Osteoarthritis overview

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Overview

Historical Perspective

Classification

Pathophysiology

Causes

Differentiating Osteoarthritis from other Diseases

Epidemiology and Demographics

Risk Factors

Screening

Natural History, Complications and Prognosis

Diagnosis

Diagnostic Criteria

History and Symptoms

Physical Examination

Laboratory Findings

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CT

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Other Imaging Findings

Other Diagnostic Studies

Treatment

Medical Therapy

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

Overview

Osteoarthritis / Osteoarthrosis (OA, also known as degenerative joint disease, degenerative arthritis, arthrosis or in more colloquial terms "wear and tear") is the most common form of arthritis, caused by wearing of the cartilage that covers and cushions joint spaces. As the cartilage wears away, the patient experiences pain with weight bearing, including walking and standing. Due to the movement limitations caused by pain, there might be a regional muscles atrophy, also ligaments may become more lax. This word is derived from the Greek word "osteo", meaning "of the bone", "arthro", meaning "joint", and "itis", meaning inflammation, although inflammation is not a common finding in this regard. OA possesses a great degree of variability in disease onset, progression, and severity.

OA affects nearly 43 million patients in United States and almost 15% of the world population, 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 is responsible to bone to bone connection) 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.

Osteoarthritis is capable of influencing any joint in human body; meanwhile, the most common affected joints are: knee and hip given the degree of weight bearing required of these joints. Other joints, such as the distal interphalangeal joints of the fingers and shoulder joints are also commonly affected as well.

Historical Perspective

The earliest descriptions of OA were provided by Heberden and Haygarth in the 19th century. [1] [2] In the 1930s and 1940s, Dr. Stecher showed that there were two forms of OA, idiopathic and post-traumatic. [3] Surgical management of OA was developed in the 1960s by Drs. Charnley and McKee. [4] [5]

Classification

Osteoarthritis is radiographically classified depending on what joint is affected.

Knee

Kellgren-Lawrence Grade

Grade Description
0 No radiographic features of osteoarthritis, normal joint space
1 Subtle joint space narrowing and osteophyte formation (bone spurs)
2 Definite osteophyte formation with subtle joint space narrowing
3 Multiple osteophytes, definite joint space narrowing, subcondronal sclerosis and possible bony deformity
4 Large osteophytes, marked joint space narrowing, severe subcondronal sclerosis and definite bony deformity

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. Heberden W. Commentaries on the history and causes of disease. London: Payne; 1802.
  2. Haygarth J. A clinical history of diseases. II. Nodosity of the joints. London: Gadell and Davies; 1805.
  3. Stecher RM. Heberden’s nodes: heredity in hypertrophic arthritis of the finger joints. Am J Med Sci 1941:201;801–809.
  4. Charnley J. Arthroplasty of the hip: a new operation. Lancet 1961;1:1129–1132.
  5. 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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