Tooth eruption is highly variable, ranging from a normally timed and sequenced process to one that results in partially or completely unerupted teeth. Molecular studies in rodent models have improved our understanding of dental eruption mechanisms significantly; defects in the differential apposition/resorption mechanism in alveolar bone cause eruption failure in rat molars. Our understanding of the molecular basis of tooth eruption is strengthened further by the finding that one gene, parathyroid hormone receptor 1 (PTH1R), is causative for familial cases of Primary Failure of Eruption (PFE). Although PFE is a relatively rare condition, knowledge of a biological mechanism underlying the development of PFE illuminates: 1) the influence of genetics on orthodontic tooth movement in general; 2) the differential diagnosis of clinical eruption disorders; and 3) the clinical management of eruption failure. In this chapter, we evaluate what is known about normal tooth eruption and eruption disorders from biological and clinical perspectives. Further, we consider a recent finding that some individuals previously diagnosed with ankylosis subsequently were found to have alterations in the PTH1R gene. This finding indicates the initial misdiagnosis of ankylosis and the necessary reclassifica-tion of PFE, and also suggests that other disturbances in tooth eruption may have a genetic etiology. Thus, recent advances in our understanding of normal and abnormal tooth eruption will allow for a refined clinical diagnostic regime based on the genetic cause versus the clinical appearance of an eruption disorder, shifting the focus in orthodontics from 'how to move teeth' to 'how teeth move.'
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