SRI KALABYRAVESHWARA SWAMY AYURVEDIC MEDICAL

COLLEDGE,HOSPITAL& RESEARCH CENTRE, BANGALORE.

OSTEO-ARTHRITIS

GUIDED BY;- DR MANJUNATH ADIGA

PRESENTED BY ;- SK TAJUDDIN UL HAQ
 CONTENTS
• INTRODUCTION
• SIGN & SYMPTOMS
• HISTORY
• PATHO PHYSIOLOGY
• PAIN MECHANISM IN OA
• ETILOGY
• PROGNOSIS
• DIAGNOSIS
• INVESTIGATION
• TREATMENT
• PREVENTION
INTRODUCTION
• Osteoarthritis is the most common type of joint disease.
• It is leading cause of chronic disability in older adults .
• It can be thought of as a degenerative disorder arising from the bio-
chemical break down of articular (hyaline) cartilage in the synovial joints
• How ever the current view holds the osteo arthritis involves not only the
articular cartilage but the entire joint organ including the sub chondrial
bone and synovium
 AP RADIO GRAPH OF THE HIP REVEALS SEVERE
SUPERIOR MIGRATION OF THE FEMORAL HEAD
(WHICH REFLECTS LOSS OF ARTICULAR
CARTILAGE MILD FLATTENING OF THE SUPERIOR
OF THE FEMORAL HEAD IS PRESENT
 SIGNS AND SYMPTOMS
• deep/ achy joint pain exacerbated by extensive use
• Reduced range of motion and crepitus
• Stiffness during rest (morning joint stiffness usually lasting for less than 30
minutes
• Dip joints are most often affected
• Pip joints and the carpometacarpal joints at the base of the thumb are
thYpically invovLed
• Heberden nodes which represents palpable osteophytes in dip joints are
most characteristic in women than in men
HISTORY
The progression of OA is characteristically slow, occurring over several
years .over the period the patient can become less and less active and
thus more susceptible to morbidities related to decreased physical acitivity
The joints may appear normal. how ever the patient gait may be antalgic if
weight bearing joints are involved
pain is usually the initial source of morbidity in OA with the primary symptom
is deep achy joint pain exacerbated by extensive use.
 PATHO PHYSILOGYY
• THE PRIMARY & SECONDARY OA are not separate on a pathologic basis
through bilateral symmetry is often seen in cases of primary oa particularly
when affected hands
• OA was thought to primarily the articular cartilage of synovial joints
,pathophysiologic changes are also known to occur in the synovial fluid as
well underlying (sub chondral)bone the overlying joint capsule and other
tissue
• In early OA, swelling of the cartilage usually occurs because of the increased
synthesis of proteoglycans this reflects an efforts by the chondrocytes to
repair cartilage damage is characterised by hypertropic repair of articular
cartilage
PAIN MECHANISM IN OA
Osteophytic periosteal elevation
Vascular congestion
Synovitis
Synovial membrane nociceptors
fatigue in muscles that cross the joint
inflammation of peri articular bursae
Psychological factors
Central pain sensitization
 ETIOLOGY
• Age
• Obesity
• Trauma
• Genetics
• Reduced level of sex hormones
• Muscle weakness
• Infection
• Crystal deposition
• Acromegaly
• Previous inf arthritis( eg burnt out rheumatoid arthritis)
• Heritable metabolic causes (eg alkap tonuria, hemochromatosis)
• Neuropathic disorders leading to a charcot joint (syringomyelia,tabes
dorsalis & diabetes)
• Dis order of bone (eg paget disease ans avascular necrosis)
• Previous Surgical procedures( eg meniscetomy)
 PROGNOSIS
• The prognosis in pt with OA depends on the joints invoved and on the
severity of the condition
• Older age
• Higher bmi
• Varus deformity
• Multiple involved joints
 PROGRESSION OF OA
• The etiopathogenesis of oa has been divided into 3 stages
• Stage1;- proteolytic break down of the cartilage matrix occurs’
• Stage 2;- fibrillation and erosion of the cartilage surface develop, with sub
sequent release of proteoglycan and collagen fragments into the synovial
fluid
• Stage 3;- breakdown products of cartilage induce a chronic inflammatory
resonse in the synovium , which in turn contributes to further cartilage
breakdown
 DIAGNOSIS
• Systemic inflammation (elevated erythrocyte sedimentation rate (esr) or c-
reactive protein level
• Positive serologies ( RF factor) or anti cyclic citrullinated peptide (anti
ccp)antibodies
• Inflammatory joint fluid with a predominance of polymorphonuclear
leukocytes
• Elevated white blood cell count
 INV >>>>>>>>PLAIN
RADIOGRAPHY

OA of right hip,including the

findings of sclerosis atsuperior
aspect of the acetabulum
OA OF PREVIOUS TRAUMA
 MRI,CT,&ULTRASONOGRAPHY
• MRI:--can depict many of the same characteristics of oa that plain
radiography can, but it is not necessary is most in most
patient.MRI..INCLUDES joint narrowing ,subchondral osseous
changes,&osteophytes.mri can directly visualize articular caritilage and
other joint tissue
• CT:- diagnosis of pri oa .it may be used in the diagnosis of malalignment of
the patellofemoral joint or foot & ankle
• USG:-no role in the routine clincal assessment of the patient.it can be used
for guided injections of joints not easily accessed with out imaging.
 EXAMINATION OF KNEE

• Inspection
• --- gait
• ---muscle wasting (QUADRICEPS)
• ---JOINT IS SWOLLEN
• NO REDNESS
• NO DISCOLOURED
• ANY EVERSION
 PALPITATION
• MIN/NO JOINT EFFUSION (PATELLA TAP)
• CHECK FOR TENDERNESS
• SYNOVIAL MEMBRANE NOT THICKENED
• PROTUBERANT (OSEOPHYTES) AT THE EDGE OF ARTICULAR CARTILAGE

• RANGE OF MOTION TESTING

• ACTIVELY (PATIENT PERFORMS)
• PASSIVELY(CLINICIan performs)
 LIGAMENT STRESS TESTS:_--
• LACHMAN TEST
• ANTERIOR DRAWER
• PIVOT SHIFT
• VALGUS STRESS
• VARUS STRESS
• SAG SIGN
• POSTERIOR DRAWER
• MCMURRAY TEST
• THESSALY TEST
 PHARMACOLOGIC TREATMENT

HAND OA Knee OA
EVALUATE THE ABILITY TO PERFORM LAND BASED EXERCISE AND STRENGTH ACTAMINOPHEN
ACTIVITIES OF DAILY LIVING TAINING
OPIOIDS
Joint protection technique AQUATIC EXERCISE
PAIN PATCHES
Instruct of use of thermal modalities SELF MANGAEMENT
INTRA ARTICULAR CORTICOSTEROIDS
Provide splints for patients with WEIGHT MANAGEMENT INJECTIONS
trapeziometacarpal joint oa
NSAIDS GROWTH FACTORE INJ/PLATELET RICH
Non steroidal anti inflammatory drugs PLASMA
including trolamine salicylate MANUAL THREAPY
INTRA ARTICULAR HYALURONIC ACID
tramadol LATERALLY DIRECTED PATELLAR
TAPING GLUCOSAMINE/CHONDROITIN
SULFATE / HYDROCHLORIDE
 HIP OA
• CARDIOVASCULAR/RESISTANCE LAND BASED EXERCISE
• AQUATIC EXERCISE
• THERMAL AGENTS
• ACETAMINOPHEN
• ORAL NSAIDS
• TRAMADOL
• INTRA ARTICULAR CORTICO STEROID INJECTIONS
 SURGERY;ARTHOSCOPIC SURGICAL TECHNIQUE IS RECOMMENDED FOR
CLEANING OF THE KNEE IN OA

View of a torn Removal of

meniscus loose
before(top) and fragements
after (bottom) of articular
removal of loose and
meniscal fragments meniscal
cartilage
 ARTHROPLASTY;;-THE SURGICAL REMOVAL OF
JOINT SURFACE AND THE INSERTION OFA METAL
AND PLASTIC PROSTHESIS

Ap of
radiograph
knee
replacement
in 1 knee & Ap radiography
arthritis in of the pelvis and
other medial hips shown an
joint spaces arthritic hip not
narrowing treated surgical
and and total hip
subchondral replacement
sclerosis
 PREVENTION
• Over weight patient is early sign of oa
• Strengthening exercise
• Life style modification
• Physical/occupational therapy
• Non pharamacologic measures
• Low vitamin D
 Thank
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