Osteoarthritis

  • 23,457 views
Uploaded on

 

  • Full Name Full Name Comment goes here.
    Are you sure you want to
    Your message goes here
    Be the first to comment
No Downloads

Views

Total Views
23,457
On Slideshare
0
From Embeds
0
Number of Embeds
0

Actions

Shares
Downloads
488
Comments
0
Likes
7

Embeds 0

No embeds

Report content

Flagged as inappropriate Flag as inappropriate
Flag as inappropriate

Select your reason for flagging this presentation as inappropriate.

Cancel
    No notes for slide

Transcript

  • 1. OSTEOARTHRITIS Disorder of hyaline cartilage and subchondral bone, though all tisues in and around involved joints are hyperthrophic.
  • 2. Incidence
    • The most common form of articular disorder.
    • First appear asymptomatically in the 2nd to 3rd decades and become universally by age 70.
  • 3. Classification
    • Oa is classified in 2 groups:
    • Primary OA: includes peripheral joints, notably the distal IFJ and PIJ ( producing Heberden´s and Bouchard´s nodes ), 1st CMTJ, cervical and lumbar spine.
    • 1st MTPJ ( big toe), hips, knees, intervertebral disks, zygapophyseal joints in the spine.
    • Several variants subset: erosive, inflammatory OA, DISH.
    • Secondary: according with the etiology
  • 4. Etiology
    • Etiology is unknown.
    • OA appears to be the result of a complex system of interacting , mechanical , biologic, biochemical, and enzymatic feedback loops.
    • When one or more fails, the clinical events follow.
  • 5. Cont;
    • Anything that change the microenvironment of the chondrocyte.
    • This includes congenital joint abnormalities, genetic defects, infectious, metabolic, endocrine, and neuropathic diseases.
    • Acute or chronic trauma including fractures.Virtually any disease process that alter the normal structure and function of hyaline cartilage.
  • 6. Pathophysiology
    • Hyaline cartilage is avascular, aneural, and alymphatic.
    • Chondrocyte divide and increase their rates of both synthesis and degradative process, they have the longest cell cycle in the body.
    • Never dividing unless some alteration occurs in the microenviroment.
  • 7. Cont;
    • Cartilage heal depends on the pumpimg action ( compression and release) of weight-bearing and use.
    • Inital event in OA : mitosis of chondrocyte with increased synthesis of the proteoglycans and type ll collagen.
    • Decrease in concentration of proteoglycans in the inmediate neighborhood of the chondrocyte.
  • 8. Cont;
    • Second event: Increased synthesis of bone by osteoblasts in the subchondral bone by intercommunication between chondrocyte and osteoblasts in the subchondral bone cells.
    • With increased bone formation in the subchondral area, physical propierties change, the bone become stiffer, and microfractures occur.
  • 9. Cont;
    • With microfractures comes callus formation and hence more stiffness and more microfracture.
    • Third event: metaplasia of the peripheral synovial cells resulting in formation of osteochondrophytes ( combination bone, connective tissue, fibrocartilage and island of hyaline cartilage on the surface.
  • 10. Cont;
    • Fourth event: formation of bony cysts
    • ( Pseudocysts) in the marrow below the subchondral bone.
    • The mechanism is that extrusion of joint fluid trough the hyaline cartilage clefts into the marrow with fibroblastic, osteoblastic cellular reaction around the synovial fluid.
  • 11. Cont;
    • The gross pathology: roughening or loss of surface of the hyaline cartilage, pitting, and irregularities, proceeding the gross ulceration with a first focal, diffuse area of loss of cartilage surface.
    • Proliferation of new bone, capsule tendon, cartilage, and synovium occur.
  • 12. Cont;
    • Deterioration and loss of bearing surface, proliferation of all osteoarticular tissue at the margin of the joints and under the detached joint surface.
    • All cases have active synovial proliferation and synovitis.
  • 13. Symptoms and signs
    • Initially, OA ..is noninflammatory and onset subtle gradual, usually involving one to only a few joints.
    • Pain is the earliest symptom, usually made worse by exercise.
    • Morning stiffness follow inactivity but last in 15-30 min, improve with exercise.
  • 14. Cont;
    • Acute episodes of severe synovitis may occur in those who have gout or pseudogout.
    • As the disease progresses joint motion become diminshed, flexion contracture occur, tenderness and crepitus or grating sensation appear.
  • 15. Cont;
    • Joint enlargement induce by the proliferative reaction of cartilage, bone ligament, tendon, capsules, and chronic synovial proliferation and inflammation is ultimately characteristic of OA.
    • As ligament become lax, the joint has increasing instability with more local pain, and cliniical appearance of a limp
  • 16. Cont;
    • Tenderness on palpation and pain on passive motion are late signs muscle spams and contracture add to the pain.
    • Mechanical block, deformities and subluxations, subchondral bone collapse, osteochondrophytes, muscle atrophy and pseudocysts.
  • 17. Cont;
    • OA of the cervical and lumbar spine: is common. In the cervical spine the symptoms may be related to radiculitis by compression of nerve roots secondary to proliferative osteochondrophytes, functional compromise of the vertebral artery, neuromyopathy secondary to compresion, spinal cord infarcts or esophageal compression, by anterior bony projection.
  • 18. Diagnosis
    • Based on symptoms and signs or by X-ray in asymptomatic patients.
    • Laboaratory and X-ray studies:
    • ESR is normal or moderately increased.
    • X-ray and radiologic criteria:
    • A) Irregular or asymmetric narrowing of the joint space.
  • 19. Cont;
    • B)- Increased in radiologic density of the subchondral bone.
    • C)-Formation of osteochondrophytes at the periphery of joints.
    • D) Formation of Pseudocysts in the subchondral bone marrow.
    • Differential diagnosis: RA, AKS, Psoriatic arthritis, seronegative spondyloarthropathies, crystal deposits, endocrine, metabolic and neoplastic disorders affecting the bone.
  • 20. Prevention and treatment
    • The most modifiable risk factor is the obesity.
    • The goals in the treatment of OA are the relieve of pain, improve function and prevent disability.
    • Patient education
    • Physical measures: exercise, supportive devices, alteration in DA, thermal modalities and psychosocial measures.
  • 21. Pharmacology therapy
    • Topical agents: Capsaicin ( depletion of substance P, neurotransmitter), topical NSADs.
    • Systemic oral agents: acetaminophen, tramadol, codeine, dextropropoxyphene.
    • Etoricoxib, lumiracoxib, celecoxib.
    • Nutraceuticals: nutricional supplements with potential pharmacologic value.
  • 22. Cont;
    • Glucosamine sulphate, chondroitin sulphate, S- adenosylmethionine (SAM-e) MSM ( methylsulphonylmethane), shark cartilage, cat´s claw.
    • Adyuvants agents: tricyclic antidepresants, antispasmodics, injection of lidocaine or depot corticosteroids.
    • Intrarticular therapy: Hyaluronan and corticoids.
  • 23. Cont;
    • Structure disease modifying agents:
    • These substances retard the progression of OA and/or enhance a normal reparative process.
    • These agents are categorized as follow:
    • Growth factors and cytokines
    • Sulfated and non-sulfated sugars.
    • Hormones and other steroids
  • 24. Cont;
    • Enzyme inhibitors: glucosamine sulfate, metalloproteinases inhibitors such as tetracyclines, growth factors and cytokines and chondrocyte stem system transplantation.
    • Collagenase inhibitors.
    • Surgical intervention: for intractable pain, and restoration of compromised function.
  • 25. Cont:
    • Total hip and knee arthroplasties, osteostomies, arthroscopy intervention
    • surgical arthroscopy for repair and for partial removal of damaged menisci, arthroscopy lavage.
  • 26.  
  • 27.  
  • 28.  
  • 29.  
  • 30.  
  • 31.  
  • 32.  
  • 33.