Osteoarthritis

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Osteoarthritis

• Randa Mahmoud Al-Harizy
• Internal Medicine department
• Faculty of Medicine, Cairo University

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OSTEOARTHRITIS

• OA is a group of diseases and mechanical
  abnormalities entailing degradation of joints,
  including articular cartilage and the subchondral
  bone next to it
• OA is derived from the Greek word ostoe,
  meaning of the bone, arthro, meaning joint,
  and itis, meaning inflammation

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DEFINITION

• There is no simple definition of OA as it
  requires consideration of three overlapping areas
  - pathological changes, radiological features and
  clinical consequences. Pathologically, there is
  an alteration in cartilage structure,
  radiologically there are osteophytes and joint
  space narrowing, and clinically some patients
  complain of pain and disability.

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EPIDEMIOLOGY

• Osteoarthritis is the most common type of
  arthritis.
• The prevalence increases with age
• 80 of people over 60 years will have some
  radiological evidence of it, although only 60 of
  those will show symptoms.

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• O.A.
• Women over 55 years are affected more commonly
  than are men of a similar age.
• There is a familial pattern of inheritance
• The resulting disabilities have major
  socio-economic resource implications,
  particularly in the developed world.

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AETIIOLOGY

• In OA, a variety of potential forces hereditary,
  developmental, metabolic and mechanical may
  initiate processes leading to loss of cartilage.
• Subchondral bone may be exposed and damaged, with
  regrowth leading to a proliferation of
  ivory-like, dense, reactive bone in central areas
  of cartilage loss, a process called eburnation.
• The patient experiences pain upon weight bearing
  
• Due to decreased movement from pain, regional
  muscles may atrophy and ligaments may become more
  lax

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PREDISPOSING FACTORS

• Obesity
• Heredity
• Gender
• Hypermobility
• Osteoporosis
• Trauma
• Congenital joint dysplasia
• Occupation
• Sport

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CAUSES

• Primary OA No known cause
• Secondary OA
• Pre-existing joint damage   RA, Gout, Seronegativ
  e spondyloarthropathy, Septic arthritis, Paget's
  disease, Avascular necrosis, e.g. corticosteroid
  therapy 
• Metabolic disease Chondrocalcinosis, Hereditary
  haemochromatosis, Acromegaly 
• Systemic diseases Haemophilia- recurrent
  haemarthrosis, Haemoglobinopathies, e.g. sickle
  cell disease, Neuropathies

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• CLINICAL PICTURE
• OA commonly affects the hands, feet, spine and
  the large weight bearing joints such as hips and
  knees
• Symptoms
• Joint pain
• Joint gelling (stiffening and pain after
  immobility)
• Joint instability
• Loss of function.

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• CLINICAL PICTURE
• Signs
• Joint tenderness
• Crepitus on movement
• Limitation of range of movement
• Joint instability
• Joint effusion and variable levels of
  inflammation
• Bony swelling
• Wasting of muscles.

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DIAGNOSIS

• Investigations in OA
• Blood tests. There is no specific test the ESR
  and CRP are normal. Rheumatoid factor and
  antinuclear antibodies are negative.
• X-rays are abnormal only when the damage is
  advanced.
• MRI demonstrates early cartilage and subchondral
  bone changes.
• Arthroscopy reveals early fissuring and surface
  erosion of the cartilage.

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TREATMENT

• Generally speaking, the process of clinically
  detectable osteoarthritis is irreversible, and
  typical treatment consists of medication or other
  interventions that can reduce the pain of OA and
  thereby improve the function of the joint.

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CONSERVATIVE CARE

• Weight control
• Appropriate rest and Exercise
• Physical therapies
• Occupational therapies

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• DIETARY TREATMENT
• Glucoseamine, chondroitin sulphate, antioxidants,
  others
• SPECIFIC MEDICATIONS
• Paracetamol
• NSAIDs
• COX-2 selective inhibitors
• Corticosteroids

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OTHERS

• Implantation of chondrocytes
• Local injection of hyaluronic acid
• Topical treatment
• Surgical treatment
• Acupuncture

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Crystal Deposition Disease

• GOUT
• Definition
• Gout is a disease which is characterized by
  tissue deposition of monosodium urate crystals
  (MSU) due to hyperuricaemia that results in
• Gouty arthritis
• Tophi
• Gouty nephropathy
• Uric acid nephrolithiasis

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ETIOLOGY

• 1- Overproduction of urate
• Endogenous
• Hyperactivity of phosphoribosylpyrophosphate
  (PRPP) synthetase
• Partial deficiency of hypoxanthine guanine
  phospho-ribosyltransferase (HGPRT)
• Myeloproliferative and lymphoproliferative
  disorders
• Hemolysis
• Psoriasis
• Exogenous
• Excess dietary purine consumption meat, liver,
  kidney, sea food, legumes, mushrooms

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Underexcretion of Urate

• Renal disease
• Lead intoxication
• Hyperparathyroidism
• Hypothyroidism
• Drugs
• Low dose aspirin
• Diuretics
• Ethambutol
• Pyrazinamide
• Cyclosporine
• Alcohol

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CLINICAL PICTURE

• 1- Asymptomatic hyperuricemia
• 2- Acute gouty arthritis
• - precipitating factors excess dietary purines,
  alcohol, drugs, surgery, trauma, dehydration
• - typically affected joints of lower limb more
  commonly than that of upper limb the first
  metatarsophalangeal joint of big toe, the
  tarsals, ankles, heels, knees, wrists and fingers
  in a descending order
• Presentation early in the course of the disease
  is monoarticular, of acute onset, often during
  night. The affected joint is exquisitely painful,
  warm, red and swollen. Subsequent attacks become
  polyarticular and persist longer

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CLINICAL PICTURE

• 3- Intercritical gout asymptomatic intervals
  between the acute attacks
• 4- Chronic tophaceous gout development of
  subcutaneous nodules of deposits of monosodium
  urate crystals

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INVESTIGATIONS

• Serum level of uric acid may be elevated
• Synovial fluid analysis for
• Cells 25.000 100.000 leukocytes/mm3
• Polarized microscopy of the synovial fluid
  reveals the typical needle shaped negative
  birefringent crystals
• Radiology soft tissue swelling, punched out bone
  erosions

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TREATMENT

• During the acute attack
• NSAIDs indomethacin , Colchicine, ACTH,
  Intraarticular steroids, systemic corticosteroids
• Treatment of chronic tophaceous gout
• Xanthine oxidase inhibitor (allopurinol)
• Uricosuric drugs probenecid
• Diet control

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PSEUDOGOUT

• Definition
• Pseudogout is an inflammatory arthropathy
  resulting from deposition of calcium
  pyrophosphate dihydrate crystals (CPPD) in and
  around joints that results in calcification of
  articular cartilage (chondrocalcinosis)

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Conditions associated with pseudogout

• Hyperparathyroidism
• Haemochromatosis
• Osteoarthritis
• Hypothyrodism
• Neuropathic arthropathy
• Idiopathic
• Familial

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Clinical picture

• Acute pseudogout
• Acute monoarthritis especially affecting knee,
  ankle, wrist or shoulder. Surgical procedures and
  acute medical illness may precipitate the attack
• Chronic pseudogout
• Presenting as osteoarthritis but distinguished
  from it by the involvement of atypical joints as
  wrists and metacarpophalangeal joints

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INVESTIGATIONS

• SYNOVIAL FLUID ANALYSIS FOR
• Cells 25.000 100.000 leukocytes/mm3
• Polarized microscopy of the synovial fluid
  reveals the typical rhomboid shaped positive
  birefringent crystals
• RADIOLOGY
• Chondrocalcinosis with evidence of calcification
  of fibrocartilage as menisci, symphisis pubis and
  triangular cartilage of the wrist

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TREATMENT

• NSAIDs
• Joint aspiration
• Intraarticular injection of steroids

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