*3.7.2 Genetic factors*

*Current Treatment of Cleft Lip and Palate*

A high incidence of enamel hypoplasia is found to occur more frequently in CLP patients compared with non-cleft populations, especially involving the maxillary

Dixon suggested that lip repair could cause enamel hypoplasia in deciduous incisors and tips of permanent incisor crowns related to the surgical area; whereas the palatal repair could cause some defects in the crowns of the permanent incisors [1].

CLP patients commonly present with anomalies in shape and size of permanent teeth, especially at the maxillary anterior region. The malformations frequently

Taurodontism [65, 88], root dilacerations [62], fusion, germination and concres-

Cleft sided central incisors are often found to be rotated, with a prevalence of 68.6% to 86.17 [48, 50, 89] reported. This has been attributed to the lack of space at

The canines on the cleft side are often palatally impacted. It has been suggested that the impaction may be due to the palatal collapse of the maxillary lateral seg-

Lai et al. suggested that when the lateral incisor is located distal to the cleft, it

Ectopic eruption of teeth, including transposition has also been reported in

ment [89] or related to the genetic factor responsible for CLP [91].

can provide guidance for the eruption of the adjacent canine [47].

Other dental anomalies associated with CLP patients include thick curved maxillary central incisors [53, 54], addition of paralabial tubercles on the central incisor and canine, missing cusp or altered cusp patterns of the maxillary molars and mandibular bicuspids [53] and smaller mesial-distal width of central incisors on the cleft side [44, 84]. Interactive compensations with dental variations in size have been reported to occur within tooth classes [85]. In non-cleft oligodontia with multiple missing teeth, the dentition was found to be reduced in size. However, in dentition with isolated tooth agenesis, tooth-size was larger compared to those of fully dentate individuals without hypodontia [86]. The premise of an odontogenic interactive compensatory mechanism was suggested in that a size reduction of a lateral incisor was a localised response to a large adjacent central incisor [87].

**3.5 Abnormalities in shape and size of permanent teeth**

exhibit as microdontia or macrodontia [47, 50, 52, 62].

cence [81] have also been associated with CLP patients.

**3.6 Abnormalities in position of permanent teeth**

*3.6.1 Rotated cleft-sided central incisors*

the end of the alveolar segment [90].

**3.4 Enamel hypoplasia**

*3.5.1 Crown abnormalities*

*3.5.2 Root abnormalities*

*3.6.2 Impacted canines*

*3.6.3 Ectopic eruption*

patients with CLP [62, 90, 92, 93].

incisors [1, 52, 62].

**10**

As the increased prevalence of dental anomalies was also found in the noncleft region, it was postulated that dental anomalies in CLP patients were affected by common developmental mechanisms that involved non-fusion of orofacial processes and the persistence of orofacial clefts during embryonic and foetal formation. Extensive studies on orofacial clefting have linked genetic susceptibility, signalling pathways and transcription factors in the regulation of -lip, palate and dentition development [94–97].

Multiple disruptions in development of a number of body tissues including the dental lamina result in frequent occurrences of dental anomalies together with and several other visceral and skeletal anomalies in CLP children [41, 98, 99].

This has led to several studies investigating the presence of dental anomalies in parents and siblings of CLP children, of which, the results have been conflicting to date. Both Jordan et al. [53] and Schroeder and Green [54] reported a higher than normal frequency of occurrence of dental anomalies in the siblings of affected CLP individuals than in the general population. More recently, Eerens et al. reported significantly higher frequency of hypodontia and asymmetric tooth formation in both cleft and unaffected sibling groups compared with normal controls [41].

On the other hand, Woolf et al. observed that the incidence of maxillary lateral incisor abnormalities in parents' dentition was similar to non-cleft controls [58]. Mills et al. demonstrated no significant differences in the oral and facial defects between cleft and non-cleft families [59].

Anderson and Moss similarly found no evidence to suggest that parents of CLP children have a higher incidence of dental abnormalities than the general population and suggested that the genes carried by the non-cleft parents of CLP cases do not produce dental manifestations [60]. This could be because the genetics of odontogenesis is complex and is influenced by many factors, genes, epigenetics, and environmental factors [60, 100, 101].
