BIOMECHANICS OF

ARTICULAR CARTILAGE

PREPARED BY
JOYCI JOSEPH
1st YEAR MPT
 INDEX
INTRODUCTION

PRIMARY FUNCTIONS OF ARTICULAR CARTILAGE

STRUCTURE OF ARTICULAR CARTILAGE

BIOMECHANICAL BEHAVIOR OF ARTICULAR CARTILAGE

WEAR OF ARTICULAR CARTILAGE

HYPOTHESES ON THE BIOMECHANICS OF CARTILAGE DEGENARATION

EFFECTS OF INTRA- ARTICULAR STEROID INJECTION ON ARTICULAR CARTILAGE

RECENT ADVANCE IN ARTICULAR CARTILAGE REPAIR

INTRODUCTION

In normal young
joints,the articulating
bone ends of
diarthrodial joints are
covered by a thin (1-
6mm), dense translucent
white connective tissue
called hyaline articular
cartilage.
Hyaline articular
cartilage is very
specialized tissue
precisely suited to
withstand highly loaded
joint environment
without failure during
an individual's lifetime.
 To distribute joint loads over a wide area,
thus decreasing the stress sustained by the
PRIMARY contacting joint surfaces.
FUNCTIONS IN
DIARTHRODIAL
JOINTS
To allow relative movement of the opposing
joint surfaces with minimal friction and
wear.
STRUCTURE
OF
ARTICULAR
CARTILAGE
 • Nature of articular cartilage viscoelasticity
• Confined compression explant loading
configuration
BIOMECHANICAL • Biphasic creep response of articular cartilage in
compression
BEHAVIOUR OF • Biphasic stress-relaxation response of articular
ARTICULAR cartilage in compression
CARTILAGE • Permeability of articular cartilage
• Behavior of articular cartilage under uniaxial
tension
• Behavior of articular cartilage in pure shear
• Swelling behavior of articular cartilage
• Lubrication of articular cartilage
 If a material is subjected to the action of constant
load and its response varies with time and then the
mechanical behaviour of the material said to be
viscoelastic.

The two fundamental responses of a viscoelastic

material are creep and stress relaxation. Creep
NATURE OF occurs when a viscoelastic solid is subjected to the
ARTICULAR action of a constant load. Typically, a viscoelastic
solid responds with a rapid initial deformation
CARTILAGE followed by a slow, progressively increasing
VISCOELASTICITY deformation known as creep until an equilibrium
state is reached. Stress relaxation occurs when a
viscoelastic solid is subjected to the action of a
constant deformation. Typically, a viscoelastic
solid responds with a rapid, high initial stress
followed by a slow, progressively decreasing stress
required to maintain the deformation; this
phenomenon is known as stress relaxation
 For articular cartilage, the compressive viscoelastic
behavior is caused by the flow of interstitial fluid
NATURE OF flow associated with frictional drag.
Recently, experimental measurements
ARTICULAR have determined that interstitial fluid pressurization
CARTILAGE supports more than 90% of the applied load to the
VISCOELASTICITY cartilage surface immediately following loading.
This effect can persist for more than one thousand
seconds and thus shields the ECM and
chondrocytes from the crushing deformations of
the high stresses resulting from joint loading.
 In articular cartilage, creep is caused by the
exudation of the interstitial fluid. Exudation is most
rapid initially, us evidence by the early rapid rate of
BIPHASIC increased deformation, and it diminishes gradually
CREEP until flow cessation occurs. During creep, the load
RESPONSE OF applied at the surface is balanced by the
compressive stress developed within the collagen-
ARTICULAR PG solid matrix and the frictional drag generated
CARTILAGE IN by the flow of the interstitial fluid during
COMPRESSION exudation. Creep ceases when the compressive
stress developed within the solid matrix is
sufficient to balance the applied stress alone.
 The stress rise in the compression phase is associated
with fluid exudation, whereas stress relaxation is
BIPHASIC associated with fluid redistribution within the porous
solid matrix. During the compressive phase, the high
STRESS stress is generated by forced exudation of the
RELAXATION interstitial fluid and the compaction of the solid matrix
near the surface. Stress relaxation is in turn caused by
RESPONSE OF the relief or rebound of the high compaction
ARTICULAR region near the surface of the solid matrix. This stress-
CARTILAGE IN relaxation process will cease when the compressive
COMPRESSION stress developed within the solid matrix reaches the
stress generated by the intrinsic compressive modulus
of the solid matrix.
 Fluid-filled porous materials may or may not be
permeable. The ratio of fluid volume (V f) to the
total volume (V T) of the porous material is known
as the porosity (β = V f/V T); thus, porosity is a
PERMEABILIT geometric concept. Articular cartilage is therefore a
material of high porosity (approximately 80%). If
Y OF the pores are interconnected, the porous material is
ARTICULAR permeable. Permeability is a measure of the ease
with which fluid can flow through a porous
CARTILAGE material, and it is inversely proportional to the
frictional drag exerted by the fluid flowing through
the porous-permeable material. Thus, permeability
is a physical concept; it is a measure of the
resistive force that is required to cause the fluid to
flow at a given speed through the porous-
permeable material. In articular cartilage,
permeability decreases exponentially as a function
of both increasing compressive drain and applied
fluid pressure.
 BEHAVIOUR OF ARTICULAR CARTILAGE UNDER
UNIAXIAL TENSION

The mechanical behavior of articular

cartilage in tension is anisotropic and
inhomogeneous. These anisotropic
and inhomogeneous characteristics in
mature joints are caused by varying
collagen –proteoglycans structural
organization of joint surface and
layering structural arrangements found
within the tissue. Thus, the collagen
rich superficial area of joint cartilage
becomes tough wear-resistant
protective skin. Articular cartilage also
exhibit viscoelastic behavior with
polymeric actin and flow of interstitial
fluid. The articular cartilage tends to
stiffen with increasing strain when the
strain becomes large.
 In tension and compression, only the equilibrium
intrinsic properties of collagen-proteoglycan solid
matrix can be determined. This is because a
volumetric changes always occurs within the
material when it is subjected to uniaxial
BEHAVIOR OF tension/compression. The volumetric changes
ARTICULAR interstitial fluid flow and induce biphasic
CARTILAGE IN viscoelastic effects within the tissue. The shear
PURE SHEAR stiffness of articular cartilage derives from its
collagen content or from the collagen-proteoglycan
interaction. It is considered that collagen is much
more elastic and load carrying element than
proteoglycans. When collagen content is increased,
it decreases the frictional dissipation.
 Cartilage is a mixture of three
miscible phases;
• Charged solid phase representing
collagen-proteoglycans network
• Fluid phase representing
SWELLING interstitial fluid
BEHAVIOUR OF • Ion phase comprising the
ARTICULAR movement cation Na+ and an
anion Cl- and others.
CARTILAGE
The swelling
behavior of tissue can be responsible
for a significant fraction of
compressive load bearing capacity of
articular cartilage at equilibrium.
 Synovial joints are subjected to an enormous range
of loading conditions, and under normal
circumstances the cartilage surface sustains little
wear. The minimal wear of normal cartilage
associated with such varied loads indicates that
sophisticated lubrication processes are at work
within the joint and within and on the surface of
the tissue. These processes have been attributed to
LUBRICATION a lubricating fluid-film forming between the
OF ARTICULAR articular cartilage surface and to an adsorbed
CARTILAGE boundary lubricant on the surface during motion
and loading. The variety of joint demands also
suggests that several mechanisms are responsible
for diarthrodial joint lubrication.

There are two fundamental types of lubrication.

1. Fluid film lubrication
2. Boundary Film Lubrication
1. Fluid film lubrication

Fluid-film lubrication uses a thin film of lubricant that causes a bearing surface separation. The
load on the bearing is then supported by the pressure that is developed in this fluid-film.

2. Boundary Film Lubrication

In boundary lubrication, the surfaces are protected by
an adsorbed layer of boundary lubricant, which
prevents direct, surface-to surface contact and
eliminates most of the surface wear. Boundary
lubrication is essentially independent of the physical
properties of either the lubricant (e.g., its viscosity)
or the bearing material (e.g., its stiffness), instead
depending almost entirely on the chemical properties
of the lubricant (Dowson, 1966/1967). In synovial
joints, a specific glycoprotein, “lubricin,” appears to
be the synovial fluid constituent responsible for
boundary lubrication (Swann et al., 1979, 1985).
Lubricin, also known as proteoglycan-4 (PRG-4), (25
× 104 mw) is adsorbed as a macromolecular
monolayer to each articulating surface. These two
layers, ranging in combined thickness from 1 to 100
nm, are able to carry loads and appear to be effective
in reducing friction
 There are two joint lubrication scenarios that can be considered a
combination of fluid-film and boundary lubrication or simply mixed
lubrication.

The articular cartilage surface, like all surfaces, is not perfectly smooth;
asperities project out from the surface. In synovial joints, situations may
occur in which the fluid-film thickness is of the same order as the mean
articular surface asperity. During such instances, boundary lubrication
between the asperities may come into play. If this occurs, a mixed mode
of lubrication is operating, with the joint surface load sustained by both
the fluid film pressure in areas of noncontact and by the boundary
lubricant lubricin in the areas of asperity contact. In this mode of mixed
lubrication, it is probable that most of the friction (which is still
extremely low) is generated in the boundary lubricated areas while most
MIXED of the load is carried by the fluid-film.

LUBRICATION
 WEAR OF ARTICULAR CARTILAGE

Wear is the unwanted removal of material from

solid surfaces by mechanical action. There are two
components of wear: interfacial wear resulting from
the interaction of bearing surfaces and fatigue wear
resulting from bearing
deformation under load.

1. Interfacial wear

Interfacial wear occurs when bearing surfaces come

into direct contact with no lubricant film (boundary
or fluid) separating them. This type of wear can
take place in either of two ways: adhesion or
abrasion. Adhesive wear arises when, as the
bearings come into contact, surface fragments
adhere to each other and are torn off from the
surface during sliding. Abrasive wear, conversely,
occurs when a soft material is scraped by a harder
one; the harder material can be either an opposing
bearing or loose particles between the bearings.
 WEAR OF ARTICULAR CARTILAGE

2. Fatigue wear

Fatigue wear of bearing surfaces results not from surface-to-surface contact but from the
accumulation of microscopic damage within the bearing material under repetitive stressing.
Bearing surface failure may occur with the repeated application of high loads over a relatively
short period or with the repetition of low loads
over an extended period even though the magnitude of those loads may be much lower than the
material’s ultimate strength. This fatigue wear, resulting from cyclically repeated deformation of
the bearing materials, can take place even in well-lubricated bearings.
In synovial joints, the cyclical variation in total joint load during most physiologic activities
causes repetitive articular cartilage stressing (deformation). In addition, during rotation and
sliding, a specific region of the articular surface “moves in and out” of the loaded contact area,
repetitively stressing that articular region. Loads imposed on articular cartilage are supported by
the collagen-PG matrix and by the resistance generated by fluid movement throughout the
matrix. Thus, repetitive joint movement and loading will cause repetitive stressing of the solid
matrix and repeated exudation and imbibition of the tissue’s interstitial fluid.
 WEAR OF ARTICULAR CARTILAGE

Once the collagen-PG matrix of cartilage is disrupted damage resulting from any of the three
wear mechanisms mentioned becomes possible: (1) further disruption of the collagen-
PG matrix as a result of repetitive matrix stressing; (2) an increased “washing out” of
the PGs as a result of violent fluid movement and thus impairment of articular
cartilage’s interstitial fluid load support capacity; and (3) gross alteration of the
normal load carriage mechanism in cartilage, thus increasing frictional shear loading
on the articular surface. All these processes will accelerate the rate of interfacial and
fatigue wear of the already disrupted cartilage microstructure.
 Articular cartilage has only a limited capacity for repair
and regeneration, and if subjected to an abnormal range
of stresses can quickly undergo total failure. It has been
hypothesized that failure progression relates to the
HYPOTHESES following: (1) the magnitude of the imposed stresses;
ON THE (2) the total number of sustained stress peaks; (3) the
BIOMECHANICS changes in the intrinsic molecular and microscopic
structure of the collagen-PG matrix; and (4) the changes
OF CARTILAGE in the intrinsic mechanical property of the tissue. The
DEGENARATION most important failure initiating factor appears to be the
“loosening” of the collagen network that allows
abnormal PG expansion and thus tissue swelling
(Associated with this change is a decrease in cartilage
stiffness and an increase in cartilage permeability which
alter cartilage function in a diarthrodial joint during
joint motion.
The magnitude of the stress sustained by the
articular cartilage is determined by both the
total load on the joint and how that load is
distributed over the articular surface contact
area. Any intense stress concentration in the
contact area will play a primary role in tissue
degeneration. A large number of well-known
conditions cause excessive stress
concentrations in articular cartilage and result
in cartilage failure. Most of these stress
concentrations are caused by joint surface
incongruity, resulting in an abnormally small
contact area. Examples of conditions causing
such joint incongruities include OA
subsequent to congenital acetabular
dysplasia, a slipped capital femoral
epiphysis, and intra-articular fractures.
Two further examples are knee joint
meniscectomy, which eliminates the load-
distributing function of the meniscus, and
ligament rupture, which allows excessive
movement and the generation of abnormal
mechanical stresses in the affected joint. In all
these cases, abnormal joint articulation
increases the stress acting on the joint surface,
which appears to predispose the cartilage to
failure.
Degenerative changes to the structure and composition of articular cartilage
could lead to abnormal tissue swelling and functionally inferior
biomechanical properties. In this weakened state, the cartilage ultrastructure
will then be gradually destroyed by stresses of normal joint articulation. OA
may also arise secondarily from insult to the intrinsic molecular and
microscopic structure of the collagen-PG matrix. Many conditions may
promote such a breakdown in matrix integrity; these include degeneration
associated with rheumatoid arthritis, joint space hemorrhage associated
with hemophilia, various collagen metabolism disorders, and tissue
degradation by proteolytic enzymes. The presence of soluble mediator such
as cytokines (e.g., interleukin-1) and growth factors (e.g., transforming
growth factor-beta 1) also appear to play an important role in OA. Another
contributing factor to the etiology of OA may be age-related changes to the
chondrocyte.
 Intra-articular corticosteroid injection has been used for decades to treat
patients with knee and hip OA, especially individuals who cannot
tolerate the side-effects of long-term pharmaceutical therapy with
acetaminophen and nonsteroidal anti-inflammatory drugs. A recent
analysis of the Medicare sample database found that more than one-
third of patients with newly diagnosed knee OA were treated with at
least one intra-articular corticosteroid injection. Although its exact
mechanism of action remains unknown, intra-articular corticosteroid
injection is thought to provide pain relief in patients with knee and hip
OA by decreasing joint inflammation. Short-term complications,
including septic arthritis, injection site pain, skin pigmentation, and
atrophy, and systemic effects are exceedingly rare.
EFFECTS OF
INTRA- Corticosteroids have been shown to be cytotoxic to articular cartilage in
both human in vitro studies and animal in vivo studies. Two
ARTICULAR randomized placebo-controlled clinical trials in study participants with
knee OA compared the progression of knee joint degeneration on
STEROID imaging studies at 2-year follow-up between study participants who
received intra-articular corticosteroid injection and control subjects
INJECTIONS ON who received intra-articular saline injection every 3 months. The results
are conflicting. One study of 68 participants with knee OA found no
ARTICULAR significant difference in the progression of joint space narrowing on
knee radiographs between participants who received corticosteroid
CARTILAGE injection and control subjects who received saline injection. The second
study involving 140 participants with knee OA found significantly
greater cartilage volume loss at knee MRI in participants who received
intra-articular corticosteroid injection compared with control subjects
who received saline injection.
Two recent retrospective studies reported an increased risk of
worsening joint degeneration on radiographs in patients with knee OA
and hip OA who received intra-articular corticosteroid injection. Thus,
there is a growing body of evidence to suggest that intra-articular
corticosteroid injection can accelerate the progression of joint
degeneration.
 RECENT ADVANCES IN
ARTICULAR CARTILAGE
REPAIR

• MICROFRACTURE(MF)

It is an articular cartilage repair

surgical procedure that works by
creating tiny fractures in the
underlying bone. This causes new
cartilage to develop from a so-called
super clot.
 AUTOLOGOUS
CHONDROCYTE
IMPLANTATION(ACI)
Autologous chondrocyte implantation (ACI,)or
mosaicplasty, is a biomedical treatment that repairs damages
in articular cartilage. ACI provides pain relief while at the
same time slowing down the progression or considerably
delaying partial or total joint replacement (knee
replacement) surgery.

This cell based articular cartilage repair procedure takes

place in three stages. In a first stage, between 200 and 300
milligrams cartilage is sampled arthroscopically from a
less weight bearing area from either the intercondylar notch
or the superior ridge of the medial or lateral femoral
condyle of the patient. The matrix is removed enzymatically
and the chondrocytes isolated. These cells are grown in
vitro in a specialized laboratory for approximately four to
six weeks, until there are enough cells to reimplant on the
damaged area of the articular cartilage. The patient then
undergoes a second treatment, in which the chondrocytes
are applied on the damaged area during an open-knee
surgery (also called arthrotomy). These autologous cells
should adapt themselves to their new environment by
forming new cartilage. During the
implantation, chondrocytes are applied on the damaged area
in combination with a membrane (tibial periosteum or bio
membrane) or pre-seeded in a scaffold matrix.
 REFERENCE

• Basic biomechanics of the musculoskeltal system-Margareta

Nordin, Victor H Frankel
• Recent advances and future trends in articular cartilage repair-
Deepak Gayal, Saumya Arthroscopy and Sports Knee
Clinic, Ahmedabad, Gujarat, India
Received:2020-05-14, Accepted:2020-05-14,
Published:2020-07-15
• Risks and Benefits of Intra-articular Corticosteroid Injection
for Treatment of Osteoarthritis-Richard Kijowski
Published Online:Oct 15, 2019
https://doi.org/10.1148/radiol.2019192034
THANK YOU