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| About
Cartilage |
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Types of cartilage
- Hyaline cartilage
covers the ends of bones within joints to allow
smooth movement (also known as articular cartilage).
It is also found in the growth plates of long bones
in children.
- Fibro-cartilage is
found in the intervertebral disc, jaw (TMJ) joint,
meniscus of the knee joint, and at the site of
fracture healing.
- Elastic cartilage is
found in the epiglottis (valve preventing food
entering the airway) and eustachian tube (connecting
the throat to the middle ear).
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Hyaline cartilage
- Hyaline (articular) cartilage has a complex
structure
whose biochemical makeup varies
between different joints. It does not have it's own
blood supply and is insensitive to pain due to the
lack of nerve fibres.
- The predominant collagen in articular cartilage
is type II, while the predominant collagen in
meniscus of the knee is type I.
- Cartilage constantly undergoes dynamic
remodelling, being eroded by matrix
metalloproteinases (MMP's), and being reformed by
chondrocyte activity (cartilage forming cells).
- It is being continuously bathed in synovial fluid
which is produced by synovial membrane at the margin
of the joint surface.
- Nutrients pass from the underlying periosteum
(superficial bony layer) through the cartilage matrix
by diffusion, to reach the chondrocytes. Nutrients
also reach the surface of cartilage from the synovial
fluid (lubricating fluid) which circulates around the
joint space.
- Hyaline cartilage has the following typical
composition:-
- 70% water
- 15% collagen
- 15% proteoglycans (protein-glycosamine
molecules), chondrocytes (cartilage producing
cells), non-collagen proteins, lipids and
inorganic material.
- The chondrocytes sit within a matrix
of proteoglycans and collagen which are
related in such a way as to give the cartilage its
important compressive and tensile properties.
- The collagen/proteoglycan matrix provides the
structural framework of the tissue and also forms a
fluid compartment for transport of nutrient, waste
products, chemical messengers and hormones, to and
from the chondrocytes.
- Hyaline cartilage is divided up in to 4 different
zones
each containing different collagen
organisation as well as different amounts of
proteoglycans:-
- Superficial tangential
zone (10-20% of the cartilage
thickness).
- Middle zone (60%
of the cartilage thickness).
- Deep zone (30%
of the cartilage thickness).
- Calcified cartilage
zone where the cartilage interfaces with
the bone.
- The superficial or tangential zone contains the
highest collagen content, about 85% by dry weight. In
addition, the collagen fibrils are oriented parallel
to the joint surface, indicating that the purpose of
this zone may be primarily to resist shear stresses.
The amount of collagen decreases in each zone moving
closer to the tidemark (see diagram), dropping to 68%
in the middle zone.
- If cartilage becomes too water-logged it swells
and loses it's resilience to injury due to a change
in it's mechanical behaviour. Factors controlling the
water content are:-
- Concentration of proteoglycans -
proteoglycans within the collagen matrix have a
strong negative electrical charge, which helps
repel water molecules.
- Organization of the collagen network
- Stiffness and strength of the collagen
network - determined by the compaction of
proteoglycans in the matrix.
- In OA degradation of the collagen matrix causes
an increase in the cartilage water content, altering
its mechanical properties and reducing its ability to
with stand injury.

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| About
Synovial Fluid |
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Synovial Fluid
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Functions:-
- Lubricate joint surfaces (Hyaluronic Acid and
water).
- Nourish chondrocytes.
- Remove waste and debris from joint.
- Medium for white blood cells to circulate and
phagocytize debris.
- Hyaluronic Acid and protein account for the
higher viscosity.
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Composition:-
- Produced as a dialysate of plasma.
- White Blood Cells = < 200/mm3.
- Monocytes and macrophages 40-50%.
- Lymphocytes 40-50%.
- Neutrophils < 8%.
- Glucose content same as plasma.
- Red Blood Cells < 100/mm3.
- Hyaluronic acid - enhances viscosity.
- Protein < 2 g/dl.
- Ionic content same as plasma.

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| About
Osteoarthritis |
- Osteoarthritis Risk Factors
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Risk Factors
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Hip
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Knee
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Hand
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Gender
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M > F
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F > M
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F > M
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Increasing Age
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++
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++
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++
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Obesity
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+
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++
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+/-
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Family History
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+/-
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+/-
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++
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Joint Shape
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++
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+
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-
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Joint Trauma
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+
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++
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+/-
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++ greatly increases risk, + increases risk
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+/- possibly increases risk, - no increased risk
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Current Theories of
Osteoarthritis (OA)
- In OA the balance between cartilage degradation
and reformation is upset, with a net loss of collagen
and proteoglycans from the matrix.
- The initial response is a proliferation of
chondrocytes, which produce an increased amount of
matrix containing collagen and proteoglycans.
- As the disease progresses, the ability of
chondrocytes to respond is outstripped by progressive
cartilage degradation.
- Fibrillation, erosion and cracking initially
appear in the superficial layer of cartilage and
progress over time to deeper layers, resulting
eventually in large clinically observable
erosions.
- There are distinct differences in the observed
changes in cartilage between old age and OA. OA
cartilage has a greater content of denatured
collagen, a different chondroitin content, and a
greater matrix metalloproteinase (MMP) activity
causing increased cartilage degradation.
- Research has shown that Interleukin-1 (IL-1), a
pro-inflammatory molecule, is an important molecule
in OA. It has the following actions:-
- Induces chondrocytes to produce more
cartilage matrix.
- Stimulates the synovial cells to produce more
metalloproteinases, the enzymes involved in
denaturing cartilage.
- Inhibits the synthesis of type II articular
cartilage.
- Inhibits the synthesis of proteoglycans by
chondrocytes.
- Therefore IL-1 not only causes degradation of
cartilage, but suppresses any attempt to repair
it.
- Cartilage repair is dependant on the production
of matrix by chondrocytes. Chondrocyte activity can
be stimulated by locally produced growth factors like
Transforming Growth Factor B (TGF-B) and Basic
Fibroblastic Growth Factor (B-FGF) These molecules
can counteract the cartilage degradation caused by
high IL-1 levels. TGF-B also switches off the
production of IL-1.
- In advanced OA however, cartilage degradation
associated with high IL-1 levels far outstrips any
attempts at repair by these growth factors.
- Future targets for treating OA include reducing
metalloproteinase (MMP) activity, and inducing
collagen matrix synthesis.
- For more about improving cartilage health through
viscosupplementation see Hyaluronic Acid and Glucosamine,
Chondroitin and MSM.
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