3. ANATOMY AND PHYSIOLOGY OF THE JOINT
• A synovial (diarthrodial) joint includes the articular cartilage
of adjacent bones; an inner synovial membrane (synovium);
an outer ligamentous capsule; and, in the normal situation, a
small amount of synovial fluid (<2 mL, even in large joints)
• The joint capsule and associated ligaments are composed
primarily of type I collagen.
• Their functions are to contain the adjacent bones in a
defined relationship to one another, and to constrain
abnormal motion. Synovium inserts at the cartilage-bone
junction; however, folds of synovial tissue extend beyond this
site.
4.
5. Normal Cartilage
• Avascular, alymphatic and aneural tissue
• Smooth and resilient
• Allows shearing and compressive forces to be
dissipated uniformly across the joint
6.
7.
8. Synovial joint
• Articular cartilage is a highly effective tissue that
provides pain-free movement with load bearing. The
very smooth, almost frictionless motion of normal
joints is put in perspective by comparison of the
significantly lower coefficient of friction of normal
articular cartilage (range, 0.003-0.006) .
• Articular cartilage is avascular and receives its
nutrition by diffusion from synovial fluid.
• Because articular cartilage is not innervated, arthritic
pain is secondary to activation of stress receptors in
the capsule and other periarticular structures.
9. Cont..
• Normal hyaline cartilage is a matrix of proteoglycan aggregates, type II collagen, and
interspersed chondrocytes. Similar to other soft tissues, cartilage comprises mostly water
(80% of wet weight); however, in contrast to other soft tissues, cartilage is a turgid gel
and is remarkably firm.
• The large proteoglycan aggregates consist of proteoglycan aggrecan molecules bound by
link protein to hyaluronate, an unsulfated glycosaminoglycan.
• The aggrecan molecules include a central protein core and radiating glycosaminoglycan
chains of chondroitin-4-sulfate, chondroitin-6-sulfate, and keratan sulfate.
• The proteoglycan aggregates, buttressed by collagen bundles, are responsible for the
compressive strength and load-absorbing properties of cartilage. The hydrophilic nature
and high density of negative charges on the glycosaminoglycan chains are key to articular
cartilage resilience when tissue pressures may be as great as 3 atmospheres
10. Cont..
• Loss of proteoglycans characterizes the early stages of a number of
arthritic diseases. As this happens, the cartilage loses its resilience,
and the resultant softening promotes further degeneration of the
proteoglycan aggregate, as well as changes in the subchondral bone.
• Type II collagen is found only in hyaline cartilage, and its
characteristic triple-helix formation of three identical peptide chains
provides tensile strength to the cartilage surface. Tensile properties
of the collagen fibers provide a counterbalancing force that
neutralizes and contains the expansile tendency of the proteoglycan
aggregates and resulting oncotic pressure.
• The minor collagens that are found in articular cartilage (types V, VI,
IX, X, and XI) contribute to matrix assembly, and their dysfunction
likely plays a role in osteoarthritic disease
11. Synovium and Synovial fluid
• The interior surface of the capsule is lined by a thin membrane, the synovium,
which is richly supplied with blood vessels, lymphatics and nerves.
• It provides a nonadherent covering for the articular surfaces and it produces
synovial fluid, a viscous plasma dialysate laced with hyaluronan.
• This fluid nourishes the avascular articular cartilage, plays an important part in
reducing friction during movement and has slight adhesive properties which assist
in maintaining joint stability.
• In normal life the volume of synovial fluid in any particular joint remains fairly
constant, regardless of movement. When a joint is injured fluid increases (as in
any bruised or oedematous connective tissue) and this appears as a joint effusion.
Synovium is also the target tissue in joint infections and autoimmune disorders
such as rheumatoid arthritis.
12. Cont..
• Synovial fluid is essentially a transudate of serum. Its purpose is joint lubrication
and nourishment of articular cartilage.
• The superficial synovial capillaries constitute an extensive fenestrated network
that facilitates rapid exchange of small solutes and water.
• To nourish articular cartilage, molecules leaving the synovial capillaries traverse
the loosely meshed synovial tissue, the synovial fluid, and the layers of cartilage
matrix.
• Intermittent cartilage compression and release provides for imbibition of synovial
fluid into the cartilage interstitial fluid.
• Synovial fluid is the lubricant for fluid film lubrication, which is the primary
means of joint lubrication. However, under high loads or with long duration of
contact, boundary lubrication adds a monolayer of lubricating glycoproteins to
augment fluid film mechanics
13.
14.
15. Osteoarthritis
• Morphologic, biochemical, molecular and biomechanical
changes of both cells and matrix which lead to softening,
fibrillation, ulceration, and loss of articular cartilage, sclerosis
and eburnation of subchondral bone, osteophytes, and
subchondral cysts
(American Academy of Orthopaedic Surgeons and the National
Institutes of Health).
• A heterogenous group of conditions that lead to joint symptoms
and signs which are associated with defective integrity of
articular cartilage, in addition to related changes in the
underlying bone at the joint margins
(American College of Rheumatology [ACR]).
16. Osteoarthritis
• Osteoarthritis (OA) is a chronic disorder of synovial
joints in which there is progressive softening and
disintegration of articular cartilage accompanied
by new growth of cartilage and bone at the joint
margins (osteophytes), cyst formation and sclerosis
in the subchondral bone, mild synovitis and
capsular fibrosis.
• It differs from simple wear and tear in that it is
asymmetrically distributed, often localized to only
one part of a joint and often associated with
abnormal loading rather than frictional wear
17.
18. RISK FACTOR ( NON MODIFIABLE)
• gender
• females >males
• increased age
• genetics
• race
• African American males are the least likely to
receive total joint replacement when compared to
whites and Hispanics
19. RISK FACTOR (MODIFIABLE)
• articular trauma
• occupation, repetitive knee bending
• muscle weakness
• large body mass
• metabolic syndrome
20. Pathologic lesions
• Primary lesion appears to occur in cartilage
• Leads to inflammation in synovium
• Changes in subchondral bone, ligaments,
capsule, synovial membrane and periarticular
muscles
22. OA cartilage
• The equilibrium between anabolism and
catabolism is weighted in favor of degradation
• Disruption of the integrity of the collagen
network as occurs early in OA allows
hyperhydration and reduces stiffness of
cartilage
23.
24. PATOPHYSIOLOGY OA
Proteolytic enzymes
•matrix metalloproteases (MMPs)
•responsible for cartilage matrix digestion
•examples
•stromelysin
•plasmin
•aggrecanase-1 (ADAMTS-4)
•Tissue inhibitors of MMPS (TIMPs)
•control MMP activity preventing excessive degradation
•imbalance between MMPs and TIMPs has been demonstrated in OA tissue
•Inflammatory cytokines
•secreted by synoviocytes and increase MMP synthesis
•examples
•IL-1
•IL-6
•TNF-alpha
25. Pathogenesis of OA
(Moskowitz RW, 1999)
Biomechanical
ChondrocyteMatrix
degradation
OA
Matrix
synthesis
•Cytokine
•Enzymes
•Nitric oxide
Loss of matrix integrityGenetic Metabolic
IGF-1
TGF-1
50. Conclusions
• Primary etiology of OA remains undetermined
• Believed that cartilage integrity is maintained
by a balance obtained from cytokine driven-
driven anabolic and catabolic processes
• Treatment is based on the stage of the
disease, whether conservartive or operative.
