5 osteoarthritis alwee

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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

5 osteoarthritis alwee

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