eMedicine Specialties > Physical Medicine and Rehabilitation > Arthritis & Connective Tissue Disorders

Osteoarthritis

Author: Todd P Stitik, MD, Professor, Department of Physical Medicine and Rehabilitation; Director, Outpatient Occupational/Musculoskeletal Medicine, UMDNJ-New Jersey School of Medicine
Coauthor(s): Patrick M Foye, MD, FAAPMR, FAAEM, Associate Professor of Physical Medicine and Rehabilitation, Co-Director of Musculoskeletal Fellowship, Co-Director of Back Pain Clinic, Director of Coccyx Pain Service (Tailbone Pain Service: www.TailboneDoctor.com), University of Medicine and Dentistry of New Jersey, New Jersey Medical School; Irim Ciolino, MD, Co-chief Resident, Department of Internal Medicine, New York Medical College/St Vincent's Catholic Medical Center
Contributor Information and Disclosures

Updated: Jul 16, 2009

Introduction

Background

Osteoarthritis (OA) is a chronic disease process affecting synovial joints, particularly large weight-bearing joints. OA is particularly common in older patients but can occur in younger patients either through a genetic mechanism or, more commonly, because of previous joint trauma.

Related eMedicine topics:
 Interphalangeal Joint Arthritis
Osteoarthritis [Orthopedic Surgery]
Osteoarthritis [Rheumatology]
Osteoarthritis, Primary
Wrist Arthritis

Related Medscape topics:
Resource Center Arthritis
Resource Center Joint Disorders

Pathophysiology

Joints can be classified as synovial, fibrous, or combination joints, based on the presence or absence of a synovial membrane and the amount of motion that occurs in the joint. Normal synovial joints allow a significant amount of motion along their extremely smooth articular surface. These joints are composed of a synovial membrane, articular or hyaline cartilage, subchondral bone, synovial fluid, and a joint capsule.

Although traditional teaching prescribes that osteoarthritis (OA) affects primarily the articular cartilage of synovial joints, pathophysiologic changes also occur in the synovial fluid, as well as in the underlying (subchondral) bone and the overlying joint capsule. The affected cartilage initially develops small tears, known as fibrillations, at the articular surface, followed by larger tears; the cartilage eventually fragments off into joints. The cartilage-forming cells (ie, chondrocytes) replicate in an attempt to keep up with the cartilage loss; however, they eventually are unable to do so, and the underlying bone becomes exposed as gross areas of the bone become denuded of cartilage.

In the early degenerative process, increased expression and content of various metalloproteinases occur. These proteinases are very much involved in the excessive matrix degradation that characterizes cartilage degeneration in OA.1 Bone along the periphery of the joint replicates to form osteophytes, while the subchondral bone along the midportion of the joint becomes sclerotic, and areas within it may eventually undergo cystic degeneration because of focal resorption. Synovial fluid is formed through an ultrafiltration process of serum by cells that form the synovial membrane (synoviocytes). Synovial cells also manufacture the major protein component of synovial fluid, hyaluronic acid (also known as hyaluronate). Synovial fluid supplies nutrients to the avascular articular cartilage; it also provides the viscosity needed to absorb shock from slow movements, as well as the elasticity required to absorb shock from rapid movements.

The osteoarthritic joint is characterized by decreased concentration of hyaluronic acid because of reduced production by synoviocytes and increased water content because of inflammation, particularly during later stages of the disease.

The onset of pain is usually insidious, is generally described as aching or throbbing, and may be the result of changes that have occurred over the previous 15-20 years of the patient's life. Most often, the pain worsens with activity involving the affected joint and is initially relieved with rest; eventually, however, pain occurs even at rest. Since cartilage itself is not innervated, the pain is presumed to arise from a combination of mechanisms, including the following:

  • Osteophytic periosteal elevation
  • Vascular congestion of subchondral bone, leading to increased intraosseous pressure
  • Synovitis with activation of synovial membrane nociceptors
  • Fatigue in muscles that cross the joint
  • Overall joint contracture

In addition to the underlying pathophysiologic changes described above, overall, the joint may undergo mechanical deformation, with resultant malalignment and instability. Alternatively, the joint can ankylose.

Related eMedicine topic:
The Approach to the Painful Joint

Related Medscape topic:
CME Management of Shoulder Osteoarthritis Reviewed

Frequency

United States

Osteoarthritis (OA) is the most prevalent musculoskeletal condition that causes joint pain. The incidence of OA increases with age, with estimates based on radiologic evidence indicating the following incidence patterns:

  • At age 18-24 years, 7% of men and 2% of women show signs of OA in the hands.
  • At age 55-64 years, 28% of men and women show signs of OA in the knee, and 23% show signs of OA in the hip.
  • At age 65-74 years, 39% of men and women show signs of OA in the knee and 23% show signs of OA in the hip.
  • At age 75-79 years, approximately 100% of men and women show some signs of OA.

Mortality/Morbidity

  • Mortality does not occur directly from osteoarthritis (OA), but it can result indirectly from complications associated with immobility and deconditioning, medications used to relieve pain associated with OA, or from joint-related surgery.
  • Morbidity can take the form of pain or loss of function.

Race

No significant correlation exists between the incidence of osteoarthritis (OA) and race, with the exception of the Chinese population, which demonstrates a decreased incidence of OA. Different prevalences are cited for different ethnic groups.

Sex

Osteoarthritis (OA) is equally prevalent in men and women aged 45-55 years. After age 55 years, the prevalence of OA increases in women in comparison with men. The primary differences in incidence between males and females are related to the sites affected by OA. The most common sites affected in females are distal interphalangeal joints, proximal interphalangeal joints, first carpometacarpal joints, metatarsophalangeal joints, hips (in those aged 55-64 y), and knees (in those aged 65-74 y). In males aged 65-74 years, the hips and knees are affected more frequently than they are in females.

Age

Most adults older than 55 years show radiographic evidence of osteoarthritis (OA).2 Males develop OA before age 45 years, possibly because of a higher incidence of posttraumatic OA. After age 55 years, women are affected more frequently by OA and tend to have more severe disease than do men.

Clinical

History

Patients with osteoarthritis (OA) generally complain of insidious throbbing arthralgias with activity. Although initially, resting relieves the pain, the patient eventually begins to suffer pain even when he/she is at rest. Morning stiffness, which usually lasts less than 30 minutes, may also be experienced in the joint. Intermittent joint swelling and give-way weakness in the knees (ie, quadriceps pain inhibition) are noted.

Physical

  • Early in the disease process of osteoarthritis, physical examination findings include the following:
    • Joints may appear normal.
    • Gait may be antalgic if weight-bearing joints are involved.
  • Later in the disease process, physical examination findings include the following:
    • Visible osteophytes may be noted.
    • Joints may be warm to palpation.
    • Palpable osteophytes frequently are noted.
    • Joint effusion frequently is evidenced in superficial joints.
    • Range-of-motion limitations, because of bony restrictions and/or soft tissue contractures, are characteristic.
    • Crepitus with range of motion is not uncommon.

Causes

  • Primary osteoarthritis (OA), which can be either localized or generalized, is most often idiopathic, except in rare cases in which a defective gene has been found to cause a familial form of OA.
  • Secondary OA can be caused by the following:
    • Obesity (increases mechanical stress)3,4
    • Repetitive use (ie, jobs requiring heavy labor and bending)5
    • Previous trauma (ie, posttraumatic OA)
    • Infection
    • Crystal deposition
    • Acromegaly
    • Previous rheumatoid arthritis (ie, burnt-out rheumatoid arthritis)
    • Heritable metabolic causes (eg, alkaptonuria, hemochromatosis, Wilson disease)
    • Hemoglobinopathies (eg, sickle cell disease, thalassemia)
    • Neuropathic disorder leading to a Charcot joint (eg, syringomyelia, tabes dorsalis, diabetes)
    • Underlying orthopedic disorders (eg, congenital hip dislocation, slipped femoral capital epiphysis)
    • Disorders of bone (eg, Paget disease, avascular necrosis)

Related eMedicine topics:
Obesity [Endocrinology]
Obesity [Pediatrics: General Medicine]

Related Medscape topic:
Resource Center Obesity

More on Osteoarthritis

Overview: Osteoarthritis
Differential Diagnoses & Workup: Osteoarthritis
Treatment & Medication: Osteoarthritis
Follow-up: Osteoarthritis
Multimedia: Osteoarthritis
References
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Further Reading

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Keywords

osteoarthritis, arthritis, joint pain, arthritis pain, knee pain, knee arthritis, hip arthritis, arthritic, degenerative joint disease, synovial, synovial joint, osteoarthritis knee, osteoarthritis treatment, treatment of osteoarthritis, arthroplasty, joint replacement, osteoarthrosis, synovial joints, osteophytes, synoviocytes, hyaluronic acid, hyaluronate, HA, repetitive joint use, crystal deposition, acromegaly, rheumatoid arthritis, obesity, alkaptonuria, hemochromatosis, Wilson disease, Wilson's disease, hemoglobinopathies, sickle cell disease, thalassemia, Charcot joint, Charcot'sjoint, syringomyelia, tabes dorsalis, diabetes, congenital hip dislocation, slipped capital femoral epiphysis, Paget disease, Paget's disease, avascular necrosis

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Contributor Information and Disclosures

Author

Todd P Stitik, MD, Professor, Department of Physical Medicine and Rehabilitation; Director, Outpatient Occupational/Musculoskeletal Medicine, UMDNJ-New Jersey School of Medicine
Todd P Stitik, MD is a member of the following medical societies: American Academy of Physical Medicine and Rehabilitation, Association of Academic Physiatrists, Phi Beta Kappa, and Physiatric Association of Spine, Sports and Occupational Rehabilitation
Disclosure: Nothing to disclose.

Coauthor(s)

Patrick M Foye, MD, FAAPMR, FAAEM, Associate Professor of Physical Medicine and Rehabilitation, Co-Director of Musculoskeletal Fellowship, Co-Director of Back Pain Clinic, Director of Coccyx Pain Service (Tailbone Pain Service: www.TailboneDoctor.com), University of Medicine and Dentistry of New Jersey, New Jersey Medical School
Patrick M Foye, MD, FAAPMR, FAAEM is a member of the following medical societies: American Academy of Physical Medicine and Rehabilitation, American Association of Neuromuscular and Electrodiagnostic Medicine, Association of Academic Physiatrists, and International Spine Intervention Society
Disclosure: Nothing to disclose.

Irim Ciolino, MD, Co-chief Resident, Department of Internal Medicine, New York Medical College/St Vincent's Catholic Medical Center
Irim Ciolino, MD is a member of the following medical societies: American College of Physicians
Disclosure: Nothing to disclose.

Medical Editor

Curtis W Slipman, MD, Director, University of Pennsylvania Spine Center; Associate Professor, Department of Physical Medicine and Rehabilitation, University of Pennsylvania Medical Center
Curtis W Slipman, MD is a member of the following medical societies: American Academy of Physical Medicine and Rehabilitation, Association of Academic Physiatrists, International Association for the Study of Pain, and North American Spine Society
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: eMedicine Salary Employment

Managing Editor

Richard Salcido, MD, Chairman, Erdman Professor of Rehabilitation, Department of Physical Medicine and Rehabilitation, University of Pennsylvania School of Medicine
Richard Salcido, MD is a member of the following medical societies: American Academy of Pain Medicine, American Academy of Physical Medicine and Rehabilitation, American College of Physician Executives, American Medical Association, and American Paraplegia Society
Disclosure: Nothing to disclose.

CME Editor

Kelly L Allen, MD, Regional Medical Director, IMX-Medical Management Services
Disclosure: Nothing to disclose.

Chief Editor

Denise I Campagnolo, MD, MS, Director of Multiple Sclerosis Clinical Research and Staff Physiatrist, Barrow Neurology Clinics, St Joseph's Hospital and Medical Center; Investigator for Barrow Neurology Clinics; Director, NARCOMS Project for Consortium of MS Centers
Denise I Campagnolo, MD, MS is a member of the following medical societies: Alpha Omega Alpha, American Association of Neuromuscular and Electrodiagnostic Medicine, American Paraplegia Society, Association of Academic Physiatrists, and Consortium of Multiple Sclerosis Centers
Disclosure: Teva Neuroscience Honoraria Speaking and teaching; Serono-Pfizer Honoraria Speaking and teaching; Genzyme Corporation Grant/research funds investigator; Biogen Idec Grant/research funds investigator; Genentech, Inc Grant/research funds investigator; Eli Lilly & Company Grant/research funds Novaritis; Novaritis  Novaritis; MSDx LLC Grant/research funds investigator; BioMS Technology Corp Grant/research funds investigator; Avanir Pharmaceuticals Grant/research funds investigator

 
 
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