Osteoarthritis overview
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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. [3] [4] In the 1930s and 1940s, Dr. Stecher showed that there were two forms of OA, idiopathic and post-traumatic. [5] And, in the 1950s the links between Heberden’s nodes and large joint OA were revealed by Kellgren and Moore. In this regard, the first x-ray grading system for OA was developed by Jonas Kellgren and John Lawrence in the 1950s. Surgical management of OA was developed in the 1960s by Drs. Charnley and McKee
Classification
Osteoarthritis is radiographically classified depending on degree of joint involvement. The Kellgren-Lawrence is a common method to classify the severity of OA in knee using five different grades. This classification was proposed by Kellgren et al. in 1957 and then it was accepted by WHO in 1961.
I: Idiopathic | |||
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A: Localized | |||
1: Hands: Heberden’s and Bouchard’s nodes (nodal), erosive interphalangeai arthritis (nonnodal), scaphometacarpal joint, scaphotrapezial | |||
2. Feet: hallux valgus. hallux rigidus, contracted toes (hammer/cockup toes), talonavicular | |||
3. Knee | a. Medial compartment
b. Lateral compartment c. Patellofemoral compartment (chondromalacia) | ||
4. Hip | a. Eccentric (superior)
b. Concentric (axial, medial) c. Diffuse (coxae senilis) | ||
5. Spine (particularly cervical and lumbar) | a. Apophyseal
b. Intervertebral (disc) c. Spondylosis (osteophytes) d. Ligamentous (hyperostosis [Forestier’s disease or DISH]) | ||
6. Other single sites: shoulder, temporomandibular, sacroiliac, ankle, wrist, acromioclavicular | |||
B. Generalized: includes 3 or more areas listed above (Kellgren-Moore) | 1. Small (peripheral) and spine
2. Large (central) and spine 3. Mixed (peripheral and central) and spine |
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II. Secondary | |||
A. Posttraumatic | |||
B. Congenital or Developmental Diseases | 1. Localized | a. Hip diseases: Legg-Calve-Perthes, congenital hip dislocation, slipped capital femoral epiphysis, shallow acetabulum
b. Mechanical and local factors: obesity (7). unequal lower extremity length, extreme valgus/varus deformity, hypermobility syndromes, scoliosis | |
2. Generalized | a. Bone dysplasias: epiphyseal dysplasia, spondyloapophyseal dysplasia
b. Metabolic diseases: hemachromatosis, ochronosis, Gaucher’s disease, hemoglobinopathy, Ehlers-Danlos | ||
c. Calcium Deposition Disease | 1. Calcium pyrophosphate deposition disease
2. Apatite atthropathy 3. Destructive arthropathy (shoulder, knee) |
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D. Other Bone and Joint Disorders: avascular necrosis, rheumatoid arthritis, gouty arthritis, septic arthritis, Paget’s disease, osteopetrosis, osteochondritis | |||
E. Other Diseases | 1. Endocrine diseases: diabetes mellitus, acromegaly, hypothyroidism, hyperparathyroidism
2. Neuropathic arthropathy (Charcot joints) 3. Miscellaneous: frostbite, Kashin-Beck disease, Caisson’s disease |
Grade | Description |
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0 | Normal articular cartilage |
I | Softening of the articular cartilage |
II | Fibrillation or superficial fissures of the cartilage |
III | Deep fissuring of the cartilage without exposed bone |
IV | Exposed bone |
Grade | Description |
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0 | No joint space narrowing (JSN) or reactive changes |
1 | Doubtful JSN, possible osteophytic lipping |
2 | Definite osteophytes, possible JSN |
3 | Moderate osteophytes, definite JSN, some sclerosis, possible bone-end deformity |
4 | Large osteophytes, marked JSN, severe sclerosis, definite bone ends 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.