Osteoarthritis overview: Difference between revisions

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==Historical Perspective==
==Historical Perspective==


The earliest descriptions of OA were provided by Heberden and Haygarth in the 19th century.
The earliest descriptions of OA were provided by Heberden and Haygarth in the 19th century. <ref> Heberden W. Commentaries on the history and causes of disease. London: Payne; 1802.</ref> <ref> Haygarth J. A clinical history of diseases. II. Nodosity of the joints. London: Gadell and Davies; 1805. </ref> In the 1930s and 1940s, Dr. Stecher showed that there were two forms of OA, idiopathic and post-traumatic. <ref> Stecher RM. Heberden’s nodes: heredity in hypertrophic arthritis of the finger joints. Am J Med Sci 1941:201;801–809. </ref> Surgical management of OA was developed in the 1960s by Drs. Charnley and McKee. <ref> Charnley J. Arthroplasty of the hip: a new operation. Lancet 1961;1:1129–1132. </ref> <ref> McKee GK,Watson-Farrar J. Replacement of arthritic hips by the McKee-Farrar prosthesis. J Bone Joint Surg Br 1966;48(2):245–259. </ref>


==Classification==
==Classification==

Revision as of 03:46, 3 January 2017

Osteoarthritis Microchapters

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]

Overview

Osteoarthritis / Osteoarthrosis (OA, also known as degenerative arthritis, degenerative joint disease, arthrosis or in more colloquial terms "wear and tear"), is a condition in which low-grade inflammation results in pain in the joints, caused by wearing of the cartilage that covers and acts as a cushion inside joints. As the bone surfaces become less well protected by cartilage, the patient experiences pain upon weight bearing, including walking and standing. Due to decreased movement because of the pain, regional muscles may atrophy, and ligaments may become more lax. OA is the most common form of arthritis. The word is derived from the Greek word "osteo", meaning "of the bone", "arthro", meaning "joint", and "itis", meaning inflammation, although many sufferers have little or no inflammation.

OA affects nearly 21 million people in the United States, accounting for 25% of visits to primary care physicians, and half of all NSAID (Non-Steroidal Anti-Inflammatory Drugs) prescriptions. It is estimated that 80% of the population will have radiographic evidence of OA by age 65, although only 60% of those will be symptomatic.[1] Treatment is with NSAIDs, local injections of glucocorticoid or hyaluronan, and in severe cases, with joint replacement surgery. Many physicians have also reported good pain relief by treating ligaments (which connect bone to bone) with Prolotherapy. There has been no cure for OA, as cartilage has not been induced to regenerate. However, if OA is caused by cartilage damage (for example as a result of an injury) Autologous Chondrocyte Implantation may be a possible treatment. Clinical trials employing tissue-engineering methods have demonstrated regeneration of cartilage in damaged knees, including those that had progressed to osteoarthritis.[2] Further, in January 2007, Johns Hopkins University was offering to license a technology of this kind, listing several clinical competitors in its market analysis.

Historical Perspective

The earliest descriptions of OA were provided by Heberden and Haygarth in the 19th century. [3] [4] In the 1930s and 1940s, Dr. Stecher showed that there were two forms of OA, idiopathic and post-traumatic. [5] Surgical management of OA was developed in the 1960s by Drs. Charnley and McKee. [6] [7]

Classification

Pathophysiology

Causes

Differentiating Osteoarthritis overview from Other Diseases

Epidemiology and Demographics

Risk Factors

Screening

Routine screening for osteoarthritis is not indicated unless the patient is symptomatic.

Natural History, Complications, and Prognosis

Natural History

Complications

Prognosis

Diagnosis

Diagnostic Criteria

History and Symptoms

Physical Examination

Laboratory Findings

Imaging Findings

Other Diagnostic Studies

Treatment

Medical Therapy

Surgery

Prevention

References

  1. Green GA. Understanding NSAIDS: from aspirin to COX-2. Clin Cornerstone 2001; 3:50-59. PMID 11464731.
  2. Hollander AP, Dickinson SC, Sims TJ; et al. (2006). "Maturation of tissue engineered cartilage implanted in injured and osteoarthritic human knees". Tissue Eng. 12 (7): 1787–98. doi:10.1089/ten.2006.12.1787. PMID 16889509.
  3. Heberden W. Commentaries on the history and causes of disease. London: Payne; 1802.
  4. Haygarth J. A clinical history of diseases. II. Nodosity of the joints. London: Gadell and Davies; 1805.
  5. Stecher RM. Heberden’s nodes: heredity in hypertrophic arthritis of the finger joints. Am J Med Sci 1941:201;801–809.
  6. Charnley J. Arthroplasty of the hip: a new operation. Lancet 1961;1:1129–1132.
  7. McKee GK,Watson-Farrar J. Replacement of arthritic hips by the McKee-Farrar prosthesis. J Bone Joint Surg Br 1966;48(2):245–259.

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