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A specific pattern of dentofacial deformity that occurs after birth and that primarily affects the mandible may be referred to as an asymmetric mandibular excess growth anomaly.* This is a useful term for name recognition, but it falls short of explaining the causes and effects of this common pattern of jaw deformity. This condition typically results in an uneven Angle Class III malocclusion, and it has been referred to by a variety of terms, including deviated mandibular prognathism, condylar hyperplasia, mandibular lateral gnathism, osteochondroma of the mandibular condyle, and asymmetric Class III dentofacial deformity. The overall effect on maxillofacial morphology also includes the secondary deformities that occur to the maxilla, the nose, the chin region, the position of the teeth, and the distortions that are visually observed in the overlying soft-tissue envelope. These effects are dependent on multiple factors, including the intensity of the mandibular hyperactivity; the patient’s age when the abnormal bone growth begins; any underlying hereditary dentofacial deformity tendency; and the treatment that was previously rendered (i.e., orthodontic, dental, or surgical) before the patient’s arrival to the surgeon for evaluation. These asymmetric mandibular excess growth patterns may be confused with other causes of maxillomandibular asymmetry (i.e., hemifacial hyperplasia, hemifacial microsomia, growth disturbance after a condyle injury during childhood).^{10,27,48,49,55,93,94,124} Most misdiagnosis are easily clarified by taking an accurate history, completing a physical examination, and reviewing the patient’s radiographs (Fig. 22-1).

Obwegeser believes that this dentofacial deformity is caused by two different growth regulators.23–25,68–91 The first is a more rare form, and it is clinically characterized by an increase in volume of all parts of the affected side of the mandible, without a lateral shift of the chin to the opposite side. Its primary effects end near the midline at the symphysis (Figs. 22-2 through 22-5). The second and more common form of this dentofacial deformity is characterized by an elongation of the affected side of the mandible, often with widening of the gonial angle and with clear displacement (i.e. lateral shift) of the midline of the chin and the mandibular dental midline to the opposite side of the face (Figs. 22-6 through 22-14).

Obwegeser also stated that these two pure forms of dentofacial deformity may present as a spectrum.23–25,68–91 He called these two pure dentofacial deformities Type I or hemimandibular hyperplasia and Type II or hemimandibular elongation. Obwegeser hypothesized that the steering mechanism for the growth of these two distinct mandibular anomalies is located entirely within the cartilaginous zone of the condylar head. This was proven to him by the fact that, whenever a very rapidly developing mandibular overgrowth (either Type I or Type II) was encountered, he was able to arrest the growth and prevent further deformity by completing a high condylar resection.

Raijmakers and colleagues carried out a meta-analysis to determine gender differences when it came to the diagnosis of asymmetric mandibular excess.¹⁰¹ Ten studies were reviewed, and these included a total of 275 affected patients. The meta-analysis showed a clear predominance of female patients in the study populations. The male and female patients had an equal distribution of left- and right-sided condylar overgrowth. The authors postulate that hormonal variations—especially of estrogen in women—may explain these differences. An alternative explanation put forth for this apparent female predilection is a difference in motivation between the sexes to seek the correction of their facial asymmetry (see Fig. 22-6).

Slootweg and Muller described four histologically different types of mandibular condylar hyperplasia.¹¹⁶ They proposed a classification system that is based on histologic criteria, and they divided hyperplastic condyles into four types, depending on the arrangement and morphology of the various layers of the condyle. These condylar layers were the fibrous articular layer; the undifferentiated mesenchyme proliferative layer; the transitional layer; and the hypertrophic cartilage layer.

Villanueva-Alcojol and colleagues attempted to correlate demographic and clinical presentations of condylar hyperplasia with the described histopathologic features and then with the associated scintigraphic and clinical findings after treatment with high condylectomy during the active phase.¹²² Interestingly, the authors were unable to find a correlation between the histologic type (as described by Slootweg and Muller¹¹⁶) and the uptake of the affected condyle on bone single photon emission computed tomography or between the patient’s age and his or her histologic type.

The preferred treatment to correct the dysmorphology for all forms of condylar hyperplasia is surgical including the repositioning and recontouring of the bones in combination with orthodontics to align the teeth.* The extent of treatment depends on the presenting dysmorphology and the status of condylar growth. If ongoing condylar growth is documented, then a form of high condylectomy should be considered to arrest progressive dysmorphology.^20,21,40,42

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