January 10, 2011

Arthritis - Osteoarthritis, Systemic lupus erythematosus (SLE or lupus)


Osteoarthritis is a disease characterized by degeneration of cartilage and its underlying bone within a joint as well as bony overgrowth. The breakdown of these tissues eventually leads to pain and joint stiffness. The joints most commonly affected are the knees, hips, and those in the hands and spine. The specific causes of osteoarthritis are unknown, but are believed to be a result of both mechanical and molecular events in the affected joint. Disease onset is gradual and usually begins after the age of 40. There is currently no cure for OA. Treatment for OA focuses on relieving symptoms and improving function, and can include a combination of patient education, physical therapy, weight control, and use of medications.


  • Also known as degenerative joint disease.
  • Most common form of arthritis.
  • Classified as: Idiopathic (localized or generalized) or Secondary (traumatic, congenital, metabolic/endocrine/neuropathic and other medical causes).
  • Characterized by focal and progressive loss of the hyaline cartilage of joints, underlying bony changes.
  • Usually defined by symptoms, pathology or combination (1)
    • Pathology = radiographic changes (joint space narrowing, osteophytes and bony sclerosis)
    • Symptoms = pain, swelling, stiffness

Rheumatoid Arthritis

Rheumatoid arthritis is a systemic inflammatory disease which manifests itself in multiple joints of the body. The inflammatory process primarily affects the lining of the joints (synovial membrane), but can also affect other organs. The inflamed synovium leads to erosions of the cartilage and bone and sometimes joint deformity. Pain, swelling, and redness are common joint manifestations. Although the definitive causes are unknown, RA is believed to be the result of a faulty immune response. RA can begin at any age and is associated with fatigue and prolonged stiffness after rest. There is no cure for RA, but new drugs are increasingly available to treat the disease. In addition to medications and surgery, good self-management, including exercise, are known to reduce pain and disability.


  • Rheumatoid arthritis (RA), an autoimmune condition, is a chronic inflammatory polyarthritis. (1)
  • Natural history studies of RA suggests that RA follows one of three courses
    • Monocyclic in 20% of people initially diagnosed with RA (i.e., had one episode which abated within two years of initial presentation and did not reoccur).
    • Polycyclic in 70% (i.e., fluctuating levels of disease activity).
    • Progressive and unremitting condition in 10%. (3)
Another natural history study found that 75% of people with RA experienced remission after five years. (4)
  • Historically, pharmacologic treatment of RA has traditionally followed the pyramid approach. That is, treatment starts with corticosteroids/non-steroidal anti-inflammatory drugs, then progresses to disease-modifying antirheumatic drugs (DMARD) and finally to biologic response modifiers (BRM) if persons are non-responsive to the previous drugs. Today, a more aggressive treatment approach is being advocated for people with early RA, with prescription of DMARDs within three months of diagnosis. (1)
  • Diagnosis
    • The 1987 American College of RheumatologyExternal Web Site Icon criteria are used in the clinical diagnosis of RA, and to define RA in epidemiologic studies. Persons must meet four of seven ACR criteria; (5) these criteria are based on clinical observation (e.g., number of joints affected), laboratory tests (e.g., positive rheumatoid factor), and radiographic examination (e.g., X-rays evidence of joint erosion). (5)
    • Early RA is typically defined as RA that is diagnosed within 6 months of symptom onset. There is extensive interest in early diagnosis of RA because early treatment may improve disease prognosis. The only U.S. study to examine time between symptom onset and diagnosis reported a median lag time of approximately 4 weeks between symptom onset and medical encounter, and a median time of 18 weeks between medical encounter and RA diagnosis (A total median lag time of 36 weeks)6. These authors noted that there was even a delay in diagnosing patients with most identifiable features of RA (e.g., morning stiffness and seropositive rheumatoid factor), and concluded that early disease recognition is challenging as only half of those who eventually develop RA initially present with features specific to the condition.
  • Risk factors
    • A range of environmental and genetic variables have been evaluated as potential risk factors for RA (e.g. hormonal exposures, tobacco use, dietary components, HLA genotype, and microbial exposures), but to date no definitive risk factors for RA have been identified.
    • Of the environmental factors examined, the most consistent evidence exists for an association between tobacco use and RA; most studies of this risk factor have found a history of smoking is associated with RA onset with increased risks ranging from 1.3 to 2.4. (2)
    • The role of the following four estrogenic factors in RA etiology has been studied extensively:
      • Oral contraceptives (OC) — Early studies found a decreased risk of RA among women who had ever used OCs, a relationship that has not been confirmed in recent studies. (19–21)
      • Hormone replacement therapy (HRT) — There is mixed evidence of an association between HRT and RA onset. (20–25)
      • Live birth history — Most studies have found that women who have never had a live birth have a slight to moderately increased risk of RA. (21,24,26,27)
      • Breastfeeding — The most recent studies have found that RA is less common among women who breastfeed; this is in contrast with earlier studies which found an increased risk associated with breastfeeding. (21,28–30)
    • Genetic susceptibility markers. Most attention has been given to the DR4 and DRB1 molecules of the major histocompatability complex HLA class II genes. The strongest associations have been found between RA and the DRB10401 and DRB10404 alleles. (2)

Systemic lupus erythematosus (SLE or lupus)

Systemic Lupus Erythematosus is an autoimmune disease in which the immune system produces antibodies to cells within the body leading to widespread inflammation and tissue damage. The causes of SLE are unknown but are believed to be linked to genetic, environmental, and hormonal factors. SLE may be characterized by periods of illness and remissions. SLE has a variety of clinical manifestations and can affect joints, skin, brain, lungs, kidneys, and blood vessels. People with SLE may experience fatigue, pain or swelling in joints, skin rashes, and fevers. A team approach in treating lupus is often warranted due to the number of organ systems involved.


  • This report is on systemic lupus erythematosus (for shorthand, SLE or lupus), and not on 2 other types of lupus: discoid lupus (skin only), and drug-induced lupus (temporary). (1,2)
  • Lupus is a prototype autoimmune disease with a wide array of clinical manifestations (rash, photosensitivity, oral ulcers, arthritis, pleuritis, pericarditis, kidney problems, seizures and psychosis, blood cell abnormalities). It is characterized by the production of antibodies to components of the cell nucleus. (1,2)
  • Primarily a disease of young women. (1,2)
  • Occurs from infancy to old age, with peak occurrence between ages 15 and 40. (1,2)
  • Females are affected far more than males (6-10:1). (1,2)
  • Blacks (and possibly Hispanics, Asians, and Native Americans) are affected more than whites. (1,2)
  • Although there is a strong familial aggregation, the disease is relatively uncommon and most cases are sporadic. (1,2)
  • May occur with other autoimmune conditions (e.g., thyroiditis, hemolytic anemia, idiopathic thrombocytopenia purpura). (1,2)
  • Diagnosis can be very difficult. The gold standard is a rheumatologist’s diagnosis. The American College of Rheumatology (ACR)External Web Site Icon uses a standard classification scheme requiring 4 of 11 criteria for research definition, although this is recognized to miss early and mild cases. Even so, there is
    • Underdiagnosis because the presenting symptoms and signs are often not specific. (1,2)
    • Overdiagnosis because doctors mistakenly use a positive blood test (present in 5% of the healthy population) by itself to make a diagnosis. (1,2)
  • Accelerated atherosclerosis among these patients is a newly recognized phenomenon responsible for premature mortality. (1,2)
  • Treatment consists primarily of immunosuppressive drugs (e.g., hydroxychloroquine [Plaquenil] and corticosteroids [prednisone]). (1,2)
  • Morbidity and mortality may be related to late diagnosis, problems in access to care, less effective treatments, and poor compliance with therapeutic regimens. (1,2)
Source: Centers for Disease Control and Prevention