - in osteoarthritis this process is disturbed.

††† Aging & mechanical effects is a most important influence.
††† Evidence includes increasing frequency of osteoarthritis with advancing age; its occurence with weight-bearing joints; & an increase in the frequency of the disease in conditions that predispose the joints to abnormal mechanical stress - e.g. obesity & previous joint deformity.

††† Genetic factors also play a role, especially in cases involving the hands & hips.
††† Specific genes have not yet been identified, but there are suggestions linking to chromosomes 2 & 11.
††† The risk of osteoarthritis is increased in direct proportion to bone density & associated with high levels of estrogens.

††† Osteoarthritis is characterized by significant changes in both the composition & mechanical properties of cartilage.
††† Early in the course of the disease, the degenerating cartilage contains increased water & decreased concentration of proteoglycans.
††† There appears to be a weakening of the collagen network, presumably caused by decreased local synthesis of type-II collagen, & increasing breakdown of preexisting collagen.
††† The levels of certain molecular messengers (e.g. IL-1, TNF & NO) are increased & appear to be responsible for some of the changes in the composition of the cartillage.
††† Apoptosis is increased, likely responsible for the decreasing number of chondrocytes.
††† Cumulatively, these changes tend to reduce the tensile strength & the resilience of the articular cartilage.

††† In response to the regressive changes, chondrocytes in the deeper layers proliferate & attempt to repair the damage by producing new collagen & proteoglycans.
††† While initially effective, molecular signals causing chondrocyte loss & changes in the extracellular matrix eventually predominate - the reasons for this phenomenon remain unclear.

Morphology
††† In early stages, the chondrocytes proliferate, accompanied by biochemical changes as water content of the matrix increases & concentration of proteoglycans decreases.
††† Degradation of the superficial cartilage layers causes vertical & horizontal fibrillation & cracking of the matrix.
††† Gross examination at this stage reveals a granular articular surface that is abnormally soft.

††† Eventually, full-thickness portions of the cartilage are sloughed, & the exposed subchondral bone plate becomes the new articular surface.
††† Friction smoothes & burnishes the exposed bone, giving it the appearance of polish ivory (bone eburnation).
††† Rebuttressing & scelrosis of the underlying cancellous bones follow.
††† Small fractures through the articulating bone are common, & the dislodged pieces of cartilage & subchondral bone tumble into the joint & form loose bodies (joint mice).
††† Synovial fluid is forced into the fracture gaps, & this loculated fluid collection increases in size, forming fibrous walled cysts.
††† Mushroom-shaped osteophytes (bony outgrowths) develop at the margins of the articular surface & are capped by fibrocartilage & hyaline cartilage that gradually ossify.
††† The synovium shows minor alterations, but is congested & fibrotic with scattered inflammatory cells.

Clinical Course
††† Osteoarthritis is an insidious disease - primary osteoarhritis is usually asymptomatic until patients are in their fifties.
††† If a young patient develops osteoarthritis, a search for underlying causes should be made.
††† Characteristic symptoms include: deep, achy pain that worsens with use; morning stiffness; crepitus; & limitation of range of movement.
††† Impingement on spinal foramina by osteophytes results in cervical & lumbar nerve root compression with radicular pain, muscle spasms, muscle atrophy, & neurological deficits.

††† Typically, only one or few joints are affected.
††† Joints commonly involved include the hips, knees, lower lumbar & cervical vertebrae, proximal & distal interphalangeal joints of the fingers, first carpometacarpal joints, & first tarsometatarsal joints of the feet.
††† Characteristic in women, but not in men, are Heberden nodes in the fingers, representing prominent osteophytes at the distal interphalangeal joints.
††† The wrists, elbows & shoulders are usually spared.