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APLEY READING
OSTEOARTHRITIS
0818501800
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THE PHYSIOLOGY OF SYNOVIAL
JOINTS
Anatomy of the joint
Articular Cartilage
Subchondral bone Synovium
Joint capsule
Tendon
Cancellous bone
Muscle
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ARTICULAR CARTILAGE
Covers the bone ends in every diarthrodeal
joint
transmit load and movement from one
skeletal segment to another
increases the area of the articular surfaces
Improve adaptability and stability component is mainly type II collagen
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CAPSULE AND LIGAMENTS
Helps to provide sability
Overstretched or torn unstable
Non-pathological ligamentous laxitystability is maintained by highly developed
muscle power&the articular cartilage is not
necessarily damaged.
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Synovium and synovial fluid
It covers the articular surface
Produces synovial fluid
Target tissue in joint infections & autoimmune
disorders ( RA )
Synovial fluid
nourishes the avascular articular cartilage
Reducing friction during movement
Also helps maintaining joint stability
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JOINT LUBRICATION
Boundary layer lubrication Fluid film lubrication
Lubrication between synovial folds
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OSTEOARTHRITIS
Osteoarthritis (OA) is a chronic joint disorder ofsynovial joints in which there is progressivesoftening and disintegration of articular cartilageaccompanied by new growth of cartilage and
bone at the joint margins (osteophytes), cystformation&schlerosis in the subchondral bone,mild synovitis and capsular fibrosis.
Asymmetric distributed
Localized only one part of a joint related to abnormal loading
Unaccompanied systemic illness
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Not a purely degenerative disorder
Dynamic phenomenon : destruction& repair
Cartilage softening and disintegrationaccompanied from hyperactive new bone
formation, osteophytosis and remodelling
Final figure determined by the relative vigourof these opposing processes
Secodary factor of progressing disorder : the
appearance of calcium-containing crystals inthe joint
Ischaemic changes (especially in elderly
people)
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secondary factors :
Joint instability
Prolonged anti-inflammatory medication.
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Etiology
Predispose factors
Age
Cartilage matrix changes (ex.crystal deposition ,
ochronosis) Inheritance
Previous trauma & inflammatory
Increase mechanical stress in the articular surfaceIncrease load
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Pathogenesis
Early stages : increase water content & extractability
matrix proteoglikan Later stages : loose proteoglikan&cartilage defects
Chondrocytes damage release cell enzymes
matrix breakdown
Forces are increasingly concentrated in the
subchondral bone focal trabecular degeneration &
cyst formation, increased vascularity, reactive
sclerosis in the zone of maximal loading Cartilage remain : regeneration, repair and
remodelling
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Pathology
The cardinal features
(1) progressive cartilage destruction
(2) subarticular cyst formation
(3) sclerosis of the surrounding bone
(4) osteophyte formation
(5) capsular fibrosis.
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PREVALENSI MEN : WOMAN 1 : 1
Age > 65 : 50 %
Most commonest : fingers, hip, knee, spine
RISK FACTORS Joint dysplasia : congenital acetabular
dyslasia, Perthes ds
Trauma : Fractures involving the articularsurface & cause joint instability secondary
OA
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Occupation: knee-bending activities, heavy
vibrating tools
Bone density
Obesity : increase joint loading
Family history
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Clinical Feature
PAIN : widespread , referred, insidiously, increases slowly, aggravated by exertion
, relieved by rest. Late stage pain in bed at night. Pain caused by
capsular fibrosis
Mild synovial inflammation
muscular fatigue bone pressure due to vascular congestion
intraosseous hypertension
STIFFNESS
occurs after periods of inactivity
Later become constant & progressive
SWELLING
intermittent /continuos
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Clinical Feature
Deformity : result from capsular contracture or
joint instability
Loss of function
A limp, difficulty climbing stairs, restriction of
walking distance or progressive inability toperform everyday tasks.
Typically, the symptoms of OA follow an
intermittent course, with periods ofremission sometimes lasting for months.
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SIGN
Joint swelling
Crepitus
Local tenderness Deformity
Instability.
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IMAGINGX-Ray
cardinal signs are asymmetric loss of cartilage (narrowing of the joint space)
sclerosis of the subchondral bone
cysts close to the articular surface
Osteophytes Late : joint displacement & bone destruction
Radionuclide scanning
shows increased activity e.c. increased vascularity &bone formation
CT and MRIArthroscopy :may show cartilage damage before x-ray
changes appear
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Arthrodesis (Bone or joint fusion surgery ) to relieve pain : hips, ankles, wrists, fingers, thumbs, or spine.
While a fused joint loses flexibility, it can bear weight better, is more stable
and is no longer painful.
for a painful or unstable joint where stiffness does not seriously affectfunction
Young, active, heavy pt with single joint involvement
Complication : pain, pseudarthrosis formation
non-union
Nerve injury
infection
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ArthroplastyHip replacement is a procedure in which the surgeon removes
damaged or diseased parts of the patient's hip joint and replaces
them with new artificial parts (called arthroplasty )
Consideration for oa:> 60 y.o
significant pain, deformity, functional loss with restricted ROM /
joint instability
If all other tx ineffective, and pain is severe
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EXCISION ARTHROPLASTY
Sufficient bone is excised to create a gap at which movementcan occur (e.g.Girdlestone's hip arthroplasty). a shaped'spacer' can be inserted; this may be tissue from another part(e.g. tendon) or artificial material like Silastic.
PARTIAL REPLACEMENTOne articular component only is replaced
The prosthesis is kept in position either by acrylic cement orby a cementless fit between implant and bone.
TOTAL REPLACEMENTBoth articular bone ends are replaced by prosthetic implants
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Complication :
Osteolysis from acrylic bone cement debris, bone
resorption and subsequent loosening or
fracture,protusio acetabuli.
Post operative sciatic nerve palsy.
Chronic pain.
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Thank you
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HAEMOPHILIC ARTHROPATHY
Manifest:
ACUTE BLEEDING (JOINT, MUSCLE,NERVE)
JOINT DEGENERATION
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Pathology
Haemorrhage (joint) synovial inflamation
synovium thick A vascular pannus on
articular surface and eroded cartilage
develop large cyst release cartilage
degrading enzymes
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Clinical features elbow joints contractures and knees - ankles
deformities recurrent haemarthrosis
chronic synovitis
acute joints or muscles bleeding
chronic arthritis
joint contractures
most in : knees,ankles, elbow, shoulders and hips.
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ACUTE BLEEDING ( JOINT, MUSCLE OR NERVE )
Feature : common in joint
a joint may rapidly fill with blood with trivialinjury .
Pain, warmth, boggy swelling,tenderness andlimited movement
large soft-tissue haematoma Neurologicaldisorder
forearm /leg bleeding potentially rise tocompartment syndrome
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JOINT DEGENERATION
The sequel to repeated bleeding.
Chronic synovitiscartilage degeneration
Arnold and Hilgartner classification :Stage I - soft-tissue swelling;
StageII - osteoporosis and epiphyseal overgrowth;
Stage III- slight narrowing of the articular space and
squaringof the bone ends;
Stage IV- marked narrowing of the
articular space; and Stage V-joint disintegration.
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Treatment
THE ACUTE BLEED
Patient : Recognize the early symptoms of
bleeding
counteract the haemorrhage as soon as
Frozen cryoprecipitate
Fresh-frozen plasma Avoid joint aspiration
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CHRONIC ARTHROPATHY
Prevent to contractures, stiffness and muscleweakness.
Operative treatment :
tendon lengthening
osteotomy
arthrodesis
Synovectomy
total hip replacement
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NEUROPATHIC JOINT DISEASE (CHARCOT'S DISEASE)
Charcot, in 1868, described a type of destructivearthropathy associated with disease of CNS arising fromloss of pain sensibility and position sense.
causes : neurosyphilis syringomyelia multiple sclerosis,myelomeningocele, spinal cord compression, peripheralneuritis, leprosy and congenital indifference to pain.
The early changes are similar to those of OA However, itsoon becomes apparent that this is a rapidly destructiveprocess; the articular surface breaks up, fragments of boneand cartilage appear in the joint or embedded in the
synovium and there is thickening of the synovial membraneand marked joint effusion. In the late stages, there iscomplete loss of articular cartilage, fragmentation of thesubchondral bone and joint subluxation
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Clinical features
complains : weakness, instability, swelling, laxityand progressive deformity of the joint
X-rays
articular space thinning
Osteophyte formation.
Joint swelling
Intra articular calcification gross erosion of the articular surfaces
joint displacement
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Charcot's disease
The vertebrae are distorted and dense, the buttocks show the radio-opaque remains of
former injections; the knee,elbow and hip joints look grotesque. Morah'lf it's bizarre,
do a WR'. Note also the happy smile (though not all Charcot joints are tabetic, nor are
they always painless).
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Treatment
No way of halting the destructive process.
Conservative treatment
Splintage of the unstable joint.
Analgesic medication.
Weightbearing joints
Arthrodesis