Systemic Conditions associated with Delayed Tooth Eruption

Delayed tooth eruption (DTE), or delayed tooth emergence is defined as the emergence, or eruption of a tooth into the oral cavity at a time statistically different from what would be expected for age, sex and ethnicity.^1–3 This is generally accepted to be greater than 12-months' delay beyond chronological norms,⁴ or greater than 6 months compared to eruption of the contralateral permanent tooth.⁵ Local factors that result in DTE are numerous, and are listed in Table 1.

Odontogenesis, or tooth eruption, is under genetic control, governed by more than 300 genes,⁶ with environmental factors playing a comparatively minor role. It is a highly complex and tightly regulated physiological process that occurs over a broad chronological age. Numerous theories have been postulated to explain the eruption process, hypothesizing involvement of many adjacent tissues and chemical mediators. More recently, the dental follicle, a sac-like membranous tissue that surrounds the developing tooth germ has been promoted as a pivotal mediator of eruption owing to its production of copious mediators (tumour necrosis factor alpha (TNF-α), transforming growth factor beta (TGF-β), receptor activator of nuclear factor kappa B ligand (RANKL), colony stimulating factor 1 (CSF-1), and interleukin-1 (IL-1)).⁷ Stellate reticulum cells of the dental follicle secrete parathyroid hormone-related peptide (PTHrP), an imperative autocrine/paracrine cytokine that exerts pleiotropic effects regulating tooth eruption.^8,9 RANKL, CSF-1, and TNF-α secreted by cells of the dental follicle are quintessential for differentiation of precursor mononuclear cells into osteoclasts, which govern eruptive tooth movement.⁷ Osteoprotegerin (OPG) is a cytokine with a role in inhibiting osteoclastogenesis and prohibits osteoclast activity by binding to RANKL.¹⁰ The RANKL/OPG axis provides an essential mechanism to regulate a balance between osteoclastic resorption and osteoblastic deposition.¹⁰ Much of our understanding of the molecular mechanisms of tooth eruption are attributable to the study of genetic diseases where functional mutations in mediators such as RANKL or PTHrP result in delayed tooth eruption or primary failure of eruption.