Osteoarthrosis

From WikiLectures

genetic, joint damage, connective tissue diseases
lies in the metabolic processes of damaged cartilage
limitation of joint movement, pain, joint deformation
physical therapy, drug therapy: NSAIDs, corticoids, chondroprotectants, TEP
limitation of function, joint swelling, septic arthritis
M15, M19, M47
165720
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Osteoarthrosis (OA) is a heterogeneous group of diseases with a common clinical picture and X-ray findings.

Epidemiology[edit | edit source]

Prevalence of OA worldwide in 2004

Globally, about 250 million people suffer from osteoarthritis, which represents 3.6% of the world's population[1].

Etiology[edit | edit source]

The disease is multifactorial, with predisposing systemic factors (genetic, hormonal, and endocrine) and local influences.

Clinical presentation[edit | edit source]

X-ray image – osteoarthrosis in typical localization of distal and proximal interphalangeal joints of the hand
  • exertional and starting pains;
  • joint stiffness after inactivity (typically in the morning), lasting for 15-30 minutes;
  • limited joint mobility;
  • sound phenomena (crepitus, grinding);
  • joint deformities.

X-ray findings[edit | edit source]

Narrowing of the joint space, subchondral sclerosis, cysts, and osteophytes on the edges of the joint surfaces.

Classification of osteoarthrosis[edit | edit source]

Primary (idiopathic)[edit | edit source]

  • localized;
  • generalized (3 or more joints);
  • erosive.

Secondary (symptomatic)[edit | edit source]

Localization of arthrotic changes

Kellgren-Lawrence[edit | edit source]

Classification based on the severity of X-ray findings

I. joint space narrowing
II. joint space narrowing, subchondral sclerosis on X-ray, osteophyte formation
III. joint space narrowing, subchondral sclerosis on X-ray, deformation of joint cavity and head, osteophytes
IV. vanished joint space, subchondral sclerosis on X-ray, deformation, cysts, osteophytes

Localization of changes in osteoarthrosis[edit | edit source]

Generalized OA[edit | edit source]

It is divided into nodal, non-nodal, and erosive types.

Pathogenesis[edit | edit source]

  • Combination of degenerative, inflammatory, and reparative changes affecting articular cartilage (loss of proteoglycans and impaired synthesis of collagen by chondrocytes), subchondral bone (sclerosis, cysts, formation of osteophytes), ligaments, tendons, and synovium.
  • As a consequence of degenerative and biochemical changes, the cartilage loses its luster, softens, and develops fissures on its surface. Gradually, it becomes less resilient and experiences losses.
  • Subchondral bone undergoes sclerosis, cysts form within it, and osteophytes (bony outgrowths) form on its edges.
  • Osteoarthritis is a disease of the entire joint structure (not just articular cartilage).
  • OA is a very common disease, affecting up to 80% of the population over the age of 50. However, degenerative changes may also occur at a younger age.

Diagnosis[edit | edit source]

The standard is an X-ray with typical changes, while laboratory tests are inconclusive.

In dif. dg. we think of:

  1. usually symmetrical polyarthritis, DIP joints are rarely affected;
  2. palpably painful joints (synovitis), pain is at rest (in osteoarthritis, it is exertional);
  3. longer morning stiffness (more than an hour);
  4. inflammatory markers and immunological indicators (RA, antinuclear antibodies…);
  • psoriatic arthritis - when DIP is affected, psoriasis should be considered;
  • crystal-induced diseases - pseudogout episodes, chondrocalcinosis on X-ray, crystals in joint aspiration.

Forms of OA[edit | edit source]

  • Gonarthrosis - most common localization, progresses slowly;
  • Coxarthrosis - often after CDH or Perthes disease, usually intermittent course;
  • Osteoarthritis of hand joints - affecting DIP (Heberden's nodes), PIP (Bouchard's nodes), rhizarthrosis (thumb base joint);
  • Osteoarthritis of the spine - affecting vertebral bodies (spondylosis - osteophytes on the edges of vertebral bodies), intervertebral joints (spondylarthrosis), discs (discopathy), unlike spondylitis, pain is exertional and better at rest.

Treatment[edit | edit source]

Total hip replacement prosthesis
  1. Regimen measures and rehabilitation, physical therapy;
  2. Pharmacological:
  3. specific COX-2 inhibitors (nimesulide, coxibs);
  4. corticosteroids intra-articularly - no more than 3 times a year;
    • symptomatic slow-acting drugs in osteoarthritis (SYSADOA) - (hyaluronic acid, chondroitin sulfate, glucosamine sulfate…) - effect after 3 months, given in series;
  5. Surgical:
    • arthroscopic abrasion (lavage, synovectomy, debridement);
    • osteotomy;
    • partial or total joint replacement.

Prevention[edit | edit source]

  • Elimination of the cause in all secondary arthritis;
  • Screening for congenital hip dysplasia in newborns;
  • Limiting meniscectomies;
  • Correction of unequal leg length;
  • Treatment of synovitis;
  • Maintaining a healthy body weight;
  • Prevention of long-term unilateral overloading of certain joints;
  • In mild initial involvement (pre-osteoarthritis), movement, preferably swimming or cycling.

Summary video[edit | edit source]


Video in English, definition, pathogenesis, symptoms, complications, treatment.

Links[edit | edit source]

Bibliography[edit | edit source]

PASTOR, Jan. Langenbeck's medical web page [online]. [cit. May 24, 2010]. <https://langenbeck.webs.com/>.

References[edit | edit source]

  1. VOS, Theo – FLAXMAN, Abraham D – NAGHAVI, Mohsen. , et al. Years lived with disability (YLDs) for 1160 sequelae of 289 diseases and injuries 1990-2010: a systematic analysis for the Global Burden of Disease Study 2010. Lancet [online]2012, vol. 380, no. 9859, p. 2163-96, Available from <https://www.ncbi.nlm.nih.gov/pubmed/23245607>. ISSN 0140-6736 (print), 1474-547X.