eMedicine Specialties > Orthopedic Surgery > Trauma

Osteoarthritis

Author: Furqan H Siddiqui, MD, Director, Research Integrity Office, University of Louisville Hospital
Coauthor(s): James Monroe Laborde, MD, MS, Clinical Assistant Professor, Department of Orthopedics, Tulane Medical School; Adjunct Assistant Professor, Department of Biomedical Engineering, Tulane University; Adjunct Assistant Professor, Department of Physical Medicine and Rehabilitation, Louisiana State University Medical School; Consulting Staff, Department of Orthopedic Surgery, Louisiana State University Health Sciences Center
Contributor Information and Disclosures

Updated: Apr 23, 2009

Introduction

Osteoarthritis (OA) is the most common joint disease and a major cause of morbidity and disability.

Arthroscopic view of a torn meniscus before (top)...

Arthroscopic view of a torn meniscus before (top) and after (bottom) removal of loose meniscal fragments.

Arthroscopic view of a torn meniscus before (top)...

Arthroscopic view of a torn meniscus before (top) and after (bottom) removal of loose meniscal fragments.


Arthroscopic view of the removal of cartilaginous...

Arthroscopic view of the removal of cartilaginous loose body.

Arthroscopic view of the removal of cartilaginous...

Arthroscopic view of the removal of cartilaginous loose body.


Osteoarthritis is commonly seen in the elderly population; however, its appearance at an early age is possible. Thus, the disease can no longer be considered a simple consequence of aging and cartilage degeneration. Unfortunately, in young patients, arthritis is often confused with traumatic arthritis, which occurs after an injury to a joint, whether by a macroincident or by repeated microincidents.1,2,3,4

For excellent patient education resources, visit eMedicine's Arthritis Center. Also, see eMedicine's patient education article Osteoarthritis.

Problem

Complications due to immobility, deconditioning, medication, and joint-related surgery can be fatal. OA is a major cause of disability in the United States, with approximately 68 million workdays lost and 4 million hospital admissions per year.

Frequency

Osteoarthritis (OA) is the most common form of progressive joint disease worldwide, affecting 16 million (6%) American adults.5

Racial differences exist for both the prevalence and the pattern of joint involvement. Compared with whites, South African blacks and persons of Chinese, East Indian, or Native American descent have a lower prevalence of hip OA.

Females have a higher prevalence of OA of the knees and hands, whereas males have a higher prevalence of OA of the hips. For knee OA, the female-to-male incidence ratio is 1.7:1.

Age is the strongest determinant of OA; the prevalence of OA at all joint sites progressively increases with age. Estimates of the true prevalence of OA are imprecise because of the difficulties associated with the diagnosis. Estimates based on the radiographic evidence of knee OA are as follows: OA affects 25-30% of persons aged 45-64 years, 60% of persons older than 65 years, and more than 80% of persons older than 75 years.5

Etiology

The daily stresses applied to the joints, especially the weight-bearing joints (eg, ankle, knee, hip), play an important role in causing osteoarthritis (OA). The hereditary component has long been recognized, particularly with generalized OA; a gene for OA has been identified and plays an important role. Potential risk factors include age, obesity, trauma, genetics, sex hormones, muscle weakness,6 and environment.7,8

Old joints and osteoarthritic joints differ. With advancing age, cartilage volume, proteoglycan content, cartilage vascularization, and cartilage perfusion are reduced and may result in certain characteristic radiologic features that include joint-space narrowing and marginal osteophytes. However, biochemical and pathophysiologic findings support the notion that age alone is an insufficient cause of OA.

Obesity increases the mechanical stress in a weight-bearing joint. It has been strongly linked to OA of the knees and, to a lesser extent, of the hips.

Traumatic insults to the articular cartilage, ligaments, or menisci lead to abnormal biomechanics in the joints and enhance their premature degeneration.

Menopause often increases the progression of OA; however, estrogen replacement therapy lowers the expected rate of radiographic and clinical findings in the knees and hips.

Muscle dysfunction compromises the body's neuromuscular protective mechanisms, leading to increased joint motion, resulting in OA. This effect underscores the need for continued muscle toning exercises in all individuals to prevent muscle dysfunction.

One should not confuse environmental factors as causes of OA, because these factors actually cause traumatic arthritis on a macrotraumatic or microtraumatic basis. This is especially true of individuals whose lifestyles require squatting, climbing stairs, or excessive kneeling.

Pathophysiology

The pathology of osteoarthritis (OA) is the result of both the combined effect of tissue damage and an immune reaction to that damage. Changes resulting from repetitive microtrauma are usually seen in the load-bearing areas of the articular cartilage. OA usually begins with the swelling of the cartilage due to the increased synthesis of proteoglycans, which reflect an effort by the chondrocytes to repair the damage sustained. This stage may last for years or decades, and it is characterized by hypertrophic repair of the articular cartilage.

As the disease progresses, the thickness of the joint surface is reduced. However, the level of proteoglycans is remarkably diminished, causing a loss of elasticity in the cartilage, which leads to its softening. As a result, loss of joint surface integrity occurs, and cartilaginous vertical clefts develop (fibrillation); deeper lesions expose the subchondral bone.

Compression of the exposed trabecular bone can cause a fracture, and new bone formation (bony eburnation) can take place. The exposed bony surface can have necrotic lesions that lead to the formation of bone cysts. Simultaneously, angiogenesis of subchondral bone marrow as a result of the initial insult to the bone tissue causes calcification of the affected cartilage that stimulates endochondral ossification (osteophytes). In addition to the articular cartilage, the synovium, subchondral bone, ligaments, and neuromuscular apparatus may also show pathophysiologic changes.

Presentation

Pain is the most important symptom of osteoarthritis (OA). It begins early in the course of the disease, usually occurs after joint activity, is mild to moderate in intensity, and is relieved with rest. When pain occurs at rest, it is indicative of severe OA.

Morning stiffness in OA is brief and localized, with the duration usually being less than 30 minutes, whereas the duration is much longer in inflammatory rheumatoid arthritis.

Stiffness after a period of inactivity and gradual improvement after a short period of movement is known as the "gel phenomenon."

Muscle activity in patients with OA is lessened because of pain and increased symptomatology, causing ambulatory episodes of giving way or buckling to occur.

Excessive pain causes a loss of full joint extension and limited range of motion (ROM) during ambulation, leading to inevitable joint deformity and a loss of function.

When an osteoarthritic knee or ankle joint is examined, bony enlargement due to proliferative change is often noted.

Frequently, in affected osteoarthritic hands, Heberden nodes occur around the distal interphalangeal joints, and Bouchard nodes are seen at the proximal interphalangeal joints.

Localized tenderness, especially in superficial joints, such as the knee or ankle, is often present, and a loss of motion and a crepitant feeling are detected. Secondary genu varum or valgum deformity may be present when patients ambulate. The tenderness experienced by osteoarthritic patients usually emanates from arthritis changes in the hip; this pain is difficult to mask and is accompanied by a hip flexion contracture. Not only is there loss of hip motion, but a loss of extension also occurs, as evidenced by the hip flexion contracture.When the spine is involved in OA, especially the lumbar spine, the associated changes are very commonly seen from L3 through L5. Symptoms include pain, stiffness, and occasional radicular pain from spinal stenosis. Spinal stenosis is caused by facet arthritic changes that result in compression of the nerve roots. The occurrence of an acquired spondylolisthesis is a common denominator of arthritis of the lumbar spine.

Indications

Before any surgical procedure is considered, its risk-to-benefit ratio must be carefully evaluated, especially in young patients with OA that is secondary to trauma or sports-related injuries.9

Although no surgical procedure is absolutely indicated or contraindicated for osteoarthritis (OA), certain general aspects are important to consider—for instance, pain at rest that requires narcotics for control. Also, limitations in a patient's ability to climb stairs and to get into and out of an automobile may affect the patient's quality of life. Another important aspect in selecting a surgical procedure is its long-term functional outcome in patients. These factors must be integrated into an overall evaluation in selecting the appropriate surgical procedure.

Relevant Anatomy

See Treatment, Surgical therapy.

Contraindications

Patients with osteoarthritis (OA) must be evaluated for contraindications to surgery. Local and remote (eg, dental, urinary) infections must be ruled out or cured. Patients may need to be medically cleared for surgery by their primary care physician. The patient's vascular status may need to be evaluated.

More on Osteoarthritis

Overview: Osteoarthritis
Workup: Osteoarthritis
Treatment: Osteoarthritis
Follow-up: Osteoarthritis
Multimedia: Osteoarthritis
References
Further Reading

References

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  2. Creamer P, Hochberg MC. Osteoarthritis. Lancet. Aug 16 1997;350(9076):503-8. [Medline].

  3. Dutkowsky JP. Miscellaneous nontraumatic disorders. In: Crenshaw AH, ed: Campbell's Operative Orthopedics. 8th ed. St Louis, Mo: Mosby-Year Book; 1992:1957-2058.

  4. Schumacher HR. Osteoarthritis. In: Primer on the Rheumatic Diseases. 10th ed. Atlanta, Ga: Arthritis Foundation;1993:184-90.

  5. Lawrence RC, Helmick CG, Arnett FC, et al. Estimates of the prevalence of arthritis and selected musculoskeletal disorders in the United States. Arthritis Rheum. May 1998;41(5):778-99. [Medline].

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  7. Outerbridge RE. The etiology of chondromalacia patellae. J Bone Joint Surg Br. Nov 1961;43-B:752-7. [Medline][Full Text].

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  13. Lanes SF, Lanza LL, Radensky PW, et al. Resource utilization and cost of care for rheumatoid arthritis and osteoarthritis in a managed care setting: the importance of drug and surgery costs. Arthritis Rheum. Aug 1997;40(8):1475-81. [Medline].

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  17. [Best Evidence] Chaipinyo K, Karoonsupcharoen O. No difference between home-based strength training and home-based balance training on pain in patients with knee osteoarthritis: a randomised trial. Aust J Physiother. 2009;55(1):25-30. [Medline].

  18. Kirkley A, Birmingham TB, Litchfield RB, et al. A Randomized Trial of Arthroscopic Surgery for Osteoarthritis of the Knee. New England Journal of Medicine. Available at http://content.nejm.org/cgi/content/short/359/11/1097?query=TOC. Accessed September 11, 2008.

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Keywords

osteoarthritis, OA, degenerative joint disease, degenerative arthritis, osteoarthrosis, arthritis

Contributor Information and Disclosures

Author

Furqan H Siddiqui, MD, Director, Research Integrity Office, University of Louisville Hospital
Furqan H Siddiqui, MD is a member of the following medical societies: American Federation for Clinical Research
Disclosure: Nothing to disclose.

Coauthor(s)

James Monroe Laborde, MD, MS, Clinical Assistant Professor, Department of Orthopedics, Tulane Medical School; Adjunct Assistant Professor, Department of Biomedical Engineering, Tulane University; Adjunct Assistant Professor, Department of Physical Medicine and Rehabilitation, Louisiana State University Medical School; Consulting Staff, Department of Orthopedic Surgery, Louisiana State University Health Sciences Center
James Monroe Laborde, MD, MS is a member of the following medical societies: American Academy of Orthopaedic Surgeons
Disclosure: Nothing to disclose.

Medical Editor

Phillip J Marone, MD, MSPH, Clinical Professor, Department of Orthopedic Surgery, Jefferson Medical College
Phillip J Marone, MD, MSPH is a member of the following medical societies: American Academy of Orthopaedic Surgeons, American College of Surgeons, American Medical Association, American Orthopaedic Society for Sports Medicine, and Philadelphia County Medical Society
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: Nothing to disclose.

Managing Editor

Samuel Agnew, MD, FACS, Associate Professor, Departments of Orthopedic Surgery and Surgery, Chief of Orthopedic Trauma, University of Florida at Jacksonville; Consulting Surgeon, Department of Orthopedic Surgery, McLeod Regional Medical Center
Samuel Agnew, MD, FACS is a member of the following medical societies: American Association for the Surgery of Trauma, American College of Surgeons, Orthopaedic Trauma Association, and Southern Orthopaedic Association
Disclosure: Nothing to disclose.

CME Editor

Dinesh Patel, MD, FACS, Associate Clinical Professor of Orthopedic Surgery, Harvard Medical School; Chief of Arthroscopic Surgery, Department of Orthopedic Surgery, Massachusetts General Hospital
Dinesh Patel, MD, FACS is a member of the following medical societies: American Academy of Orthopaedic Surgeons, American Association of Physicians of Indian Origin, American College of International Physicians, and American College of Surgeons
Disclosure: Nothing to disclose.

Chief Editor

Mary Ann E Keenan, MD, Professor, Vice Chair for Graduate Medical Education, Department of Orthopedic Surgery, University of Pennsylvania School of Medicine; Chief of Neuro-Orthopedics Program, Department of Orthopedic Surgery, Hospital of the University of Pennsylvania
Mary Ann E Keenan, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Orthopaedic Surgeons, American Orthopaedic Association, American Orthopaedic Foot and Ankle Society, American Society for Surgery of the Hand, and Orthopaedic Rehabilitation Association
Disclosure: Nothing to disclose.

 
 
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