The Mandible

Embryology

At birth, the mandible consists of two lateral halves united in the midline at the symphysis by a bar of cartilage (Fig. 22-1, e-Fig. 22-2, and Figs. 22-3 and 22-4). Bony fusion of the symphysis usually occurs before the second year, but segments of the fissures may persist beyond puberty. The body of the mandible is large at birth compared with the relatively short rami and poorly differentiated coronoid and condylar processes. The rami form an angle of about 160 degrees with the body at birth.

Figure 22-1 Important anatomic features of the normal mandible.

Figure 22-3 Anatomy of a normal temporomandibular joint. The zygomatic arch and a portion of the ramus of the mandible are cut away to expose the articular disk.

Figure 22-4 A, A mandible in an 8-week-old infant with hereditary ectodermal dysplasia shows failure of calcification of dental crowns and defective dental sacs. B, A radiograph of a normal 8-day-old newborn shows normal dental development in the neonatal period.

e-Figure 22-2 The relative size and shape of neonatal and adult mandibles. The rami form an angle with the body of 160° at birth; this angle is reduced to 130° at adolescence and 120° in adulthood. (Modified from Arey LB. Developmental anatomy. Philadelphia: Saunders; 1942.)

Formation of the dental buds is visible by 20 weeks’ gestation. Beginning mineralization in the first molar tooth occurs between gestational weeks 33 and 34, and in the second molar tooth, it occurs between gestational weeks 36 and 37. In contrast to bone age, dental age is little affected by endocrine aberrations.

All or some of the teeth may be missing developmentally, as in persons with anhidrotic ectodermal dysplasia (Fig. 22-4).¹ Because infants and children with normal dentition seem to have a plethora of teeth in radiographs (deciduous and permanent dentitions), the condition may be recognized in a newborn by the lack of dental buds. Many diseases cause loss of dentition, and recognition of premature loss of teeth can lead to important diagnoses (Box 22-1).²

Box 22-1 Premature Loss of Primary or Permanent Teeth

Most Common

Hypophosphatasia

Early-onset periodontitis

• Secondary to any condition with impaired polymorphonuclear leukocyte function

• Diabetes mellitus (usually poorly controlled)

Medications

Membrane ion chamber blockers

Antiepileptic drugs

Antihypertensive calcium antagonist

Cyclosporine (alone or in combination with nifedipine)

Steroids

Other Systemic Diseases

Human immunodeficiency virus

Histiocytosis syndromes

Acrodynia

Genetic Disorders

Down syndrome

Chronic granulomatous disease

Papillon-Lefèvre syndrome

Chédiak-Higashi syndrome

Ehlers-Danlos syndrome

Wiskott-Aldrich syndrome

The opposite condition—too many teeth with little alveolar bone—can be seen in persons with cleidocranial dysplasia, who have marked delay in shedding of the deciduous teeth. Early tooth extraction has no effect on the subsequent eruption of the permanent dentition and may result in a lengthy edentulous period for the child.³

Anatomy

The mandible is the only freely movable bone of the face; it articulates with the temporal bone in the temporomandibular fossa anterior to the external auditory canal (see Fig. 22-3). The range of motion is free in all directions, and the condyle moves downward and forward in the articular fossa upon opening of the jaw.

The temporomandibular joint (see Fig. 22-3) is a complex joint in which a biconcave fibrous disk divides the articular space into upper and lower compartments.^4–6 Gliding movements occur in the upper compartment, whereas the lower compartment functions as a true hinge joint. The articulating bony surfaces are not covered by hyaline cartilage as in other joints, but by an avascular, fibrous tissue that is separated from the underlying bone of the condyle by growth cartilage.⁷

Diseases of the Mandible

Significant congenital malformations of the mandible are rare, with the most important being hypoplasia (micrognathia), which may be a cause of congenital stridor. The short, small mandible apparently causes a retrodisplacement of the tongue and obstruction to airflow (Fig. 22-5).

Figure 22-5 Hypoplasia of the mandible in a 1-day-old newborn—lateral projection. The short dorsoventral diameter of the mandible is evident; the tongue is displaced posteriorly and fills the greater part of the pharynx (black arrow). The displaced tongue impinged on the epiglottis and interfered with the flow of air to and from the larynx (white arrow).

Micrognathia occurs in a variety of dysmorphic syndromes. The combination of cleft palate and hypoplasia of the mandible defines the Pierre Robin sequence radiographically. The Pierre Robin association is nonspecific and occurs with several genetic and drug-induced syndromes and some loosely associated anomalies, as well as an isolated symptom complex.⁸ In the cerebrocostomandibular syndrome, it is associated with posterior rib defects, cleft palate, and, occasionally, mental retardation.⁹

Elongation of the body of the mandible and widening of its arc occur in conditions associated with an enlarged tongue, including lymphatic malformations and Beckwith-Wiedemann syndrome. Relative enlargement of the mandible is observed in several craniofacial syndromes. The angle of the mandible is markedly increased in persons with pyknodysostosis. Rare cases of hyperplasia of the coronoid process are observed; the enlargement impinges on the zygomatic arch and interferes with normal opening of the jaw. The temporomandibular joints frequently are involved in persons with juvenile rheumatoid arthritis. Rarely, the mandible may be partially duplicated.

Temporomandibular Joint Disorders

Disorders of the temporomandibular joint are infrequent but not rare.10,11 Adventitious sounds on mandibular movement, muscle tenderness or pain, and deviation of the mandible during movement are the most common signs and symptoms. Magnetic resonance imaging (MRI) is the most precise imaging modality.^12,13