Malocclusion

From bonepath

Malocclusion is a general term referring to the misalignment of the upper and lower teeth, and there are several ways this can manifest. Overjet / overbite refers to the maxillary dental arcade being positioned anterior to the mandibular arcade, and is clinically referred to as Class II malocclusion or molar relationship (McNamara 1981). Contrarily, in negative overjet / under-bite the mandibular arcade is anterior to the maxillary, and is clinically referred to as a Class III malocclusion (Guyer et al. 1986). Class I molar relationship is more or less ‘normal’ or neutral positioning of the upper and lower dentition (i.e. not really maloccluded). Dibbets (1986) argues that these antero-posterior malocclusions form a morphological continuum (overbite/Class II → neutral/Class I → under-bite/Class III). Cross-bite is the transverse malocclusion of the upper and lower dentition (McNamara 2009). Finally, dental crowding is a malocclusion in which individual or multiple teeth are misaligned because there is not enough space in the jaw (Howe et al. 1983). Indeed, many malocclusions may result from too small a maxilla (“maxillary deficiency syndrome”; McNamara 2009) Malocclusion appears to be a fairly recent dental phenomenon. A number of studies have found that the frequency and severity of (various) malocclusions have increased in modern versus archaeological samples (e.g. Evansen and Øgaard 2007), and in post-industrial versus “traditional” or hunter-gatherer modern societies (Begg 1954, Beecher and Corruccini 1981). Beecher and Corruccini (1981) reported that malocclusion affected up to 50% of Americans, and Evansen and Øgaard (2007) report a prevalence of 40-80% of malocclusion in modern populations. While malocclusion does seem to have at least a small heritable and/or congenital component (Beecher and Corruccini 1981, Dibbets 1986), most researchers would argue that the recently-high frequency is due to environmental factors (Begg 1954). Most notably, irregular muscle forces acting on the jaws during growth and dental eruption probably seem to influence occlusal relationships (McNamara 1981). Thilander and colleagues (2002) found a significant association between various types of malocclusion and temporomandibular dysfunction (TMD, a general term describing various “clinical signs and symptoms” affecting the temporomandibular joint and masticatory musculature). Mouth-breathing has been one suspected source of some TMD responsible for malocclusion (Evansen and Øgaard 2007). Begg (1954) and Beecher and Corruccini (1981) have argued, though for different reasons, that the soft-diet of industrialized populations is responsible for malocclusion. Begg (1954) argues that soft-diet reduces the amount of interproximal (between adjacent teeth in the same jaw) attrition and mesial drift, which results in jaws that cannot sufficiently accommodate excessive “tooth substance.” Beecher and Corruccini (1981), on the other hand, argue that the soft diet requires insufficient stimulus for adequate jaw growth. Supporting the latter hypothesis, Howe and colleagues (1983) found that crowding and other malocclusions were due to insufficient maxilla size, as opposed to large tooth size. Nevertheless, it is likely that both reduced interproximal wear and lessened jaw growth, engendered by a softened modern diet, are responsible for a majority of recent cases of malocclusion. A number of authors review skeletal morphologies associated with various forms of malocclusion (e.g. Class I-III: Dibbets 1996; Class II: McNamara 1981, Franchi et al. 2007; Class III: Brezniak et al. 2002). Malocclusion can be ‘corrected’ by tooth extraction to better accommodate teeth in a reduced jaw (e.g. Begg 1954), or by various orthodontic apparatuses to increase jaw size (e.g. McNamara 2000).

References

Beecher RM, Corruccini RS. 1981. Effects of dietary consistency on craniofacial and occlusal development in the rat. Angle Orthod 51: 61-9.

Begg PR. 1954. Stone age man's dentition with reference to anatomically correct occlusion, the etiology of malocclusion, and a technique for its treatment. Am J Orthod 40: 298-312.

Brezniak N, Arad A, Heller M, Dinbar A, et al. 2002. Pathognomonic cephalometric characteristics of Angle Class II Division 2 malocclusion. Angle Orthod 72:251-7

Dibbets JM. 1996. Morphological associations between the Angle classes. Eur J Orthod 18: 111-8.

Evensen JP, Øgaard B. 2007. Are malocclusions more prevalent and severe now? A comparative study of medieval skulls from Norway. Am J Orthod Dentofacial Orthop 131: 710-716.

Franchi L, Baccetti T, Stahl F, McNamara JA. 2007. Thin-plate spline analysis of craniofacial growth in Class I and Class II subjects. Angle Orthod 77: 595-601.

Guyer EC, Ellis EE, McNamara JA, Behrents RG. 1986. Components of class III malocclusion in juveniles and adolescents. Angle Orthod 56: 7-30.

Howe RP, McNamara JA, O'Connor KA. 1983. An examination of dental crowding and its relationship to tooth size and arch dimension. Am J Orthod 83: 363-373.

McNamara Jr JA. 1981. Components of Class II malocclusion in children 8-10 years of age. Angle Orthod 51: 177-202.

McNamara Jr JA. 2000. Maxillary transverse deficiency. Am J Orthod Dentofacial Orthop 117: 567-570.

McNamara Jr JA. 2009. Maxillary Deficiency Syndrome. In Current Therapy in Orthodontics. Nanda and Kapila, eds: 137-42.

Thilander B, Rubio G, Pena L, De Mayorga C. 2002. Prevalence of temporomandibular dysfunction and its association with malocclusion in children and adolescents: An epidemiologic study related to specified stages of dental development. Angle Orthod 72: 146-152.