Cartilage- Secondary or Primary

Condyle- secondary
cartilage-a misnomer

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INDIAN DENTAL ACADEMY
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Cartilage
It’s a type of connective tissue found on
the ends of bones, which protects and
cushions them, and absorbs the forcses
transmitted throughout the body;a living
tissue without a direct blood supply.


Facts about cartilage
Mesenchymal in origin
Consists of cartilage cells called chondrocytes
and a ground substance
Rigid and firm, but not hard
Matrix is noncalcified and avascular
Can grow both interstitially and appositionally
Is covered by perichondrium but can exist
without one.
Uniquely Pressure tolerant.

Types of Cartilage and their
Distribution
Hyaline cartilage - 1. Costochondral Junctions
2. Articular surfaces of most
joints
3. Some laryngeal cartilages
4. Walls of Trachea and large
bronchi
5. Epiphyseal plate of long bones


Fibrocartilage –

1. Secondary cartilaginous joints or symphysis
2. Articular discs of Synovial joints
3. Shoulder and hip joints

Elastic cartilage – 1. Auricle
2. Medial part of auditory tube
3. Epiglottis


Methods of Ossification
Endochondral Ossification
Intramembranous Ossification


Steps in Endochondral Ossification
Mesenchymal condesation at
site of bone formation
Differentiation of mesenchymal
cells to form chondroblasts.
Those on the surface form
perichondrium
Calcification of intercellular
substance
Formation of PRIMARY
AREOLAE
Invasion of calcified
cartilaginous matrix by the
PERIOSTEAL BUD

Formation of SECONDARY
AREOLAE
Differentiation of osteogenic
cells to osteoblasts
Formation of Osteoid and it’s
subsequent calcification


Primary Vs Secondary Cartilage
According to Stutzmann (1976)
Primary Cartilage – exists in the axial skeleton,
skull base and limbs; the dividing cells , the
differentiated chondroblasts are surrounded by a
cartilaginous matrix that isolates them from local
factors able to restrain or stimulate cartilaginous
growth


Secondary Cartilages – exist in the condylar and
coronoid processes and sometimes in sutures;the
dividing cells ,prechondroblasts, are not
surrounded by a cartilaginous matrix and thus are
not isolated from local growth modifications


Origin of the term “Secondary
Cartilage
A common theory of the 18th and 19th
century – that cartilage always preceded
and turned into bone.
That most bone was not transformed
cartilage but formed by an independent
process ( intramembranous ossification) –
gave forth the revolutionary idea of
“Secondary Cartilages “.

Schaffer’s Definition of Secondary
cartilages
Schaffer defined as secondary or accessory any
cartilage forming after and separate from the
primary cartilaginous skeleton.
Examples – mandibular symphysis, condyle,
coronoid process , ends of clavicle,on several
bones of the cranial vault, cartilage participating
temporarily in callus formation.
Heterotrophic cartilage – secondary cartilages
that are occasional abnormal malformations not
typical of the site and species – eg.cartilage in
human arterial walls.

Apart from differing times of first
formation can one otherwise
justify a separation of secondary
cartilage from primary?


Fuch’s refutation of Secondary
cartilage
Argued that the relation between secondary
cartilages and pressure / mechanical stimulation
was inconsistent.
Noted that the mechanical action of the condyle
played no role in the formation of cartilage.
That no criterion – whether of timing, histology or
etiology precisely seperated the two categories.
Contended that he had positive evidence that
secondary cartilages were in fact primary.
Claimed to have recognized a
CHONDROBLASTEM at sites of futures
secondary cartilage.

Key points of Fuch
Mechanical forces cannot be seen to play a role
in the origin of all secondary cartilages.
There is overlap between the first appearance of
primary and secondary cartilages.
The secondary cartilages vary greatly in their
histologic appearance.
He called to attention the secondary nature of
structures not included by Schaffer -


If the boundaries of Schaffer’s
class of secondary cartilages so
vulnerable, has the concept any
value?


Differences between condylar
and epiphyseal cartilages
Biologic criteria

Epiphyseal growth
plates

Condyle

Origin

Derivative of
primordial cartilage

Secondary cartilage
formation on original
membrane bone

Growth

Interstitial

Peripheral in
Fibrocartilage
covering; proliferating
cells are not cartilage
cells but
undifferentiated
mesenchymal cells.

Mechanical Stimuli

Unresponsive

Responsive


Biologic Criteria

Epiphyseal
Growth Plates

Condyles

Maturation

Secondary ossification
centers,final fusion and
disappearance of all
cartilage

Conversion from
hypertrophic to non
hypertrophic state but
not complete conversion
to bone

Histology

Only the degenrative
zone is mineralizing

Whole hypertrophic area
is in state of
mineralization, structural
organization is lacking

Hormonal control

Marked response to
thyroxine deficiency,after
final fusion no further
response to growth
hormone

Minimal response to
thyroxine
deficiency.Mature
condyle can be
reawakened by growth
hormone


Growth of Mandible


Effects of Orthodontic forces on the
Mandible
It is fair to say that controlling excessive mandibular growth is an
important unsolved problem in orthodontics.
If growth stimulation is defined as producing a larger mandible at the
end of total growth period than would have existed without
treatment; it is much harder to demonstrate a positive effect.
The ultimate size of mandible in treated and untreated patients is
remarkably similar.
Muscle activity is not necessary to obtain growth modification.
When the mandible is protruded or restrained, changes occur on the
temporal as well as the mandibular side of the TMJ.
The Herbst appliance is potentially the most effective of functional
appliances in altering jaw growth probably because of its full time
action, but is also rather unpredictable in terms of the amount of
skeletal versus dental changes likely to be produced.


Acceleration of mandibular
growth often occurs but a long
term increase in size is difficult
to demonstrate and,if it exists
at all, is so small to be
clinically significant.
Functional appliances that are
aimed at stimulating
mandibular growth produce a
highly variable response,but
the growth acceleration that
sometimes occurs can be
useful


Tentative interpretation of the
method of operation of functional
appliances
Functional Appliance

Increased contractile
activity of the LPM

Intensification of
repetitive activity of
the retrodiscal pad
Increase in growth stimulating
factors

Increase in growth stimulating factors

.Change in condylar trabecular orientation
.Additional Growth of condylar cartilage
.Additional subperiosteal ossification of the posterior border of
The mandible

Supplementary lengthening of the
mandible


Functional Appliances believed to
stimulate growth of condylar
cartilage
Class II elastics – believed to stimulate growth rate and
amount of condylar cartilage; the stimulating action
mediated primarily through the retrodiscal pad.
Herren (L.S.U activator) – increase growth of condylar
cartilage if the appliance is worn for 12 – 18 hours.
Increased repititive activity of retrodiscal pad produces
hypertrophy of condylar chondroblasts.
Neither the functional regulator nor the Harvold activator
are capable of altering the size of the mandible.


Condylar Cartilage before and after
resection of LPM and retrodiscal Pad
Resection of LPM and
retrodiscal pad produces a
significant slowdown of
condylar cartilage growth rate
Interruption of blood supply to
the differentiating
skeletoblasts;originating from
the LPM may be the probable
cause.


Demise of the Lateral Pterygoid
Hypothesis
Anatomic research has
not found significant
attachments of the LPM
to the condylar head.
Hyperactivity of the LPM
during mandibular
advancement thereapy is
doubtful as the muscle
actually shortens during
this procedure.


New bone formation at
the condyle was
associated with
decreased postural EMG
activity in the LPM,
masseter and digastric
muscles
This has led to the
evolution of NON
MUSCULAR
HYPOTHESIS.

Lateral Functional Shift of the mandible –
effects on condylar cartilage thickness and
proliferation
Condyle on the side opposite the direction of shift is
displaced anteriorly or protruded while the condyle on
the side towards the shift is more stable positionally and
is less likely to be retruded.
Growth of the Mandibular Condylar Cartilage (MCC)
adapts to its local functional biomechanical environment
Thus differential changes in the metabolic activity of the
MCC would be expected on the non protruded and
protruded sides.
Increased thickness of the MCC was followed by
temporary increased proliferation of prechondroblastic
cells on the protruded side.

Clinical implications
Functional appliances which protrude or
retrude the mandible and alter the local
functional-biomechanical environment;
can alter the growth of the MCC.


What exactly affects the growth of
the condylar head?
Genetic theory -

suggests that condylar growth is
strongly under the influence of genes.

Functional Matrix Theory – though attractive
could not satisfactorily explain how condylar growth
would be stimulated by the growth of the soft tissues.
Endow and Hans – mandibular growth is a composite of
regional forces and functional agents of growth control
that interact in response to specific extracoronal
activating signals.


Growth Relativity Hypothesis –
John Voudouris
Based on three main
foundations –
Glenoid fossa
promotes condylar
growth with the use of
mandibular
advancement
thereapy.


Growth Relativity Hypothesis
Viscoelastic tissues
anchored between
glenoid fossa and the
condyle insert directly into
condylar fibrocartilage
and affect its growth.
Transduction of forces
over the fibrocartilaginous
cap of condylar head
occurs as the viscoelastic
tissues are stretched
during mandibular
advancement

Light Bulb Analogy of Condylar
growth and Retention
The condyle lights up
like a LIGHT BULB on
a dimmer switch
when it is
continuously
advanced.
The reactivated
muscle activity dims
the light bulb and
returns it to normal
growth activity at the
end of treatment.

Conclusions of John Voudouris
Propulsive mandibular appliances such as herbst and twinblock cause
growth modification of the condyle fossa region that involves–
Displacement of mandible
Viscoelastic tissue extension forces to the condyle
Transduction of forces radiating beneath the fibrocartilage of the condyle
and glenoid fossa.
Condylar growth modifications occur relative to the glenoid fossa and not
necessarily as an independent and isolated phenomenon.
New bone formation at the condyle and glenoid fossa is associated with
decreased postural EMG activity in the LPM, masseter and anterior digastric
muscles.
Fixed functional appliances (Herbst) produce consistent and reproducible
condyle fossa changes compared with inconsistent results reported for
removable functional appliances.
Bone formation in the glenoid fossa and condyle was statistically significant
compared to controls.
Condylar response appears to be age determined.


Unique features of the mandibular
condyle
A major site of growth having considerable clinical
significance.
Not a pacesetting “master center” with all other regional
growth fields subordinate to and dependant on it .
The condylar cartilage has a secondary type of cartilage
which developed because of changed functional and
developmental conditions imposed on this part of the
mandible.
The condylar cartilage is not the pacemaker for the
growth of the mandible. It functions to provide regional
adaptive growth.
The condyle performs a dual role –
Provides pressure tolerant articular contact.

Makes possible a multidimensional growth
capacity in response to ever changing
developmental conditions and variations.
The condylar cartilage does have some
measure of intrinsic genetic programming.The
cartilage cells are coded to divide and divide but
extracondylar features are needed to sustain this
activity.
Condylar prechondroblasts are randomly
arranged providing an opportunity for selected
multidirectional growth potential in contrast to
long bones.

Conclusions
Secondary cartilages resemble each other in many respects eg-the clavicle
and mandibular condyle have a similar layering and disorder in their growth
cartilages.
Secondary cartilages alike in many ways differ in others.
No one secondary cartilage can represent all the properties in it’s class.
The argument that secondary cartilage can validly be distinguished from
primary one has hinged not only on morphology and histochemistry but on
whether a mechanical factor underlies secondary chondrogenesis.
Secondary cartilages have no manifest unity being in the first place non
primary cartilages.They cannot be unified by a known mechanical etiology.
Condylar cartilage can at best be considered a modified periosteum.
Condylar cartilage is rather like an epiphysis at the end of a long bone but
unlike the clavicle it has no secondary center of ossification.


following people who helped me immensely during
the preparation of this seminar.

Dr.Uma Shankar
Dr.(Ms.) Uma Shankar
Dr.Vinod
Dr.Kuber Sood
Dr.Ramesh
Dr.Kartik
Dr.Divya
Dr.Balaji
Thanks for making it all worthwhile

Cartilage matrix production and chondrocyte
enlargement as contributors to mandiular
growth in Animals ( AJODO Oct.1991)
Mandibular growth in length at the condyle
results from
Perichondral and
Chondral components
Matrix production depends on systemic
influences while chondrocyte enlargement might
be affected by local factors.
One could speculate that chondrocyte
enlargement rather than matrix production
should be primarily affected by orthopedic
appliances aimed at altering condylar growth
though this aspect has never been investigated.

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Cartilage- Secondary or Primary

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