structure of articular cartilage

ARTICULAR CARTILAGE

Applied anatomy

Articular cartilage is a specialized connective tissue

covering joint surfaces. Macroscopically, it has a
glistening, white appearance. Microscopically, it is
composed of water, collagen, proteoglycans,
chondrocytes and other matrix proteins and lipids.
It is avascular and alymphatic and is sheltered from
the immune system .

It also has no nerve supply and is therefore not

sensitive to early injuries. It also has poor repair
properties, because there are relatively few cells in
the tissue, the metabolic rate is low, and the
capacity of chondrocytes to divide and migrate in
the articular cartilage is restricted by the matrix
fibres. As a consequence, it is generally agreed that
articular cartilage does not repair significantly after
injury to the collagen mesh.

Structure & importance of tide-mark

Articular cartilage has been subdivided into five zones depending on the alignment of collagen
fibers, which give each zone particular biomechanical advantages:

1. Superficial zone - resistant to shear due to tangential arrangement. Low metabolic

activity and hence low healing potential.
2. Transitional (middle) zone - resistant to compression, high concentration of collagen
obliquely arranged at right angles to each other.
3. Radial (deep) zone - resistant to compression, This zone contains the largest-diameter
collagen fibrils, the highest concentration of proteoglycans, and the lowest concentration of
water. Cells are arranged in columns.
4. Tidemark - resistant to shear. Changes of the tidemark were found to be multiform and
metabolically active in the osteoarthritic process. Endochondral ossification depletes the
structure of articular cartilage

calcified cartilage at the cartilage/bone interface and the tidemark has been thought of as
a calcification front advancing in the direction of non-calcified cartilage. Duplication of the
tidemark is cited as evidence of this advancement.

Reestablishment of the tide mark is inconsistent in most cartilage repair techniques. In the
adult, there is heavy deposition of apatites in the calcified zone, which prevents diffusion
of nutrients across the tide-mark.The calcified zone also functions as an efficient barrier to
cellular invasion. This may explain the apparent immunity of cartilage transplants to the
allograft rejection process.
5. Calcified zone - acts as an anchor between articular cartilage and subchondral bone

Composition

Chondrocytes

Chondrocytes are highly

specialized mesenchymal
cells that are responsible for
the production of the
structural components of
articular cartilage including
collagen, proteoglycans and
other matrix proteins and
lipids.

They are located in lacunae,

usually scattered individually
throughout articular
cartilage. During growth of
the articular cartilage,
chondrocytes have a
constant, usually roundish
shape, but their shape
becomes more variable
depending on age, pathological state and the cartilaginous layer to which they correspond.
Chondrocytes are anaerobic, and receive their nutrition via diffusion of substances within synovial
fluid.

Matrix

Water contributes up to 80% of the wet weight of articular cartilage, and the interaction of water
with the matrix macromolecules significantly influences the mechanical properties of the tissue.

The principal articular cartilage collagen, type II, accounts for 90% to 95% of the cartilage
collagen. They are responsible for the tensile strength.

Proteoglycans are responsible for compressive strength of articular cartilage and are composed of
aggrecan molecules linked to hyaluronic acid to form an aggregate macromolecule. Aggrecan
molecules are composed of a protein core with multiple glycosaminoglycans subunits. The
glycosaminoglycans include chondroitin-4-sulphate, chondroitin-6-sulphate and keratin sulphate.
In ageing, the level of chondroitin-4-sulphate decreases and that of keratin sulphate increases.

Note: Proteoglycans are long chain polysaccharides linked to hyaluronate that are negatively
charged and hold water within the cartilage by osmotic pressure, thus maintaining the
tension of the collagen mesh. However, if the proteoglycans are damaged by trauma or by
other agents such as enzymes in inflammatory disease or infection then the proteoglycan
structure disintegrates and the water holding capacity is lost, and progressive breakdown of
the collagen meshwork then occurs. This leads to exposure of the bone beneath, causing
severe pain and disability.
structure of articular cartilage

Functions

1. Decrease friction and joint lubrication: The predominant method of lubrication of articular
cartilage during joint motion is elastohydrodynamic lubrication. This occurs when pressure
in the fluid film deforms the articular surface, increasing the surface area and reducing
escape of fluid from between the surfaces as they glide over each other.
2. Load transmission: stiffness to compression and an exceptional ability to distribute loads,
thereby minimizing peak stress on subchondral bone.

Response to injury

Deep lacerations of articular cartilage extending beyond the tidemark heal with fibrocartilage
produced by undifferentiated mesenchymal cells. Superficial lacerations do not heal, although
some proliferation of chondrocytes may occur. Immobilisation of joints leads to atrophy of the
articular cartilage and therefore continuous passive motion is believed to be beneficial to healing.
In arthritic cartilage, chondrocytes are recovered in clusters of up to thirty cells, which probably
represents an attempt at tissue regeneration.

Basic science in repair

Articular cartilage injuries. Buckwalter JA. Clin Orthop Relat Res. 2002 Sep;(402):21-37
University of Iowa Department of Orthopaedics, Iowa City 52242, USA.

The acute and repetitive impact and torsional joint loading that occurs during participation in
sports can damage articular surfaces causing pain, joint dysfunction, and effusions. In some
instances, this articular surface damage leads to progressive joint degeneration. Three classes of
chondral and osteochondral injuries can be identified based on the type of tissue damage and the
repair response:

(1) damage to the joint surface that does not cause visible mechanical disruption of the articular
surface, but does cause chondral damage and may cause subchondral bone injury;

(2) mechanical disruption of the articular surface limited to articular cartilage; and

(3) mechanical disruption of articular cartilage and subchondral bone. In most instances, joints can
repair damage that does not disrupt the articular surface if they are protected from additional
injury.

Mechanical disruption of articular cartilage stimulates chondrocyte synthetic activity, but it rarely
results in repair of the injury. Disruption of subchondral bone stimulates chondral and bony repair,
but it rarely restores an articular surface that duplicates the biologic and mechanical properties of
normal articular cartilage.

In selected patients, surgeons have used operative treatments including penetrating subchondral
bone, soft tissue grafts, and cell transplants and osteochondral autografts and allografts to restore
articular surfaces after chondral injuries. Experimental studies indicate that use of artificial
matrices and growth factors also may promote formation of a new joint surface. However, an
operative treatment of an articular surface injury that will benefit patients must not just provide a
new joint surface, it must produce better long-term joint function than would be expected if the
injury was left untreated or treated by irrigation and debridement alone. Therefore, before
selecting a treatment for a patient with an articular cartilage injury, the surgeon should define the
type of injury and understand its likely natural history.
structure of articular cartilage

Why do we need hyaine cartilage repair tissue?

In fibrocartilage the matrix component is minimal, and the fibrous one greatly predominates. The
chondrocytes are less numerous and much more widely separated than in other types, but most of
them are still enclosed in lacunae. Repair tissue that fills osteochondral defects is less stiff and
more permeable than normal articular cartilage, and the orientation and organization of the
collagen fibrils in even the most hyaline-like chondral repair tissue do not follow the pattern seen
in normal articular cartilage. The decreased stiffness and increased permeability of repair cartilage
matrix may increase loading of the macromolecular framework during joint use and result in
progressive structural damage, thereby exposing the repair chondrocytes to excessive loads that
additionally compromise their ability to restore the matrix. depletion of matrix proteoglycans,
fragmentation and fibrillation, increasing collagen content, and loss of cells with the appearance of
chondrocytes within 1 year or less. The remaining cells often assume the appearance of fibroblasts
as the surrounding matrix comes to consist primarily of densely packed collagen fibrils. This
fibrous tissue usually fragments and often disintegrates, thus leaving areas of exposed bone. The
inferior mechanical properties of chondral repair tissue may be responsible for its frequent
deterioration.

Cartilage in disease

The mechanisms of genetic regulation and degeneration of articular cartilage are important to our
understanding the evolution of many degenerative and traumatic diseases. The available evidence
indicates that normal matrix turnover depends on the ability of chondrocytes to detect alterations
in the macromolecular composition and organization of the matrix, including the presence of
degraded molecules, and to respond by synthesizing appropriate types and amounts of new
molecules. In addition, the matrix acts as a signal transducer for the cells. Loading of the tissue
due to use of the joint creates mechanical, electrical, and physicochemical signals that help to
direct the synthetic and degradative activity of chondrocytes. In arthritis, proteoglycan
degradation is thought to be an early and reversible process, whereas the breakdown of the
collagen network is believed to be irreversible, contributing to loss of joint function.

Changes in OA

 Increased water content

 Reduced proteoglycan concentration
 Reduction in chondrocyte number
 Breakdown of matrix framework

Infection and inflammatory arthritis

Articular cartilage is extremely sensitive to proteolysis induced by contaminant bacteria.

Inflammatory cytokines and tissue-damaging proteinases play important roles in joint destruction
in Rheumatoid Arthritis. The pannus is a sheet of inflammatory granulation tissue that spreads
from the synovial membrane and invades the joint in rheumatoid arthritis.

What happens in Osteochondritis Dissecans and

AVN

Osteochondritis dissecans (OCD) is a relatively

common condition causing knee pain in children
and young adults. It is a condition affecting
subchondral bone that manifests as a pathologic
spectrum. Initially stages have intact articular
surface but softening. This can progress to early
articular cartilage separation, partial detachment
of an articular lesion, and eventually osteochondral
structure of articular cartilage

separation with loose bodies. In the knee potential locations are the lateral aspect of the medial
femoral condyle (75%), the weight-bearing surface of the medial (10%) and lateral femoral
condyles (10%), and the anterior intercondylar groove or patella (5%).

Although the etiology of these lesions is unclear, it is believed that repetitive microtrauma may
interrupt the already tenuous epiphyseal blood supply in the growing child and contribute to the
development of osteochondritis dissecans lesions. differences between osteochondrotic and normal
cartilage.

There is a decrease in acidic glycosaminoglycans in OCD with thinned subchondral growth plate
compared to normal osteochondral samples. Borders to the healthy tissue are clearly visible micro-
and macroscopically. Scanning electron microscopy revealed structural differences in the
subchondral area. Immunohistochemistry found a general decrease in glycosaminoglycan content
and a change in composition. Only faint staining for chondroitin and keratan sulfates was observed
in osteochondritic cartilage, whereas increased staining was shown for keratan sulfate in bone. The
intraosseous supply to the medial femoral condyle appeared to consist of a single nutrient vessel
supplying the subchondral bone with an apparent watershed area of limited supply compared to
the lateral femoral condyle.
structure of articular cartilage

Role of Chemokines/Chemokine Receptor Systems in

Cartilage Degradation
by Guo-Hua Yuan, Kayo Masuko-Hongo and Kusuki Nishioka

Summary
The underlying mechanism of the degradation of
articular cartilage is an imbalance between anabolic and
catabolic pathways, which are under the control of
cytokines. Chemokines are a novel class of small
cytokines and have a wide range of effects in many
different cell types, both inside and outside of the
immune system. Their actions are mediated by a family
of 7-transmembrane G-protein coupled receptors.
Recent studies have demonstrated that chondrocytes co-
express chemokines and their receptors, and that the
interaction of chemokines with their receptors results in
the release of cartilage matrix-degrading proteinases,
and affect proteoglycan metabolism in chondrocytes.
structure of articular cartilage

These data reveal a catabolic pathway primed by

chemokine/chemokine receptor system in articular
cartilage, thus proposing a novel therapeutic approach
against cartilage destruction in arthropathy. © 2001
Prous Science. All rights reserved.
structure of articular cartilage