[Normal and abnormal medial diastema. II. Diastema, frenulum and pin].
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Diastema↗
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Origin and developmental fate of vestigial tooth primordia in the upper diastema of the field vole (Microtus agrestis, Rodentia).
OBJECTIVE: Odontogenesis in voles is a convenient model to test hypotheses on tooth development generated from investigations in the mouse. Similar to other rodents, the functional dentition of the vole includes a toothless diastema. At its mesial end, a vestigial tooth bud has been found in the upper jaw of vole embryos. The aim of this study was to analyse the developmental dynamics of vestigial tooth structures in the upper diastema of the field vole and to compare it with the situation in the mouse. DESIGN: The development of odontogenic structures in the upper diastema of the field vole was investigated using serial histological sections and three-dimensional (3D) computer-aided reconstruction. RESULTS: A transient continuous dental lamina in the upper diastema of the field vole extended mesially to the first molar primordium, but was not continuous with the dental lamina in the incisor region. At its mesial limit, a large vestigial tooth primordium was regularly present. A further distinct vestigial bud was located mesially to the first molar primordium. The segmentation of the dental lamina suggested a potential to give rise to further vestiges in the upper diastema of the vole. CONCLUSIONS: In the prospective diastema of the vole exists as in the mouse a continuous dental lamina. Beside the prominent vestigial tooth bud in the mesial diastema, a further large bud was transiently located in front of the molars. The incorporation of dental epithelium into the first upper molar (M(1)) primordium in the vole differs from that in the mouse.
Animals↗
Characteristic tissue interaction of the diastema region in mice.
Rodents have a toothless diastema between the incisor and the first molar, which may contain rudimentary tooth germs. In the lower diastema region of mice at E13, the rudimentary tooth germs, which developed into the bud stage before its removal by apoptosis, was found. The immunoreactivity to tenascin was observed in the condensed mesenchyme around the normal tooth bud and was detected in only the basement membrane in the diastema bud. This result shows that the relationship between mesenchymal condensation and tooth development. The similar patterns of Msx-1 and Msx-2 expression between the tooth bud and the diastema bud show that the diastema bud may have some other genetic mechanism in the developmental arrest of the rudimentary tooth germs rather than the Msx-1 and Msx-2 expression. Strikingly, the induction of the tooth formation was possible using tissue recombination between the oral epithelium of the diastema bud and the dental mesenchyme of the molar tooth bud, which indicates the potential capability of the diastema in the tooth formation. In conclusion, it is suggested that the condensed mesenchyme may be the key to tooth development.
Animals↗
Incidence and etiology of midline diastema in a population in south India (Madras).
In a cross-sectional study of midline diastemas in a South Indian (Madras) population, 9,774 patients aged 13-35 years were screened. True midline diastema was defined as one without periodontal/periapical involvement and with the presence of all anterior teeth in the arch. Sample purification resulted in a research sample of 166 patients with true midline diastemas. The incidence of true maxillary midline diastema (160/9774-1.6%) was greater than that of true mandibular midline diastemas (31/9774-0.3%). No direct etiologic factor for the midline diastemas was noted. Spacing in the anterior region was the most significant factor associated with the midline diastema.
Adolescent↗
Gene expression patterns associated with suppression of odontogenesis in mouse and vole diastema regions.
Rodents have a toothless diastema region between the incisor and molar teeth which may contain rudimentary tooth germs. We found in upper diastema region of the mouse (Mus musculus) three small tooth germs which developed into early bud stage before their apoptotic removal, while the sibling vole (Microtus rossiaemeridionalis) had only a single but larger tooth germ in this region, and this developed into late bud stage before regressing apoptotically. To analyze the genetic mechanisms of the developmental arrest of the rudimentary tooth germs we compared the expression patterns of several developmental regulatory genes (Bmp2, Bmp4, Fgf4, Fgf8, Lef1, Msx1, Msx2, p21, Pitx2, Pax9 and Shh) between molars and diastema buds of mice and voles. In diastema tooth buds the expression of all the genes differed from that of molars. The gene expression patterns suggest that the odontogenic program consists of partially independent signaling cascades which define the exact location of the tooth germ, initiate epithelial budding, and transfer the odontogenic potential from the epithelium to the underlying mesenchyma. Although the diastema regions of the two species differed, in both species the earliest difference that we found was weaker expression of mesenchymal Pax9 in the diastema region than in molar and incisor regions at the dental lamina stage. However, based on earlier tissue recombination experiments it is conceivable that the developmental arrest is determined by the early oral epithelium.
Animals↗
[Maxillary central diastema. A case study].
A case is presented with loss of two maxillary central incisors in a 12 year old girl due to the use of elastics around the teeth to close a median diastema. The patients complaint was an increased mobility of these teeth. She presented a Class I malocclusion and a supraposition of the upper central incisors. There was however an extreme periodontal destruction, as a consequence of which the central incisors had to be extracted. In connection with this case report considerations are made concerning the normal development of the dentition and the need for orthodontic treatment of a median diastema in the maxilla. A median diastema normally closes when the canines erupt. A hypertrophic superior labial frenum rather seems to be a consequence than a cause of a median diastema. Thus, it is no use to close a median diastema before eruption of the upper canines. If a median diastema is to be treated, use of elastics around the central incisors is contraindicated.
Child↗
Dental lamina develops even within the mouse diastema.
In embryos of albino mice of ICR strain, collected between days 13 and 15, the epithelial lining within the future upper maxillary diastema was studied using frontal histological sections stained with hematoxylin-eosin and PAS methods. In embryos harvested on the 12th hr of day 13 (stage 13/12), a continuous epithelial rudiment of dentition was found in the anterior extension of the epithelial anlage of the first upper molar, up to the level of the lower anterior margin of the primary choana. In this stage the rudiment acquired, in the most anterior region of the future diastema, an arrangement typical for the dental lamina. In its dorsal extension there was found a distinct tooth anlage at the transitory stage lamina bud, which further (at stage 13/24) disintegrated into several segments. Starting with the day 14 (stage 14/12), the epithelial rudiment of dentition within the future upper diastema began to regress. From the stage 14/24 on, the anlage persisted only in its posterior terminal part where it merged with the epithelial lamina extending anteriorly from the anlage of the first upper molar. The existence of the dentition rudiment within the future mouse diastema constitutes the ontogenetic evidence that the diastema originates only secondarily--by regression. In some mutant strains of mice (tabby, crooked, sleek), the regression appears incomplete. The odontogenic potency of mouse diastema tissues should be considered when interpreting the results of in vitro experiments investigating the odontogenic inductive tissue interactions in mouse.
Animals↗
The midline diastema: a review of its etiology and treatment.
A midline diastema usually is part of normal dental development during the mixed dentition. However, several factors can cause a diastema that may require intervention. An enlarged labial frenum has been blamed for most persistent diastemas, but its etiologic role now is understood to represent only a small proportion of cases. Other etiologies associated with diastemas include oral habits, muscular imbalances, physical impediments, abnormal maxillary arch structure, and various dental anomalies. Effective diastema treatment requires correct diagnosis of its etiology and intervention relevant to the specific etiology. Correct diagnosis includes medical and dental histories, radiographic and clinical examinations, and possibly tooth-size evaluations. Appropriate treatment modalities have been described. Timing often is important to achieve satisfactory results. Removal of the etiologic agent usually can be initiated upon diagnosis and after sufficient development of the central incisors. Tooth movement usually is deferred until eruption of the permanent canines, but can begin early in certain cases with very large diastemas.
Adolescent↗
Mouse rudimentary diastema tooth primordia are devoid of peripheral nerve fibers.
The tooth is a well-defined peripheral target organ for trigeminal nerve fibers. However, only limited information is available regarding pioneer axon guidance to the developing tooth target field. In rodents there is a toothless diastema region between incisors and molars that in the mouse maxilla contains three rudimentary tooth anlagen. Their development stop at the early bud stage when the primary nerve axons grow towards the developing first molar tooth germs. In order to provide background information for studies of regulatory mechanisms of pioneer axon guidance to the developing tooth germs, we investigated the distribution of nerve fibers in the mouse diastema tooth buds, and compared it to the axon growth to the maxillary and mandibular first molar tooth germs by immunohistochemical localization of peripherin and PGP9.5. Analysis of serial sections showed that trigeminal nerve fibers emerging from the trigeminal maxillary and mandibular nerve trunks started to grow towards the developing molar tooth germ at the early bud stage, and subsequently they diverged into buccal and lingual branches next to the condensed dental mesenchyme. During the cap stage, nerve fibers were observed around the tooth germ in the dental follicle region. In contrast, no nerve fibers were located in the vicinity of the diastema tooth primordia at any stage studied, nor did any nerve fibers appear to grow towards this region. Our results show that the development and subsequent disappearance of the diastema tooth primordia takes place without peripheral trigeminal innervation. The diastema tooth primordia may therefore be a useful model system for future studies on molecular regulatory mechanisms of pioneer axon guidance to the tooth germs, and possibly also for evolutionary studies of peripheral axon guidance mechanisms.
Animals↗
The diastema, the frenum, the frenectomy: a clinical study.
1. The pretreatment relationship between a clinically "abnormal"-appearing maxillary midline frenum and a midline diastema showed a strong, but not absolute, correlation. A certain percentage of patients demonstrated (1) a diastema but not an "abnormal" frenum or (2) no diastema but an "abnormal" frenum. 2. Diastema cases in which there were "abnormal" pretreatment frenums demonstrated a decidedly stronger potential for relapse after orthodontic closure. The exceptions to the rule were explained by the clinician's inability to differentiate between "normal" and "abnormal" frenums and by the periodontium's apparent (if not consistent) ability to recognize the frenal and interdental tissues following orthodontic tooth movement. 3. A three-stage surgical procedure was shown to be very effective in alleviating the relapse phenomenon following orthodontic treatment of diastemas. The surgical procedures were successful in avoiding many of the hazards to the periodontium associated with previous techniques.
Child↗
Sprouty genes control diastema tooth development via bidirectional antagonism of epithelial-mesenchymal FGF signaling.
Unlike humans, who have a continuous row of teeth, mice have only molars and incisors separated by a toothless region called a diastema. Although tooth buds form in the embryonic diastema, they regress and do not develop into teeth. Here, we identify members of the Sprouty (Spry) family, which encode negative feedback regulators of fibroblast growth factor (FGF) and other receptor tyrosine kinase signaling, as genes that repress diastema tooth development. We show that different Sprouty genes are deployed in different tissue compartments--Spry2 in epithelium and Spry4 in mesenchyme--to prevent diastema tooth formation. We provide genetic evidence that they function to ensure that diastema tooth buds are refractory to signaling via FGF ligands that are present in the region and thus prevent these buds from engaging in the FGF-mediated bidirectional signaling between epithelium and mesenchyme that normally sustains tooth development.
Adaptor Proteins, Signal Transducing↗
Occurrence of midline diastema and frenum attachments amongst school children in Nairobi, Kenya.
The aim of this study was to determine the prevalence of midline diastema, tongue tie and frenum attachments amongst school children in Nairobi. A total of 1802 children aged between 4 and 16 years were selected randomly using multistage sampling technique. To avoid oversampling in either sex, a proportionate sampling procedure was used. Thereafter, a thorough intra-oral examination was carried out using a mouth mirror under artificial or natural light with the children lying on a supine position. Presence or absence of midline interdental spaces unusually bigger than other interdental spaces were noted and recorded on a prepared dateacollection form. Accurate location of the origin of the frenum was done using Placek et al Morphological-functional classification of the labial frenum attachments. Data was analyzed manually by tally method. Results showed that 35% had upper and lower midline diastema. 55% were females and 45% were males. Their mean age was 7.6 years. 0.2% had a high lingual frenum. The commonest location of frenum attachment amongst children with lower midline diastema was the mucogingival junction (86%) whereas amongst those with upper midline diastema it was attached gingiva (50%). None of the children had frenum attachment on the interdental papilla. It was concluded that the maxilla had a higher prevalence of midline diastema than the mandible and that papillary penetrating frenum attachments amongst these patients were higher in the maxilla than the mandible.
Adolescent↗
Midline diastema and frenum morphology in the primary dentition.
PURPOSE: The purpose of this study was to determine the prevalence of different types and insertions of labial frenums as well as midline diastema in Peruvian children between 0 and 6 years of age. METHODS: A sample of 1,355 children was selected for the study. A clinical examination was done to classify the labial frenum, measure gingival insertion levels, and quantify midline diastema. Descriptive statistics and the Spearman test were used. RESULTS: The most prevalent frenums were the simple frenum (59%) and the persistent tectolabial frenum (25%). The level of gingival insertion moved apically with age. The midline diastema was wider in younger children and decreased with age. A significant inverse relationship (r=-0.27; P=.001) was found between the level of gingival insertion and the midline diastema. CONCLUSION: The most prevalent frenum was the simple frenum. A significant inverse correlation between the gingival insertion level and the midline diastema was found.
Age Factors↗
Maxillary diastema: indications for treatment.
1. In comparing characteristics associated with the presence or absence of diastema at the age of 16 years, generalized spacing was the only significant factor. 2. In the 230 children who had a diastema of 0.5 mm. or greater at age 9, there was a significant association between the diastema and the amounts of crowding or spacing at age 16. 3. A clinician must analyze the individual case in order to determine whether the diastema is to close through normal development or if there exists a likelihood of its persistence.
Adolescent↗
A postretention study of patients presenting with a maxillary median diastema.
The purpose of this study was to assess postretention stability of maxillary midline diastema closure, to search for predictors of relapse, and to test for associations between relapse and other postretention changes. The sample consisted of 35 patients with pretreatment diastemas ranging from 0.9 mm to 3.0 mm (mean 1.4, SD = 0.5) following eruption of the maxillary canines. Data were gathered from treatment charts, study models, periapical radiographs, and cephalograms taken pretreatment, posttreatment, and 1 to 26 years postretention (mean 11.4, SD = 6.4). Measurable diastema relapse was observed in only 12 cases. The majority of the relapse was 0.6 mm or less, and maximum relapse was 3.0 mm. Abnormal frenums and/or intermaxillary osseous clefts did not appear to be risk factors for relapse, and no pretreatment predictors of relapse could be established. The only posttreatment change associated with diastema relapse was proclination of the maxillary incisors (p < 0.01).
Adolescent↗
Relapse after orthodontic correction of maxillary median diastema: a follow-up evaluation of consecutive cases.
An evaluation of 96 treated orthodontic patients with maxillary median diastema ranging from 0.50 mm to 5.62 mm (mean 1.22, SD 0.85) was performed 4.0 to 9.0 years after completion of active treatment. Pre- and posttreatment data were gathered from available records. Follow-up data were gathered from records and interviews of 37 patients, and from phone interviews of 59 patients. The incidence of diastema relapse was 49% when scored as either presence of a measurable space at follow-up, a history of orthodontic or prosthetic retreatment to close a reopened space, or continued use of a retainer to control relapse tendency. Logistic regression analysis revealed that pretreatment diastema size and presence of a family member with a similar condition were the only significant risk factors for relapse (p<0.05), while pretreatment spacing in the maxillary anterior dentition approached significance (p = 0.10). No association was found between relapse and presence of an abnormal frenum or an osseous intermaxillary cleft, although patients with an abnormal frenum had a wider pretreatment diastema than those with a normal frenum (p<0.05). Fremitus of the maxillary incisors was the only parameter at follow-up associated with space reopening (p<0.01).
Adolescent↗
Unerupted canine without median diastema.
The eruption of the canine is known to be a factor for diastema closure. In this study the relative changes in the orientation of the unerupted canine were assessed using the orthopantomographs of 9854 patients who sought consultation between April 1984 and March 1993. A total of 38 canines in 32 patients, all aged 11 years or older, were identified as unerupted canines. The features of the patients with unerupted canine showed no significant relation to diastema closure status, but some patients had unerupted horizontal or inverted canine without diastema even in the absence of a history of orthodontic treatment, suggesting the presence of a mechanical force due to some phenomenon other than canine eruption as a factor in diastema closure.
Adolescent↗
[Histomorphologic evaluation of upper lip frenum in relation to the method of treating diastema].
The aim of this study was to determine collagen density in the hypertrophic upper lip frenum and scar forming after frenectomy and to compare the results with collagen density in a normal population (autopsy specimens). Differences in collagen density may cause problems in diastema closure and may eventually result in relapse of this condition. The study was done in 47 patients treated for diastema. Histomorphology was performed in 15 patients of this group. Autopsy material was obtained from 27 persons. Histomorphometric assessment of collagen density was done after staining of collagen fibers according to van Gieson. A computerized image analysis system was used for interactive detection of stained collagen fibers on the digitized microscopic image. The percentage of positive staining expressed as ratio of positive area to whole area of the field studied was determined and recorded as an Excel file. Collagen density was increased in the pathologic frenum and in the scar as compared with the normal frenum. The difference was statistically significant. Diastema treatment with frenectomy, fixed appliance and retainer produced more stable results as compared to treatment with a removable appliance without frenectomy. The results suggest that the similar collagen density observed in hypertrophic upper lip frenum and scar after frenetomy may hinder complete closure of diastema and facilitate relapse after treatment.
Adolescent↗