This document discusses a presentation by Dr. Sagal Omar's group on osteoarthritis and ganglion cysts. It provides details on the pathogenesis, morphology, clinical course, and treatment of osteoarthritis. It describes osteoarthritis as a degenerative joint disease characterized by cartilage breakdown. Ganglion cysts are also discussed, noting they are fluid-filled sacs near joints that lack a cell lining. The document contrasts ganglion cysts with synovial cysts which communicate with joints.

1. Instructor : Dr. Sagal Omar
Group : four
Presentation : Osteoarthritis/Ganglion cyst.

2. Osteoarthritis
Osteoarthritis (OA) also called degenerative joint
disease is characterized by degeneration of cartilage
that results in structural and functional failure of
synovial joints.
It is the most common disease of joints.
Although the term osteoarthritis implies an
inflammatory disease, it is considered an intrinsic
disorder of cartilage in which chondrocytes respond
to biochemical and mechanical stresses resulting in
the breakdown of the matrix and failure of its repair.

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 In most instances OA appears insidiously without
apparent initiating cause (idiopathic or primary
osteoarthritis).
 In about 5% of cases, Osteoarthritis appears in younger
individuals with some predisposing condition, such as
joint deformity, a previous joint injury or an underlying
systemic disease that places joints at risk.
 In these settings the disease is called secondary
osteoarthritis.
 The prevalence of OA increases exponentially beyond
the age of 50, and about 40% of people older than 70
are affected.

4. Pathogenesis
 The lesions of OA stem from degeneration of the articular
cartilage and its disordered repair. Articular cartilage
serves as a low-friction surface that transmits loads to the
underlying bone.
 Cartilage resists compression through the viscoelastic
properties of the extracellular matrix (principally type II
collagen, proteoglycans and water) secreted by
chondrocytes.
 Repeated biomechanical stress contributes to development
of OA, but genetic factors, including genes encoding
components of the matrix and signaling molecules, also
play a role.

5. MORPHOLOGY
 In the early stages of OA, chondrocytes proliferate,
forming clusters. This manifests as a granular soft articular
surface. Eventually, full thickness portions of the cartilage
are sloughed.
 Outgrowths (osteophytes) develop at the margins of the
articular surface and are capped by fibrocartilage and
hyaline cartilage that gradually ossify.
 The exposed subchondral bone plate becomes the new
articular surface and friction with the opposing surface
burnishes the exposed bone, giving it the appearance of
polished ivory (bone eburnation).

8. Clinical Course
Characteristic symptoms include
 Joint pain that worsens with use,
 Morning stiffness,
 Crepitus, and limitation of range of movement.
 Impingement on spinal foramina by osteophytes results
in cervical and lumbar nerve root compression and
radicular pain, muscle spasms, muscle atrophy, and
neurologic deficits.

11. Therapeutic uses
 Management of pain,
 NSAIDs to reduce inflammation,
 Intra-articular corticosteroids,
 Activity modification,
 Severe cases, arthroplasty.

12. Ganglion and Synovial Cysts
 A ganglion is a small (1–1.5 cm) cyst that is almost
always located near a joint capsule or tendon sheath.
 A common location is around the joints of the wrist,
where it appears as a firm, fluctuant, pea-sized
translucent nodule.
 It arises as a result of cystic or myxoid degeneration of
connective tissue; hence the cyst wall lacks a cell
lining.
 The lesion may be multilocular and enlarges through
coalescence of adjacent areas of myxoid change.

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 The fluid that fills the cyst is similar to synovial fluid,
however, there is no communication with the joint space.
 Despite the name, the lesion is unrelated to ganglia of the
nervous system.
 Herniation of synovium through a joint capsule or massive
enlargement of a bursa may produce a synovial cyst.
 A well-recognized example is the synovial cyst that forms
in the popliteal space in the setting of RA or OA (Baker
cyst).
 The synovial lining may be hyperplastic and contain
inflammatory cells and fibrin.