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CRANIOMANDIBULAR
DISORDERS
With the term Craniomandibular
Disorders, is meant a muskuloskeletal disorder affecting mandibular
function. It is characterised by pain and/or tenderness in the
temperomandibular joints and in the masticatory muscles, limitation or
asymmetry in the range of opening/closing of the mouth, and noises in the
joints. In infancy, deviation or displacement during jaw movements and
noises in the joints are the symptoms most frequently
encountered.
Epidemiology
There have been
several studies done on the prevalence of craniomandibular disorders in
the paediatric population, showing a presence that varies from 20 to 61%
in samples studied.
Etiology
In the
past it was thought that occlusal anomalies were a primary factor in the
development of craniomandibular disorders. Nowadays, the role of these
factors needs to be seen in the light of many other contributing factors.
Amongst these should be mentioned the specific morphological structure of
the joint, noxious parafunctional habits, eventual congenital
malformations of the condylar, meniscal and temporal components and the
premature loss of part of the occlusal support.
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1 and
2:Etiology: nailbiting. 3 and
4:Etiology: noxious habitual positioning of the cervical
spine. | |
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Oral parafunctional
activities in side shift.
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Bruxism | |
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Infantile
bruxism |
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Teeth marks (scalloping) on the
tongue edge from parafunctional
habits | |
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Habitual tongue biting
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Acute trauma of accidental or
sporting origin causing intracapsular lesions (meniscal and synovial
compression, etc.) should also be considered a cause. The lesions may be
immediate (acute traumatic arthritis), or delayed (post-traumatic
arthritis). Following damage induced in the intracapsular ligamentous
structures, from continual overloading or from acute trauma, a state of
localized inflammation sets in. This causes a further breakdown of
connective tissue giving lieu to a hypermobile structure (joint
instability). (Fig. Post-traumatic arthritis.)
Pathogenisis
This hypermobility
(instability), in turn, causes a change in function and subsequently,
organic changes. Increased friction and hence also wear, increase
proportionally with the velocity and acceleration of joint
movements.
The capacity of the ligamentous and synovial joint
structures to adapt is related to their mesodermic mesenchymal (connective
tissue) origin.
They are therefore subject to the general laws of
biomechanics governing connective tissue. They will suffer a ‘strain’
while under a functional ‘load’, or an abnormal parafunctional ‘stress’,
up to the limit of elastic stretch allowed by their collagen and elastic
fibres. They will become irreversibly deformed when the tension goes
beyond their maximum limit (different for the collagen and the elastic
fibres)(Fig. Stress/strain curve).
At this stage permanent changes or
‘deviation in form/ DIF’, occur.
The ability to tolerate ´stressful´
forces, (persistent trauma) has even been calculated in terms of time. It
has been estimated that it takes three to four weeks (one month), for a
‘permanent condition’ to become established, or rather one that is
irreversible and curable if treated, but without ‘restitutio ad integrum’.
Already at this stage objective pathological joint sounds can be produced
in the patient by the dental clinician, defined as: ‘crepitus’, ‘clicks’
and ‘thuds’, with appropriate provocatory manoeuvres.
If unchecked,
this condition of joint laxity leads to further damage of the intrinsic
ligamentous structures and to dislocation of the condylar –meniscal-
temporal complex.
| 6a, 6b.
Pathological condition of the temperomandibular joint
complex showing anterior dislocation of the meniscus with mouth open
and shut. Legend: C = condyle; T = temporal bone (articular
eminence); D = disc (meniscus). |
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A, B.
Magnetic resonance image of mouth open and shut showing non
reducing dislocation of the disc
Legend 1= mandibular condyle;
2 = temporal component of the joint; 3 =
meniscus. |
Usually this gives rise to an
anteromedial migration of the disc and a posterolateral displacement of
the condyle that leads to a lack of coordination (dyskinesis), between the
condylar, meniscal and temporal components in the functional movements of
the mandible. This lack of coordination in opening and closing of the
mouth, chewing, lateral movement and protrusion, is highlighted by the
appearance or worsening of noises such as crepitus in the joint. Sometimes
this state can lead to locking of the condyle as a result of a
non-reducing dislocation (usually anterior dislocation of the disc, with
posterior dislocation of the condyle).
Pain may appear at
this stage spontaneously or there may be pain on palpation of the affected
joint area and/or musculature:
- Arthrogenous, as a consequence of
chronic inflammation, of further acute episodes, and of intra and
pericapsular states of compression;
- Miogenous, as a result of muscle
involvement from a secondary reaction to joint damage, from chronic
inflammation of connective tissue (myofibrositis), or from overuse in
parafunctional activities.
The degenerative type of arthritic
changes (degenerative arthropathy/arthrosis) that take place if the state
of dysfunctional arthropathy persists and shows further signs of evolving,
can lead to marked anatomical derangement and to a significant loss of
function. It brings about marked changes in structure of the condylar
and temporal components, severe deformation of the disc, perforation of
the posterior ligaments of the disc with disintegration of the bilaminar
zone, intra-articular oedema, temperocondylar osteophytes, adhesions,
etc.
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Tomografia di un articolazione
temporomandibolare affetta da segni e sintomi gravi di artrosi
disfunzionale |
The patient may notice the onset of
crepitus, a persistent lateral deviation, or a marked limitation in
opening the mouth, and will often experience pain radiating to the angle
and horizontal ramus of the mandible.
The correction of orofacial anomalies in childhood and
adolescence could therefore prove an important preventative and
therapeutic approach to such conditions, even if it may not, in itself, be
curative in the majority of cases.
Many authors have claimed
that there exists a very close relationship between craniofacial structure
and craniomandibular function.
It also seems widely accepted that
specific aspects of the occlusal mechanism can be related to particular
combinations of dysfunctional symptoms.
The etiological relationship
that links occlusion, states of malocclusion and functional
craniomandibular disorders remains however a subject of controversy.
Long-term studies taking into account retrospective data, that have
evaluated the prevalence of dysfunctional symptoms in patients with normal
occlusion, pathological occlusion and those treated orthodontically, do
not seem to show any significant differences between the three
groups.
The main criticism that can be directed at most of the
above studies, is the differing criteria adopted for the evaluation of the
function of the occlusal craniomandibular mechanism. Case history and
clinical data research already show marked discrepancies in possible
findings, not only within a single research project, but also when one
compares them with those of other researchers.
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