Osteoarthritis.pdf

If you’re a medical student in your orthopedic or rheumatology rotation, this could help, good luck.

1. OSTEOARTHRITIS “OSTEOARTHROSIS”

2. THE OBJECTS OF THE LECTURE:
1.Definition
2.Cause
3.Pathology
4.Risk factors
5.Clinical features
6.X-Rays
7.Treatments

3. Suture
JOINT:Is the meeting between 2 bones or more.
This classification of joints is according to the
material which fill the gab between the bones
Intervertebral discsEpiphyseal plate
TMJ, acromioclavicular joint, Shoulder
joint Elbow, radioulnar joint, wrist,
carpometacarpal joint of the thumb, Hip
joint and knee.

4. -Osteoarthritisinvolves primarily the synovial joints which are found in (Hips, Knees and fingers) Which
each bone is covered by articular cartilage “Collagen type II” and laterally we have synovial membrane.
“Synovium” which secretes the synovial fluid to fill the synovial cavity which one of its components
Hyaluronic acid and that is the typical structure of synovial joint.
Osteoarthritis(OA) is the most common
degenerative chronic joint disorder
in which there is progressive softening and
disintegration of articular cartilage accompanied
by new growth of cartilage and bone at the joint
margins (osteophytes), and capsular fibrosis.
It
is defined as primary when no cause is
obvious,
and secondary when it follows a
demonstrable abnormality.

5. -The most obvious feature of OA is that it increases in frequency with age. This does
not mean that it is an expression of senescence; it simply shows that OA takes many
years to develop. To be sure, cartilage ageing does occur, resulting in splitting and
flaking of the surface, but these changes are not progressive and they do not cause
symptomatic arthritis.
1.OAresults from a disparity between the stress
applied to articular cartilage and the ability of the
cartilage to withstand that stress. This could be
due to one or a combination of two processes: (1)
weakeningof the articular cartilage (possibly due to
genetic defects in type II collagen or to enzymatic
activity in certain inflammatory disorders such as
rheumatoid disease); and (2) increasedmechanical
stressin some part of the articular surface.
Idiopathic in 80% of cases (Primary OA)
EXAMPLES OF Extra stress on joints
can be risk factor of OA? Deformities,
Obesity Excessive use of joints e.g.
handsin typists especially the DIP
“Bouchard’s” and PIP “Heberden” nodes
-shoulderin basketball players
Diseases affecting the cartilage such as
Hemochromatosis which is the
deposition of iron in cartilage leading
to degenerate it. (Rare)

6. Increased
stress on
some parts of
the articular
surface
Inflammatory
disorder which
weakness the
cartilage and
renders it
unable to bear
even normal
loads
Abnormality
(defects) of
subarticular
bone leads to
stress
concentratio
n at
particular
sites

7. Defect in chondrocytes response to biochemical and mechanical stresses resulting in breakdown of
the matrix leading to injury in the articular cartilage SO, it is false response to the stress, it is releasing
inflammatory mediators, IL’s, more matrix and proteases, but the degradation exceeds synthesis
so ending with breaking-down of the chondrocytes.
The prevalence of OA increases
expoenetillay beyond the age of 50,
and about 40% of people older than
70 are affected.
5% occur in younger individuals due to: joint
deformity a previous joint injury or an underlying
disease such as DM, hemochromatosis and obesity
Knees and hands in female
Hips joint in males.
The joints commonly involved
are cervical and lower lumbar
vertebrae, PIP, DIP, 1
st
carpometacarpal joint and 1
st
tarsometatarsal joint

8. Small fractures through the articulating bone are
common and the fracture gaps allow synovial fluid to
be subchondral cyst
SO releasing of the cytokines
motivate the inflammation process so
it is calling Osteoarthritis.
The earliest morphological change is
softening of the articular cartilage. The
normal smooth and glistening surface
becomesfrayed and fibrillated, and
eventually it is worn away to expose
the underlying bone

10. 1.Occupation: there is good evidence of an association between OA and certain
occupation which cause repetitive stress, for example OA of the knees in workers
engaged in continuous knee-bending activities.
1.Trauma: fractures involving the articular surface are obvious precursors of secondary OA;
so too are lesser injuries which result in joint instability.
1.Joint dysplasia: disorders such as congenital acetabular dysplasia, Perthes’ disease and
slipped upper femoral epiphysis presage a greater than normal risk of OA in later life.
Minor degrees of dysplasia are often asymptomatic and are spotted only later in life when
OA starts to develop.
1.Family history: women whose mothers had generalized OA are more likely to develop the
same condition. The particular trait responsible for this is not known.

11. -Patients with primary OA are often asymptomatic until they are in their 50s
-Deep dull “achy” pain that worsens with use and relieved by rest
-Morning stiffness
-Crepitus “Can be listened by stethoscope” or by examination feeling crackling or grinding
-Limitation of range of movement
-Spinal roots compression by osteophytes may occur with radicular pain, muscle spasm,
atrophy and neurological deficits
-Swelling, deformity, tenderness and muscle wasting are features of advanced disease.
-The ankylosing “effusion of the bones” doesn’t occur in OA “
Varus deformity of the right knee due to OA
medially

12. Heberden nodes in DIPBouchrad’s nodes in PIP
Spinal root compression
Crepitus

13. The characteristic changes of OA on X-RAY are:
1.Narrowing of the joint space due to cartilage depletion
2.Subarticularcyst formation and sclerosis
3.Osteophyte formation
4.Initially the first two features are restricted to the major loadbearingpart of the joint, but in
Late cases the entire joint is affected
5.Evidence of previous disorders (congenital defects, old fractures, rheumatoid arthritis) may be
present
spurs, lipping or
osteophytes
Narrowing of
joint space
Subarticular sclerosis

14. There are three principles in the treatment of early OA:
(1)relieve pain
(2)increase movement
(3)reduce load
Pain relief is achieved by analgesics and nonsteroidal
anti-inflammatory drugs (NSAIDs). Rest
periods and modification of activities may also
be necessary. NSAIDs are powerful
prostaglandin inhibitors, which reduce the
vascular congestion
in the subchondral bone. Unfortunately they
have a serious drawback: they cause
gastrointestinal irritation and in some patients
this leads to ulceration and bleeding. NSAIDs
should be used only under medical supervision
Joint mobility can often be improved by
physiotherapy; even a small increase in
range and
power will reduce pain and improve function
Load reduction can be achieved by using a
walking stick, wearing soft-soled shoes, avoiding
prolonged, stressful activity and by weight
reduction
CONSERVATIVE TREATMENT

15. joint debridement which is meaning removal of interfering osteophytes, cartilage tags and
loose bodies can be performed arthroscopically.
Joint replacement “Arthroplasty” in one form or another, is now the procedure of choice
for OA in patients with severe symptoms, marked loss of function and significant restriction of daily
activities. For OA of the hip and knee in middle-aged and older patients, total joint replacement by
modern techniques promises improvement lasting for 15 years or longer, but techniques are
improving year by year.
Arthrodesis is
sometimes indicated for
joints in
which permanent
stiffness is not a
drawback

16. THANK YOU ALL
DONE BY: Ghaidaa Al-Sarayreh
THANK YOU
DONE BY: Ghaidaa Al-Sarayreh