Osteoarthritis

Pathophysiology

Presentation

Epidemiologic concepts

Pharmacotherapeutics

Information technologies

Medical resources

Medical History Questions?

Disease Management

Physical Examination

Testing

Psychosocial

Lifestyle Changes

Health Promotion

Patients should be encouraged to participate in self-management of their OA. Providers can empower them to manage their weight, exercise, and have a positive outlook on their disease.

Cultural

Treatment Plan

When to Refer?

Symptoms

Preventing complications

Question: What are the hallmark signs of osteoarthritis?

Community Resources

Genetic factors

  • Rare mutations in collagen types II, IX, or XI can cause premature OA
  • Mutations in GDF-5 are thought to predispose to OA due to altered joint shape
  • Multiple genes are needed for a more substantial OA risk
    (Loeser, 2021)

Risk Factors

  • Joint abnormalities
  • Obesity
  • Female Sex
  • Age
  • Joint injury

Weight loss

Pain (3 stages) All include use related pain and improvement with rest

Stage 3: Constant dull/aching pain with episodes of severe pain. Results in severe limitations of function

Stage 2: Pain becomes more constant and starts to affect daily activities. May be unpredictable episodes of stiffness

Stage 1: Predictable sharp pain - only modest effect on function

  • Boney swelling
  • Joint deformity
  • Limitation of active & passive movement
  • Instability (knee)

Seen most commonly in knees, hips, finger interphalangeal joints, first CMC joints, first MTP joints, and apophyseal (facet) joints of the lower cervical and lower lumbar spine
(Doeherty & Abhishek, 2023)

Radiography allows for detection of characteristic features of OA, include marginal osteophytes, localized joint space narrowing, subchondral sclerosis, and cysts.

Ultrasonography can identify OA-associated structural changes and is useful for detecting features such as synovial inflammation, effusion and osteophytosis.

Synovial fluid from OA joints is usually noninflammatory, predominately mononuclear cells.

Differential diagnosis to consider: Rheumatoid arthritis, psoriatic arthritis, crystalline arthritis, hemochromatosis, infectious arthritis, soft tissue abnormalities.

Clinical Diagnosis: 1) Persistent usage-related joint pain in one or few joints, 2) Age >45 y.o. 3) morning stiffness greater than 30 min.

Joint pain and functional impairment are hallmark signs.

Loss of at least 10% body weight has been associated with a 50% reduction in pain scores in patients who are overweight with knee OA after 18 months.

Oral and Topical NSAIDs

Topical capsaicin

Duloxetine

Lowest dose required to control symptoms on an as needed basis.

For patients with OA in multiple joints and concomitant comorbidities that may contradict oral NSAIDs

One or few joints are involved and other interventions are ineffective or contraindicated.

Intraarticular glucocorticoids

Not a routine injection d/t short duration of effects and evidence it may have deleterious effect on the hyaline cartilage and may accelerate OA progression.

Acetaminophen is no longer considered the first line analgesic for the treatment of knee and hip OA by clinical guidelines.

Surgical treatment is dominated by total joint replacement, which is highly effective in patients with advanced knee and hip OA when conservative therapies have failed to provide adequate pain relief.

Excess mortality due to all causes has been observed in patients with knee and hip OA.

Patients with walking disability, impaired physical function, and associated comorbid conditions such as diabetes and other CV risk factors are at a higher risk of mortality

OA is the most common forms of arthritis, representing 62% of all arthritic conditions in 2017-2018.

Substantial morbidity associated with OA, including disability and reduced quality of life.

Incidence of OA increases with age and is higher in females compares with males

Globally, 595 million people are affected by OA.

The knee is the most commonly reported site of OA, with 368 million prevalent cases in 2020. Hip OA is less common than knee or hand OA.

Knee OA in the US is similar to that of Europe, with lower rates reported in southern Asia.

Non-pharmacological

Aerobic and strengthening exercises
such as water aerobics

Walking aids and knee braces for joint malalignment. Foot orthoses.

Goals are to minimize pain, optimize function, and modify joint damage process. Treatment plans are individualized based on patient need and severity of OA.

Caution with pharmacologic therapy needs to occur. Patients are taking NSAIDS and Tylenol regularly.

Studies have shown that cognitive behavioral therapy can be beneficial in patients struggling with chronic pain related to OA.

Weight loss tools/programs

CBT referrals if needed for pain management or processing their disability/disease.

Exercise programs, chair exercises, ROM examples. Many offices have these as pamphlets to give to patients,

All cultures express pain differently. It is important to take this into consideration when we evaluate pt's for OA.

Providers need to understand the impact that disability and/or surgery will have on patients based on their culture.

The understanding and acceptance of their OA can have an affect on the support the patient receives from their family/friends.

Obesity and an unhealthy diet is more prevalent in certain countries (the U.S.), and this can create difficulties in patients losing weight or incorporating exercise.

YMCA offers mobility friendly exercise classes

Many gyms/pools offer water aerobics

The Arthritis Foundation

The city of Rochester, MI has a gym called the Older Persons Commission. Many mobility friends exercise classes are available. They also have social groups for people to get involved in which can help the psychosocial aspect of OA.

  • When did the pain in your joints begin?
  • Have you ever broken a bone?
  • Do you have a family history of joint disease?
  • What makes the pain worse?
  • What makes the pain better?
  • What time of day is the pain the worst?

Inflammatory mediators may play a role in the pathogenesis of OA as potential drivers of joint tissue destruction

The destruction of joint tissues in OA is mediated by a variety of proteases including several MMPs, cysteine proteinases and serine proteinases.

Treatments for OA targets pain, none have been proven to alter the structural progression of the disease.