DR AJAY SRINIVASDEPT OF ORTHODONTICS
PG STUDENT
MANAGEMENT OF CRANIOFACIAL ANOMALIES
INTRODUCTION
The term craniofacial anomalies literally encompasses all congenital deformities of the cranium and face. More specifically however the term has come to imply congenital deformities of the head that interfere with the physical and mental well being (Marsh and Vannier 1985)
The main problem in craniofacial developmental biology is understanding when, where and how are genes expressed and how is differential gene regulation associated with specific pattern of morphogeneis.
HOX HOMEOBOX NETWORK
Patterning of much of the craniofacial region is laid down by cluster of genes, the Hox homeobox network. These are expressed through patterning of rhombomeres. The structures of the craniofacies are largely derived from neural crest cells. They undergo extensive migrations and interactions in the facial region they give rise to almost all the skeletal and connective tissues.Interaction of crest cells with other cells, with matrix and growth factors at various locations along the migratory path, or at their destination determine the differentiation of the cells.
Failure of neural crest to migrate, inadequate migration, failure to proliferate during migration, and premature cell death (necrosis) serve as a basis for the many syndromes, collectively known as neurocristopathies.
ETIOLOGY
Chromosomal disorders Single gene disorders Multifactorial inheritance Maternal infections in pregnancy Maternal metabolic derangements Maternal use of medication Radiation exposure Disturbances of embryonic differentiation
and fetal growth
Cleft lip and palate
They are one of the most common congenital anomalies occurring in about 1.97 to 1.23 /1000 in Indians and 2/1000 in mongoloids In 2/3rd of the cases cleft palate is on the left than the right side CL(P) is seen more in male and CP alone more in females.
The pathogenesis is heterogeneous and multifactorial and is ultimately due to deficiency of neural crest mesenchyme failing to migrate and/or proliferate to coalesce individual embryonic prominences and processes that combine into the fetal orofacies.
cleft lip results from failure of fusion of the median nasal ;lateral nasal and the maxillary processes on either or both sides.
Reasons
Hypoplasia of the facial processes Altered facial geometry Defective ability of surface epithelia to
participate in the fusion process Excessive cell depth in the fusing palatal
seams, mesenchymal deficiency and post fusion rupture
Thus they can be unilateral or bilateral clefting ; complete or incomplete , of the lip and/or primary palate till the incisive foramen.
Reasons
Hypoplasia of the palatal shelves Failure of the palatal shelf elevation at the
correct time due to diminished intrinsic force increased resistance mainly by the tongue
position being high.an under developed mandible also prevents
the descent Excessive head width causing failure of
normal sized palatal shelves to meet
Dentofacial relationships in unoperated cases
Unilateral cleft - nasal septum and columella is deviated to the non cleft side of facial midline whereas incisors deviate towards the cleft
In UCLP and BCLP - tendency for the mandible to be retruded and for the mandibular plane to be steep with a relatively shorter posterior facial height and a longer anterior facial height.
Mandibular incisors- labially proclined in UCLA while lingually inclined in CLP
In BCLP -maxillary intercanine dimension were much smaller than UCLP and UCLA
In maxillary arch the non cleft segment has a tendency to rotate forwards hence increasing the overjet while the cleft side rotates medially hence edge to edge bite of the canines. Teeth also tend to roll superiorly hence an openbite on that side due to infraocclusion .
Maxillo-mandibular clefting
It is not formed between the maxillary and mandibular bone but between the facial processes with the same names. It is essentially a soft tissue defect affecting skin, muscle and mucosa, is usually called macrostomia. It may be unilateral or rarely bilateral. Its range of malformations varies from minor elongation of the oral angle to a wide cleft extending towards the tragal area
In the majority of cases it is associated with preauricular appendages or fistulae that may be found anywhere between the angle of the mouth and the tragus occasionally also with temporoaural and/or mandibular abnormalities.
CRANIOFACIAL DYSPLASIAS WITH DYSOSTOSIS
MEDIAN CLEFT FACE SYNDROME/ fronto-nasal syndrome/Internasal dysplasia
A whole spectrum of malformations may be observed and the severity of the reported examples can be graded in a sequence.
At one end is bifidity of the nasal tip or dorsum, sometimes associated with a median cleft lip and with duplication of the labial frenulum. Grooves and folds along the dorsum nasi are also occasionally observed.
At the other end widely separated nasal halves and extreme orbital hypertelorism, including other anomalies caused by frontonasoethmoidal dysplasia, www.indiandentalacademy.com
Premaxilla may be retarded in development and bifid, The maxilla may show a keel-shaped deformity, with the incisors rotated upward in each half of the alveolar process. Sometimes a medial cleft of the palate is also found and this may extend upwards to the cribriform plate as an inverted V .
NASAL APLASIA - characterized by complete absence of one nasal half. The nasal cavity is missing and pneumatiziation of the maxillary ethmoidal and frontal sinuses has failed . There is no nasolacrimal duct. The affected half of the maxilla is hypoplastic and the palatal vault is high and acutely arched . www.indiandentalacademy.com
NASAL DUPLICATION-ranges from a supernumerary nostril in an otherwise normal nose to duplication of the upper face (diprosopia). The supernumerary nostril is usually the medial one. It may end blindly, be stenotic or open into a nasal cavity..
In the milder cases there may be one continuous midline septum, while in the more severe cases duplication of the anterior part of the septum or full duplication may be observed
Treacher Collins' syndrome /Zygomatic dysplasia / mandibulofacial dysostosis
caused by a change in a single gene & this Treacher Collin gene is located on chromosome 5 inherited as an autosomal dominant gene with complete penetrance but variable expressivity
Features
Malar & zygomatic hypoplasia Anti mongoloid slant of the palpebral fissures Coloboma in the outer third of the lower
eyelid(75%) deficiency of eyelashes in the medial third of
these eyelids Unusual tongue shape (25% cases)
Hair extending down & forward from the temporal region on to the cheek. flattening of the cheeks body of the mandible is frequently hypoplastic and the chin severely retruded.
Radiographs show antigonial notch in the lower border of the mandible along with hypoplasia of coronoid & condylar processes. Cleft palate is found in approximately 30% of the cases.
Posterior maxillary height is decreased and anterior height is increased resulting in a steep anteroinferior cant. open bite is related to shortening of the mandibular rami and premature posterior teeth contact .
Deformed external ear,ear tags & pre-auricular pits,absence of external auditory meatus frequently accompanied by malformations of the middle ear
Miller syndrome / Postaxial acrofacial dysostosis
Has resemblance to that of mandibulofacial dysostosis but there is postaxial limb deficiency. Malar bones are hypoplastic with downslanting palpebral fissures.Eyelids may exhibit coloboma Cleft lip and/or cleft palate are common
Pinnae tend to be cup-shaped. The external auditory canals and middle ears are often malformed. Various congenital heart defects have been documented
Nager syndrome / Preaxial acrofacial dysostosis
Similar to mandibulofacial dysostosis. The zygomatic hypoplasia results in downslanting palpebral fissures. The lower eyelids exhibit colobomas reduced number
External ear defects and cleft palate are common Velopharyngeal insufficiency ‘
Micrognathia is usually more marked mild mental retardation www.indiandentalacademy.com s of eyelashes.
HEMIFACIAL MICROSOMIA
Temporo-auromandibular dysplasia / Goldenhars syndrome
Facial asymmetry with deviation of the chin towards the affected side and ear anomalies are the 'hallmarks' of this entity
Ear - anotia to an ill-defined mass of tissue that is displaced anteriorly and inferiorly, to a mildly dysmorphic ear are found in over 65%. Preauricular tags of skin and cartilage are extremely common, and maybe unilateral or bilateral.
Both the horizontal and ascending ramus of the mandible may have macrostomia. malformations are most severe in the condylar region and less near the middle sector, with flattening of the gonial angle .
Hypoplasia of the maxilla on the affected side is shown by obliquity of the occlusal plane entuation of the antegonial notch.
A depression and recession of the inferiolateral angle of the orbit indicates involvement of the malar bone. Orbital dystopia may be observed temporalis, masseter and lateral pterygoid may be differentially hypoplastic. A fused mass may be observed on CT scans, containing elements of each of these muscles.
Aplasia of the levator veli palatini, resulting in abnormal elevation of the soft palate towards the unaffected side parotid gland may be absent,producing a preauricular concavity.
Maxillary, temporal, and malar bones on the involved side are reduced in size and flattened Narrow external auditory canals are found in more mild cases; atretic canals are seen in more severe cases.
Unilateral or bilateral cleft lip and/or cleft palate occurs in 7-15% of patients Tooth development tends to be delayed and missing on the affected side 35% have velopharyngeal insufficiency.
CRANIOSYNOSTOSIS
conditions in which one or more sutures close too early causing problems with normal brain & skull growth Occurs 1 in 2000 live births Affects males twice as often as females .Most often occurs sporadically .Can be inherited as: Autosomal recessive Autosomal dominant
Pachycephaly
Premature closure of the lambdoid sutures found isolated, associated with synostosis of the sagittal suture or as part of multiple synostoses. It causes hypoplasia and flattening of the occiput, with slight compensatory development of the ipsilateral anterior cranial region.
Scaphocephaly/ interparietal
Elongated narrow shape of the skull, resembling the hull of a ship resulting from early fusion of the interparietal sagittal suture. From front, the skull is high and narrow ; from side, skull is elongated from front to back with posterior occipital protrusion and excessive bulging of the frontal bones anteriorly.
Trigonocephaly / interfrontal
Premature closure of the frontal suture. The frontal area becomes triangular. extent of skull malformation depends on how early the synostosis takes place; this usually occurs during intra-uterine life. Results in a prominent ridge running down the forehead Forehead may look pointed like a triangle with closely placed eyes
Plagiocephaly
Asymmetric malformation secondary to fusion of one half of the coronal suture. Mainly affecting the sphenotemporal suture . Produces flattening of forehead & the brow on the affected side with forehead excessively prominent on the opposite side.
Brachycephaly / frontoparietal
Refers to craniofacial dysmorphism secondary to premature bilateral coronal stenosis the skull is shortened in the sagittal plane and compensatory lateral development occurs in breadth or in height.
Binder's syndrome / Maxillo-nasal dysostosis
Nasomaxillary deformity which mainly affects the lower part of the nose and the premaxilla It is due to an alteration of the inferior mesenchymal portion of the medial strut formed by the vomer pushing the premaxilla forward.
Philtrum is poorly developed Premaxilla is hypoplastic with shortening of
the dental arch All patients have relative mandibular
prognathism with anterior crossbite
Crouzon syndrome
The term refers to a typical deformation, but this anomaly may be due to various causes. The developmental arrest affects the Maxilla, the Orbit and the Vault .It is an autosomal dominant condition. Two genes known to be associated are FGFR2 and FGFR3.
Cranium- Some people have craniosynostosis at birth in which several sutures are always involved . A very pronounced bregmatic boss “Clown’s Hat” may be observed. The severity of cranial malformations does not parallel that of face
Eyes – Exopthalmos, the cardinal sign is constant eyes give the patient a ‘ toad like ’ appearance. This appearance is due to hypoplasia of the maxilla, of the malar bone and of the orbital roof, resulting in the reduction in the size of the orbital cavities Divergent strabismus or defective convergence is frequent.
Face – flattened and sometimes concave. Parrot beak appearance of nose b’coz of maxillary retrusion. Dental malpositioning is common, sometimes with supernumerary or abnormal ‘peg-top’ teeth. Palate is high, arched, narrow & pointed nasal root is flat, the dorsum and the nostrils are wide.
Vision- Lack of skeletal protection may result in exposure keratitis or even dislocation of the globe. Respiration Constriction of airway may result in chronic or intermittent respiratory problems.
Apert's syndrome
Inherited in an autosomal dominant manner. The gene involved is FGFR2 (fibroblast growth factor receptor 2) located on chromosome 10 of those having craniosynostosis, 4-5% have Apert’s syndrome.
Down slanting palpebral fissures, strabismus, orbital hypertelorism.
ears may appear low set and Otitis media is common
Midface deficiency (maxillary hypoplasia). Class III malocclusion is present, with
anterior open bite and anterior and posterior crossbite
Delayed dental eruption
Palate is high arched; constricted, and has a median furrow. Lateral palatal swellings (Hyaluronic acid) are present, which increase in size with age. The maxillary dental arch is Vshaped with severely crowded teeth and bulging alveolar ridge
Pfeiffer syndrome
Mostly autosomal dominant transmission Main features-craniosynostosis,broad thumbs, broad great
toes, and soft tissue syndactyly of the hands skull is usually
turribrachycephalic. Craniofacial asymmetry may be present
Maxillary hypoplasia
Hypertelorism, downslanting palpebral fissures,ocular proptosis, and strabismus are common
palate is highly arched, alveolar ridges are broad, and teeth are crowded
thumbs and great toes are broad Mild soft tissue syndactyly.
Saethre-Chotzen syndrome
Craniosynostosisis is a facultative feature Brachycephaly or acrocephaly with coronal
sutural synostosis is seen, producing plagiocephaly and facial asymmetry
Frontal bossing, parietal bossing, and flattened occiput with late-closing fontanels are seen.
Oral anomalies include narrow or highly arched palate, cleft palate supernumerary teeth, enamel hypoplasia .Some degree of brachydactyly and partial cutaneous syndactyly is present.
Cloverleaf anomaly ,Triphyllocephaly
Characterized by hydrocephalus and a trilobular skull with synostosis of the lambdoidal and coronal and metopic sutures, with bulging of the cerebrum through the open sagittal sutures and a widely patent anterior fontanelle.
Main characteristics
hydrocephaly Retrusion of orbital roof exorbitism maxillary retrusion & severe downward
displacement of ears and zygomatic arches
antimongoloid slanting, nasal flattening and an arched palate
Macrostomia;macroglossia oblique facial clefting Iris colobomas and blindness Obstructed nasolacrimal ducts Absent external auditory canals
Ectodermal dysplasia
affect series of ectodermal derivatives including the teeth, the sweat glands and adnexa of the skin derivatives(nails, hairs, setaceous glands).
Hypohydrosis,hypotrichosis, hypodontia are the main characteristics
sex-linked recessive trait. It occurs in males
Main features
Thin hair Thin and/or small nails Person cannot perspire and consequently
suffers from hyperpyrexia & inability to endure warm temp
The midface is retruded due to deficient alveolar growth.
Jaw and facial development are normal forehead is prominent and the nose flattened
the skin is thin and dry with multiple ridges hairs are scarce and underdeveloped.
complete or partial absence of teeth & when present teeth may be truncated or cone shaped.
Palatal arch is frequently high and a cleft palate may be present.
Forehead is prominent and nose flattened xerostomia may be present. Hypoplasia of the nasal & pharyngeal mucous glands which leads to chronic rhinitis &/or pharyngitis, sometimes associated with dysphagia & hoarseness.
NEUROFIBROMATOSIS
characterized by neurofibromas or other neural tumours and by focal cutaneous hyperpigmentation (cafeaulait spots) caused by aggregation of melanoblasts in the basal layer of the epidermis. derivatives from the neural crest, are primarily affected.
Skeletal malformations – macrocranium interosseous cysts and perforating defects,
expansion of the middle cranial fossa hypoplasia of the sphenoid resulting in wide
areas of communication between the cranial cavity and the orbit
downward displacement of the zygoma, maxilla and the mandible on the affected side.
Pierre Robin syndrome
It’s a combination of problems that begins with Micrognathia . Causing not enough room for the tongue to lie flat in the mouth, so it rests at the back of the mouth. Glossoptosis prevents palate from closing resulting in Cleft palate.
It is a disturbance of muscular maturation of nervous origin which affects the masticatory mu
Retromandibulism is caused by deficient activity of the pterygoid muscle, which is unable to bring the mandible forward.
Stickler syndrome
It is a connective tissue disorder caused by a change in one of the 3 genes for connective tissue.
Features
Cleft palate and a small lower jawOf those with stickler syndrome , 60% have
pierre robbin syndrome Eyes - near sightedness. increased risk of
cataracts & retinal detachment.
Mobius syndrome
involves paralysis of certain facial nerves (unilateral or bilateral). Mainly the intra-cerebral nuclear part of the 6th & 7th nerves are affected. face is motionless with a characteristic nasiolabial grin.
Patient cannot do side to side eye movements, but they will be able to move them up & down. Blinking action may be difficult hypoglossia & microstomia may be seen skeletal involvement include clubfoot, missing or webbed.
Hemangioma
A type of birth mark. Most common benign tumor of the skin. May be present at birth (faint red mark) or may appear in the first months after birth. Also known as port wine stain, strawberry hemangioma, and salmon patch.
Hemangiomas are usually not present at birth or are very faint red marks After birth, they grow rapidly- often faster than the child’s growth. Over time, they become smaller (involute) and lighter in colour
Vascular malformations- These are present at birth. Enlarge proportionately with growth of the child. They do not involute spontaneously and may become more apparent as the child grows.
Velocardiofacial syndrome
Autosomal dominant inheritance Features Face -Approx 40% are
microcephalic face is long with vertical maxillary excess malar flatness and mandibular retrusion. nose is prominent with squared nasal root, hypoplastic alae nasi, and narrow nasal passages
Adenoids are hypoplastic Narrow palpebral fissures with blue suborbital coloring occurs Small ear auricles and minor thickening of the helical rims have been seen Multiple cardiac anomalies are present in over 80%, especially VSD.
Cleft palate (35%), submucous cleft palate (33%), and occult submucous cleft palate or velar paresis (33%) resulting in hypernasal speech have been found in nearly all patients Class I malocclusion is common .The pharynx is hypotonic
Cleidocranial dysplasia
autosomal dominant inheritance individuals are usually short skull is brachycephalic, with pronounced
frontal and parietal bossing. maxilla and zygomas are hypoplastic.
skull is large and short Closure of the anterior fontanel and sagittal
and metopic sutures is delayedSecondary centers of ossification appear in
the suture lines, and many Wormian bones are formed
Delayed union at the mandibular symphysisis characteristic.
nose is broad at the base, with the bridge depressed.
neck appears long, and the shoulders are narrow and droop markedly
Clavicles are absent unilaterally or bilaterally
variations in size, origin, and insertion of muscles related to the clavicles, especially the sternocleidomastoid,trapezius, deltoid, and pectoralis major.
palate is highly arched. Submucous cleft of palate and complete cleft
of the hard and soft palates is seen Development of the premaxilla is poor with
relative prognathism
multiple supernumerary teeth Multiple crown and root abnormalities, crypt
formation around impacted teeth, ectopic location of teeth, and lack of tooth eruption
CFA TEAM
It is agreed worldwide that management of patients with CFAs is best provided by a multidisciplinary team of specialists.
Plastic /craniofacial surgeon Neurosurgeon Pediatrician Orthodontist Pediatric dentist Speech & language specialist Otolaryngologist Audiologist
Opthalmologist Genetic councellor Nurse team coordinator Social worker Psychiatrist
The surgeon and the orthodontist plan at the very beginning for diagnosis and treatment planning . A detailed treatment plan should be written, including a specific definition of what orthodontic teeth movement is to be done prior to surgery; how the orthodontic appliance will be used for surgical fixation; and what orthodontic tooth movement will be required to finish the case following surgery.
he efficacy of orthodontic and orthopedic treatment in case of craniofacial anomalies depend on the type of deformity, taking mainly into consideration the growth potential.
Presurgical orthodontic treatment
The main objective of this stage is to arrange the teeth so that they will approximately fit when the arches are surgically moved.
Continuous arch wire technique Segmented arch technique
Continuous arch wire technique Used for total maxillary surgical procedures. progressively the size of the arch wires is
increased to achieve final stability in the postsurgical occlusion.
If .018 slot is used, the minimum size of arch wire for a total maxillary surgical splint is .016x.022 without palatal splinting and .016x.016 if acrylic or metal palatal splinting
Segmented arch technique-used in preparation for a segmented surgical
procedure. orthodontic treatment time is shortened
because alignment of each segment is done without being concerned about the relationship of the segments to each other.
Disadvantage- when surgical suspension wires are used inadequate fixation will allow the crowns of the segments to be buccally torqued, causing posterior buccal overjet and open bite
Post surgical orthodontic treatment - Involves various final adjustments in the occlusal relationships and the final tooth alignment. This final phase usually lasts form 3 to 4 month.
Transverse Maxillary Deficiency
3 main factors should be considered amount of arch length discrepancy In moderate to minimal space deficiency,
RME will increase arch circumference sufficiently to permit alignment of the crowded anteriors without the necessity of extraction of premolars
Arch morphology
Cases in which a transverse deficiency exists will exhibit a narrow, tapering arch form. The discrepancy will be most pronounced in the canine region.
If nonextraction orthodontic therapy is decided lateral maxillary osteotomies and rapid maxillary expansion is the treatment of choice to achieve proper arch morphology
Cases which do not exhibit severe constriction in the anterior region, a two-piece maxillary procedure with a midline osteotomy and resultant diastema may be done consideration to wound healing after creation of an interincisal space should be done.
When excessive the gingiva may detach and interproximal bone may be exposed with a possibility of devascularization and osteonecrosis of the underlying bone
vertical dimension
In cases exhibiting an anterior open-bite with a severely accentuated maxillary curve of spee ; orthodontic treatment by extrusion of incisors and/or intrusion of posterior teeth may compromise the postsurgical stability. Segmentalized orthodontic therapy with a three-piece or four-piece maxillary surgical procedure is indicated
True Unilateral Transverse Maxillary Deficiency
should be treated by maxillary segmental surgery with the osteotomy mesial to the most anterior tooth in palatal cross-bite. Orthodontic management of such patients will depend upon the necessity of extra In some cases the apparent maxillary deficiency may be due to the ectopic eruption of one or two posterior teeth in one quadrant and be treated by orthodontic means ctions for alignment of crowded anterior teeth.
Transverse Maxillary Excess
Seen mostly in cases with skeletal class II The aim of presurgical orthodontics in these cases is to position the malaligned teeth over their bases so that the maxilla can be surgically positioned into satisfactory overbite-overjet relationship.
Many technical modifications of the Le Fort I osteotomy are feasible to facilitate simultaneous anteroposterior, vertical, or horizontal movements of the anterior and posterior segments of the maxilla
Hemifacial Microsomia
Harvold advocates the use of activators to guide eruption of teeth and prevent midline shift until the time of surgery. This approach may have a stimulator effect on muscle development and serves to prevent canting of the occlusal plane. conventional orthodontic tooth movement is of little value.
In a cephalometric study by Bachmayer, Ross and Munro (AJO 1986) on maxillary growth following Le Fort III osteotomy in children with Crouzon-Apert Pfeiffer (CAP) syndromes it was found that the maxillary growth after surgery is negligible. Vertical maxillary growth following surgery is identical to that in unoperated CAP and normal children, amounting to 1.3 mm/yr.
Olow-Norderam and Thilander (AJO 1989) studied the influence of orthodontic treatment on Binder's syndrome . Although the orthodontic treatment led to acceptable dental conditions in some patients, no influence on craniofacial growth could be demonstrated
Graysun et al ( AJO 1983) in a study on unilateral craniofacial microsomia said that the lateral ceph analysis of patients with unilateral craniofacial microsomia confirmed the clinical impression of an increased gonial angle and decreased ramal height and body length on the affected side.
The ramal height on the unaffected side was also decreased. The mandibular plane angle was greater than normal on both affected and unaffected sides. They conclude that the unaffected side too is characterized by abnormalities in the skeletal anatomy.
Schudy ( JCO 1986) described the surgical correction of Crouzon's and Apert's syndromes by Dr. Paul Tessier. The orthodontic treatment involves no special procedures and is performed in the usual manner. Good arch forms were established for the prospect of good future occlusion before the surgery was performed. After the surgery was done brackets remained on for a further 24 months to improve the occlusion
Skeletal Mandibular Deficiency. 3 types of dentoalveolar problems that require orthodontic treatment often accompany it – Malalignment of the teeth ie: crowding or protrusion.
Most of these are dental compensation for the skeletal deficiency crossbite tendency appears as the mandible is advanced.
Deep bite, with an accentuated curve of Spee due either to elongation of the mandibular incisors or due to vertical under development of the premolar segment of the arch.
Distraction ostegenesis.
specially effective in cases of unilateral mandibular deficiency involves the deliberate fracturing of the bone side and holding it in close but not exact approximation by means of a complex system of extra oral positioners.
Principle
osteogenesis takes place in the intervening space. As soon the bone formation is complete the set up is adjusted so that the bone segments move a bit away from each other. The bone segments are held in that place till new bone is formed and so forth, till the bone achieves the required length.
General principles of treatmentOrthodontic intrusion of teeth must be done
prior to surgery. Extrusion of teeth can be done following
surgery. tooth movement in the transverse or crossbite plane of space can be deferred until after surgery
Tooth movement that occurs immediately after surgery, while the patient is in IMF but before bone healing occurs should also be considered. Orthodontic tooth movement takes place to maintain the dental relationship.
The mandibular dentition slips forward on the mandible (2mm) increasing the prominence of the lower incisors. The maxillary dentition is retracted, decreasing the prominence of the maxillary incisors.
Moving teeth laterally for crossbite correction introduces interferences along the line of the cusps and leads to some lengthening of the posterior vertical dimension and a downward positioning of the mandible.
desirable - skeletal deep bite undesirable - steep mandibular plane angle
Orthodontic Procedures To Be Avoided Prior To Surgery For Mandibular Deficiency.
use of Class II intermaxillary elastics to reduce overjet
produces forward positioning of the lower incisors.
will cause vertical extrusion of the anterior maxillary segment, tending to extrude teeth.
Mandibular excess characterized by a prominent lower third of
the face. orthodontic treatment modalities- Chin-cap therapy Activator appliances
Fully banded orthodontic appliances.
Chin-cap therapy the pressure against the chin would be transmitted to the growing areas of the mandible and the growth would be impeded or at least directed more favorably
Two approaches
impede mandibular growth by applying heavy pressure in the vicinity of the growing condyle of the mandible.
The force is applied upward and backward, opposite to the vector of downward and forward mandibular growth. redirect the growth of the mandible.
It is based on the principle that when the mandible is rotated downward it rotates backward.
Activator appliances: effective in the treatment of class I I I malocclusion using a class III activator causing a downward and backward displacement of the mandible. It may be trimmed to allow posterior teeth to erupt so that the vertical dimension is maintained
Fully banded orthodontic appliances can only be carried out satisfactorily without surgery only when the problem is minor, because it is very difficult to position mandibular teeth so as to camouflage the mandibular prominence.
CONCLUSION
Although craniofacial anomalies have been reported and depicted from ancient times; a team approach to diagnosis ; management and treatment of dysmorphic patients is a recent event. understanding of normal and pathogenesis helps us diagnose and treat to the best of our capabilities
REFERENCES