**3.3. Permanent dentition**

In the permanent dentition, the etiology of the diastemas is multifactorial [2, 16–19] and can be associated to the following factors: abnormal labial frenulum [1, 2, 16, 17, 20–22], microdontia, agenesis of maxillary incisors [2, 10, 16, 17, 20], dental discrepancy [2, 17, 23], shape of the anterior teeth (barrel) [10], brachyfacial pattern [17], a positive tooth-bone discrepancy [2, 16, 17], overbite, congenital anomalies such as soft tissue fissure, hybrid brake, or supernumerary teeth [2, 10, 16, 24], cysts and tumors [2, 24], periodontal disease [2, 25], macroglossia or neuromuscular imbalance of the tongue [10], acromegaly [26, 27], and orthodontic treatment [2, 20, 24].

The etiology of diastemas is also very well explored in a review article published by Bishara [2]. In this study, the authors divided diastemas into two categories, according to the etiology: (1) those not caused by orthodontic treatment, present before its accomplishment; and (2) those that appeared during or after orthodontic treatment. In the first category, the etiological factors mentioned are: physiological spaces in the deciduous dentition; developmental spaces in the mixed dentition phase, which are closed, according to the authors, after the canine eruption; genetic factors such as large jaws and small teeth; tooth size, interarch discrepancy, agenesis, and micro-diseases; characteristics relating to ethnic groups; low insertion of the upper labial frenulum, preventing the mesial migration of the maxillary central incisors during canine eruption; dental rotations; supernumerary teeth, among which a classic example is the mesiodens; pathological conditions, such as proximal caries, periodontitis, cysts, and tumors; and, finally, the deleterious habits, exemplified by the lingual interposition and sucking lip. In the second category, the author refers to dental extractions and occasional dental size discrepancies, caused by extractions as diastematic agents during orthodontic treatment.

biogenetic course of the deciduous dentition, Baume [11] classified the dental arches according to the spaces designated by him as type I, with anterior spaces, and type II, without such

Moyers [14] reported that there is a generalized spacing in the anterior region of the upper and lower arches in the deciduous dentition, which increases significantly after this dentition

In the mixed dentition phase, the diastemas continue to appear as a physiological characteristic, mainly the diastema between the permanent maxillary incisors. The germs of these teeth remain separated within the maxilla, respecting the intermaxillary suture interposed between

Broadbent [12] published a study of 5000 individuals observed over 12 years. The author called the "ugly duckling stage" the period that ranges from the eruption of the upper incisors, around the age of 7 years, until approximately 10 years of age, when the upper canines erupt. At this stage, the lateral incisors remain with the converging roots until the maxilla size is sufficient to assume a more vertical position. With sufficient increase in the size of the subnasal area, and in the presence of normal growth, the canines move down, forward, and laterally to the lateral incisor roots. Correction of the ugly duckling stage will occur in the period between

Burstone [13], observing the normal changes during development, identified that during the "ugly duckling phase" of Broadbent [12], protrusion of the crowns, overjet, and anterosuperior spaces occurs. He also reported that the upper central interincisive diastema would be closed with the eruption of the other permanent teeth, especially the canines, and that the overjet of the incisors would be corrected by the pressure of the labial musculature and the

In the permanent dentition, the etiology of the diastemas is multifactorial [2, 16–19] and can be associated to the following factors: abnormal labial frenulum [1, 2, 16, 17, 20–22], microdontia, agenesis of maxillary incisors [2, 10, 16, 17, 20], dental discrepancy [2, 17, 23], shape of the anterior teeth (barrel) [10], brachyfacial pattern [17], a positive tooth-bone discrepancy [2, 16, 17], overbite, congenital anomalies such as soft tissue fissure, hybrid brake, or supernumerary teeth [2, 10, 16, 24], cysts and tumors [2, 24], periodontal disease [2, 25], macroglossia or neuromuscular imbalance of the tongue [10], acromegaly [26, 27], and orthodontic treatment [2, 20, 24]. The etiology of diastemas is also very well explored in a review article published by Bishara [2]. In this study, the authors divided diastemas into two categories, according to the etiology: (1) those not caused by orthodontic treatment, present before its accomplishment; and (2) those that appeared during or after orthodontic treatment. In the first category, the etiological factors mentioned are: physiological spaces in the deciduous dentition; developmental spaces in the mixed dentition phase, which are closed, according to the authors, after the canine

spaces. In this work, the author cites that one type cannot progress to the other.

has been completed.

98 Current Approaches in Orthodontics

**3.2. Mixed dentition**

8 and 12 years of age.

**3.3. Permanent dentition**

irruption of the other permanent teeth.

them [16].

Steigman et al. [9] evaluated the stability of permanent denture spaces during adolescence in untreated patients, and also investigated the association of tooth spacing with tooth size and dental arch dimensions. They observed that women with spaced dentition had smaller dental widths and similar arch dimensions than those without dental spacing. In them, the spaces were equally distributed in both arches. On the other hand, in men, there was an equivalence of the dental dimensions, but the intercanine distances and superior interpremolars were greater in those with a spaced dentition. This is the reason why, in males, a greater number of spaces were found in the maxilla than in the mandible.

Oesterle and Shellhart [27] mentioned that the presence of generalized spaces in the dental arches may be the result of discrepancies between the size of the teeth and their respective apical bases, muscular imbalances, deleterious habits, and loss or absence of teeth. The large jaw and/or jaw combination with normal or slightly reduced teeth size is related to inherited characteristics, but may also be a sign of endocrine imbalances, which result in excess growth hormone, such as acromegaly.

Gass et al. [18], when evaluating the correlation between the heredity and the presence of the medium diastemas in leucodermas and melanodermas, found that the genetic expression was more significant for the whites than for the black ones, where the existence of an interincisive diastema is more related to environmental factors, such as excessive protrusion of the incisors, a predisposing periodontal tissue, habits, and absence of teeth. However, in relation to the stability of the treatment, an association between heredity and median diastema recurrence has been reported [28].

In the same year, Mondelli et al. [24], in a comprehensive review work describing the etiology and the various diastema treatments, add that there are diastemas of iatrogenic etiology. As examples, the authors cited the rapid expansion of the maxilla and a type of mechanics inadequate for diastema closure, where an elastic band is positioned on the central incisors, but slides in the cervical direction, causing periodontal damage and root approximation, with consequent divergence of the crowns, making the diastema even wider.
