This document discusses diseases of the joints, focusing on osteoarthritis and rheumatoid arthritis. It defines osteoarthritis as the most common form of chronic joint disorder, characterized by progressive degeneration of cartilage over years, especially in weight-bearing joints. It then describes the types and pathogenesis of osteoarthritis, including primary osteoarthritis which occurs in the elderly due to wear and tear, and secondary osteoarthritis which results from previous joint injuries or inflammation. The document also defines rheumatoid arthritis as a chronic inflammatory disease of unknown cause affecting mainly the hands and feet. It involves persistent symmetric polyarthritis and may result in joint destruction over time. The pathogenesis involves genetic susceptibility and an autoimmune reaction triggering synovial hypertrophy and chronic inflammation. Both

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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10. 10
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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