Musculoskeletal system: rheumatoid and osteoarthritis

1. Musculo-skeletal System III
Associate Prof.
PhD (UK), MD(Egypt)

2. DISEASES OF THE JOINTS

3. Osteoarthritis

4.  Definition: Osteoarthritis (OA) (also called
osteoarthrosis or degenerative joint disease)
is the most common form of chronic disorders
of synovial joints.
 It is characterised by progressive
degenerative changes in the articular
cartilages, over years, particularly in weight-
bearing joints.
Osteoarthritis

5.  Types and Pathogenesis of OA:
I- Primary Osteoarthritis (OA):
II- Secondary Osteoarthritis (OA):
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6. I-Primary Osteoarthritis (OA):
 Occurs in the elderly
 More commonly in women than in men.
 The process begins by the end of 4th decade
and then progressively and steadily increases
producing clinical symptoms.
 Wear and tear with repeated minimal trauma,
heredity, obesity, aging per se, all contribute to
focal degenerative changes in the articular
cartilage of the joints.
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7. II- Secondary Osteoarthritis (OA):
 May appear at any age
 It is the result of any previous wear and tear
phenomena involving the joint such as
previous injury, fracture, inflammation, loose
bodies and congenital dislocation of the hip.
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8.  Pathologic changes:
 Occur in the articular cartilages, adjacent
bones and synovium.
 1. Articular cartilages: The changes are
most marked in the weight bearing regions of
articular cartilages. Initially, there is loss of
cartilaginous matrix (proteoglycans)
 2. Bone: The sub-chondral bone (which is
stripped of covering by cartilage) appears like
polished (smooth) ivory.
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9.  3.The death of superficial osteocytes and
↑osteoclastic activity cause: rarefaction,
microcyst formation and occasionally
microfractures of the bone.
 4. Osteophyte or spur (projection)
formation. Osteophytes are outgrowths at
the joint margins.
 5. Synovium: Initially, there are no
pathologic changes in the synovium. In
advanced cases, there is low-grade chronic
synovitis and villous hypeplasia.
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Osteoarthritis

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Osteoarthritis
Typical hand deformities. Heberdens’s nodes are seen on the distal
interphalngeal joints & Bouchard’s nodes on the proximal ones.

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Osteoarthritis

13. Rheumatoid Arthritis (RA)
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14. Rheumatoid Arthritis (RA)
 Definition & Background:
 Rheumatoid arthritis (RA) is a chronic multi-
system inflammatory disease of unknown
cause.
 The hallmark feature of this condition is
persistent symmetric polyarthritis that affects
mainly the hands and feet, although any joint
lined by a synovial membrane may be
involved.
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15.  The severity of RA may fluctuate (rise & fall
irregularly) over time, but chronic RA most
commonly results in the progressive
development of various degrees of joint
destruction, deformity, and a significant
decline in functional status.
 Extra-articular involvement of organs such as
the skin, heart, lungs, and eyes can be
significant.
 The presence of anti-cyclic citrullinated
protein antibody (ACPA) and rheumatoid
factor (RF) are highly specific for this
condition. 15

16.  Aetiology:
 The cause of RA is unknown.
 Genetic, environmental, hormonal,
immunologic, and infectious factors may play
significant roles.
 Socioeconomic, psychological, and lifestyle
factors (e.g., tobacco smoking) may influence
disease outcome.
 Incidence & gender:
 RA is a common disease having peak
incidence in 3rd to 4th decades
 There is 3-5 times higher preponderance in
females. 16

17.  Pathogenesis:
 The pathogenesis of RA is not completely
understood.
 An external trigger (e.g., cigarette smoking,
infection, or trauma) causes an autoimmune
reaction, leading to synovial hypertrophy
and chronic joint inflammation along with
the potential for extra-articular
manifestations, is theorized to occur in
genetically susceptible individuals.
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18.  Genetic factors and immune system
abnormalities contribute to disease
propagation.
 CD4 T cells, mononuclear phagocytes,
fibroblasts, osteoclasts, and neutrophils play
major cellular roles in the patho-physiology of
RA, whereas B cells produce autoantibodies
(ie, RFs).
 Abnormal production of numerous cytokines,
chemokines, and other inflammatory
mediators has been demonstrated in patients
with RA.
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19.  The articular lesions include: Uncontrolled
inflammation, pannus formation, synovial
membrane thickenening and destruction of
various tissues (including cartilage, bone,
tendons, ligaments, and blood vessels).
 Systemic manifestations, are seen in
some organs, in the form of nonspecific
inflammation in the vessels (acute
vasculitis) & rheumatoid nodules.
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20.  Pathologic changes:
1. Articular lesions:
A. RA involves first the peripheral small joints of hands and feet
in the form of symmetrical polyarthritis then affects the Joints
of wrists, elbows, ankles and knees. The proximal inter-
phalangeal and metacarpo-phalangeal joints are more
affected. The involved joints ’re swollen, painful & stiff.
B. Chronic inflammation of synovial membrane & thickenening:
there is hyperplasic villous projections of the membrane..
C. Pannus formation: Excessive formation of granulation tissue
which creeps under the cartilage over the eroded bone &
also over the articular cartilage stimulating fibrous ankylosis.
D. Articular cartilage is destroyed which is followed by fibrous or
bony ankylosis.
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Rheumatoid Arthritis (RA)

22. 2. Extra-articular lesions:
 It is seen in some organs like lungs,
pleura, pericardium, myocardium, lymph
nodes, eyes & peripheral nerves.
 One of the characteristic extra-articular
manifestations of RA is occurrence of
rheumatoid nodules in the skin.
Microscopically, the nodules are formed of
Fibrinoid necrosis surrounded by
Histeocytes.
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23.  RA in certain age groups
 Felty's Syndrome: RA occurs in older age
which is accompanied by splenomegally and
pancytopenia.
 Still's diseas: Juvenile RA occurs in young
patients under the age of 16 years. It is
characterized by acute onset, hi fever,
leucocytosis, splenomegally and skin rash.
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24.  Diagnosis:
 No test results are pathognomonic; instead, the
diagnosis is made by using a combination of
clinical, laboratory, and imaging features.
Potentially useful laboratory studies in suspected
RA include the following:
• 1. Erythrocyte sedimentation rate
• 2. C-reactive protein level
• 3. Complete blood count
• 4. Rheumatoid factor assay
• 5. Antinuclear antibody assay
• 6. Anti−cyclic citrullinated peptide and
anti−mutated citrullinated vimentin assays 24

25.  8. Potentially useful imaging modalities include the
following:
 Radiography (first choice): Hands, wrists, knees,
feet, elbows, shoulders, hips, cervical spine, and
other joints as indicated
 Magnetic resonance imaging MRI: Primarily cervical
spine
 Ultrasonography of joints: Joints, as well as tendon
sheaths, changes and degree of vascularization of
the synovial membrane, and even erosions
 9. Joint aspiration and analysis of synovial fluid may
be considered, including the following: Gram stain,
Cell count, Culture
 10. Assessment of overall appearance
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