Other systemic conditions associated with impairment of growth, such as anemia (hypoxic hypoxia, histotoxic hypoxia, and anemic hypoxia) and renal failure, have also been correlated with DTE and other abnormalities in dentofacial development.
DTE has been found to be a feature in many genetic disorders and syndromes. Various mechanisms have been suggested to explain DTE in these conditions. A generalized developmental delay in permanent tooth formation is seen in Apert syndrome. Supernumerary teeth have been found to be responsible for DTE in Apert syndrome, cleidocranial dysostosis, and Gardner syndrome. There is considerable evidence to implicate the periodontal tissues’ development in DTE. Abnormalities in these tissues, as have been found in some syndromes, might be a factor in DTE. Lack of cellular cementum has been found in cleidocranial dysplasia; cementum-like proliferations and obliteration of periodontal-ligament space with resultant ankylosis have been noted in Gardner syndrome.
Tooth eruption is also regulated by various cytokines, including epidermal growth factor, transforming growth factor, interleukin-1, and colony stimulating factor. Lack of appropriate inflammatory response, an inadequate expression of some cytokines, and increased bone density that impedes resorption have been noted to be factors for DTE in some syndromes. In osteopetrosis, sclerosteosis, Carpenter syndrome, Apert syndrome, cleidocranial dysplasia, pyknodysostosis, and others, underlying defects in bone resorption and other operating mechanisms might be responsible for DTE. Conversely, bone resorption is enhanced in hyperimmunoglobulin E syndrome, but DTE has been noted as a feature of this condition. This has been suggested to be due to defective root resorption of the deciduous teeth or the presence of a protective factor on the root that resists physiologic resorption. Tumors and cysts in the jaws can also cause interference with tooth eruption. Occasionally, some syndromes or genetic disorders are associated with multiple tumors or cysts in the jaws, and these might lead to generalized DTE. Gorlin syndrome, cherubism, and Gardner syndrome are such disorders, in which DTE might be the result of interference to eruption by these lesions.
Occasionally, families are found in which a generalized delay in the eruption of teeth is noted. Patient medical history might be totally unremarkable, with DTE as the only finding. The presence of a gene for tooth eruption has also been suggested, and its “delayed onset” might be responsible for DTE in “inherited retarded eruption.” Delayed development of isolated teeth has also been reported.
This is most commonly seen in the premolar region. Profitt and Vig hypothesized that a “gradient of eruption” might exist distally along the dental lamina. This could explain the frequency of DTE in posterior teeth. Some patients who have delayed eruption of the second molars alone might fall into the category of mild eruption failure syndrome.
Accurate diagnosis of DTE is an important but complicated process. When teeth do not erupt at the expected age (mean _ 2 SD), a careful evaluation should be performed to establish the etiology and the treatment plan accordingly. The importance of the patient’s medical history cannot be overstated. A wide variety of disorders has been reported in the literature to be associated with DTE. Family information and information from affected patients about unusual variations in eruption patterns should be investigated. Clinical examination should be done methodically and must begin with the overall physical evaluation of the patient. Although the presence of syndromes is usually obvious, in the mild forms, only a careful examination will reveal the abnormalities.
Right-left variations in eruption timings are minimal in most patients, but significant deviations might be associated with (for example) tumors or hemifacial microsomia or macrosomia and should alert the clinician to perform further investigation.
Intraoral examination should include inspection, palpation, percussion, and radiographic examination. The clinician should inspect for gross soft tissue pathology, scars, swellings, and fibrous or dense frenal attachments. Careful observation and palpation of the alveolar ridges buccally and lingually usually shows the characteristic bulge of a tooth in the process of eruption. Palpation producing pain, crackling, or other symptoms should be further evaluated for pathology. In patients in whom a deciduous tooth is overretained, with respect to either the contralateral side or the mean
exfoliation age for the patient’s sex and ethnicity, the deciduous tooth and the supporting structures should be thoroughly examined. Ankylosed teeth also interfere with the vertical development of the alveolus. Retention of the deciduous tooth might lead to deflection of the succedaneous tooth and resorptive damage of the adjacent teeth.
Schour and Massler, Nolla, Moorrees et al, and Koyoumdjisky-Kaye et al have developed tables and diagrammatic charts of the stages of tooth development, starting from the initiation of the calcification process to the completion of the root apex of each tooth. Norms with the average chronologic ages at which each stage occurs are also provided. Root development, with few exceptions, proceeds in a fairly constant manner.