Dental Impaction

From bonepath

Impaction refers to the failure or extreme delay of a tooth’s eruption into the mouth. The two most commonly impacted teeth are the canine and third molar. Canine impaction is found in 0.8 – 4.9% of orthodontic cases (Thilander and Jakobsson 1966, Peck et al. 1994, Chung et al. 2011, Kazanci et al. 2011). Canine impaction is most often unilateral, involving a palatally (as opposed to labially) displaced tooth, and found in girls (Thilander and Jakobsson 1966, Kazanci et al. 2011). Support for the idea that canine impaction is due to reduced space in the dental arch is mixed (e.g. yes in Thilander and Jakobsson 1966, no in Chung et al. 2011). It has been suggested that because impacted canines are often found in association with other dental anomalies such as hypodontia or tooth agenesis, there is some genetic basis for impaction (Peck et al. 1994, Chung et al. 2011); in spite of such claims, specific genes have yet to be identified as causing dental impaction (and associated anomalies).

The third molar is the other most commonly-impacted tooth, affecting up to more than 50% of dental samples (Dachi and Howell 1961, Richardson 1977, Eliasson et al. 1989, Celikoglu et al. 2010). Eliasson and colleagues (1989) reported relatively few pathologies associated with long-term M3 impaction, the greatest being resorption of the second molar or its alveolar bone. A number of studies have suggested that M3 impaction may be of epigenetic origin: a lack of space in the jaws preventing the eruption of the last molar (i.e. Begg 1954, Richardson 1977, Forsberg 1988). Richardson (1977), for example, found that patients with impacted M3s tended to have larger M3s and reduced jaw growth compared to individuals whose M3s had fully erupted. Forsberg (1988) found that girls with M3 impaction tended to have longer overall dental arcades (mesiodistally), and that boys with impaction tended to have a higher incidence of dental crowding. This growth-related (epigenetic) etiology of M3 impaction contrasts with the proposed genetic etiology of canine impaction, which is more often associated with other dental anomalies (Peck et al. 1994).

References

Celikoglu M, Miloglu O, Kazanci F. 2010. Frequency of agenesis, impaction, angulation, and related pathologic changes of third molar teeth in orthodontic patients. Journal of Oral and Maxillofacial Surgery 68:990-5.

Chung DD, Weisberg M, Pagala M. 2011. Incidence and effects of genetic factors on canine impaction in an isolated Jewish population. American Journal of Orthodontics and Dentofacial Orthopedics 139:e331-5.

Dachi SF, Howell FV. 1961. A survey of 3,874 routine full-mouth radiographs:: II. A study of impacted teeth. Oral Surgery, Oral Medicine, Oral Pathology 14:1165-9.

Eliasson S, Heimdahl A, Nordenram A. 1989. Pathological changes related to long-term impaction of third molars. A radiographic study. International Journal of Oral and Maxillofacial Surgery 18:210-2.

Forsberg CM. 1988. Tooth size, spacing, and crowding in relation to eruption or impaction of third molars. American Journal of Orthodontics and Dentofacial Orthopedics 94:57-62.

Kazanci F, Celikoglu M, Miloglu O, Ceylan I, Kamak H. 2011. Frequency and distribution of developmental anomalies in the permanent teeth of a Turkish orthodontic patient population. Journal of Dental Sciences 6: 82-9.

Peck S, Peck L, Kataja M. 1994. The palatally displaced canine as a dental anomaly of genetic origin. The Angle Orthodontist 64:249-56.

Richardson ME. 1977. The etiology and prediction of mandibular third molar impaction. The Angle Orthodontist 47:165

Thilander B, Jakobsson SO. 1968. Local factors in impaction of maxillary canines. Acta Odontologica Scandinavica 26:145-68.