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ExperimentaL Oral Medicine
Published in Samuel Dreizen, Barnet M. Levy, Handbook of Experimental Stomatology, 2020
Samuel Dreizen, Barnet M. Levy
Odontogenic keratocysts have an aggressive growth potential, a tendency towards multiplicity, and a marked propensity to recur or to persist, properties not possessed by any other form of odontogenic cyst. The pathogenesis of such cysts is uncertain. Suggested origins are offshoots of the dental lamina before odontogenesis or remnants of the dental lamina after odontogenesis. In the course of transplantation studies in mice by Bartlett et al.68 using molar tooth germs, cysts containing keratin were produced during development of the transplanted teeth. First maxillary molars from 2-day-old C57B1/10 mice neonates were carefully removed and transplanted to a subcapsular site in the kidney of anesthetized adult isologous mice. Nephrectomies were performed on the recipient mice after 1 to 180 days posttransplantation. The kidneys were fixed in 10% neutral formol saline, decalcified, and processed for histologic examination. Sections were stained with hematoxylin and eosin, and some were subjected to special technics for demonstrating keratin or keratinlike material. As the tooth germs were forming teeth, keratin-producing cysts also developed in the epithelium of the enamel organs. By 120 days posttransplantation, many of the cysts had completely enveloped the crowns of the developing teeth. These studies show that tooth germ epithelium was capable both of cystic change and keratin production. The experimentally induced keratin-producing cysts were histologically similar to human odontogenic keratocysts.
Cysts and Tumours of the Bony Facial Skeleton
Published in John C Watkinson, Raymond W Clarke, Terry M Jones, Vinidh Paleri, Nicholas White, Tim Woolford, Head & Neck Surgery Plastic Surgery, 2018
Julia A. Woolgar, Gillian L. Hall
The odontogenic cysts arise from remnants of the tooth-forming apparatus.1 There are three distinct types of epithelium which persist once odontogenesis is complete (Table 25.2). First, the dental lamina, which, in the developing embryo, is the downgrowth of surface oral epithelium that extends into the underlying developing mesenchymal tissue and gives rise to the enamel organ (Figure 25.1). Once tooth formation is complete, this structure fragments, but its persistence as small, rounded islands of epithelium within the bone and alveolar soft tissues, the rests (glands) of Serres, is well recognized (Figures 25.2–25.4). These dental lamina residues give rise to the developmental lateral periodontal and gingival cysts (and the keratocystic odontogenic tumour, formerly the odontogenic keratocyst). Second, once enamel formation is complete, prior to eruption, the tooth is covered by a layer of reduced enamel epithelium, formed by fusion of the two layers of inner and outer enamel epithelia. This is the source of epithelium for dentigerous (follicular), eruption and inflammatory paradental cysts. The third epithelial residue is the rests of Malassez within the periodontal ligament between the tooth root and the bony tooth socket which results from the fragmentation of Hertwig’s root sheath on the completion of root formation, and gives rise to the inflammatory radicular cysts. The classification of odontogenic cysts used in this chapter (Table 25.3) is based on that recommended by the World Health Organisation.2
Oral cavity
Published in Paul Ong, Rachel Skittrall, Gastrointestinal Nursing, 2017
Primary thickening of the oral ectoderm in week 6 of gestation forms an epithelial band. The epithelial band forms a continuous ‘horseshoe’-shaped ridge around the margins of the developing oral cavity. This is called the dental lamina. It is from here that the tooth buds arise. The formation of the dental lamina in the lower jaw precedes that of the upper jaw.
Recurrent odontogenic keratocyst with orbital invasion
Published in Orbit, 2022
Valerie Juniat, Alistair Varidel, James Badlani, James Nolan, Paul Sambrook, Dinesh Selva
OKCs are acquired, non-choristomatous lesions which arise from the remnants of the dental lamina with secondary proliferation of enamel epithelium.1 It is difficult to know the true incidence of OKC involving the orbit due to the rarity of the condition. This is further complicated by inconsistencies in the nomenclature, with OKCs being named in 2005 by the WHO as keratocystic odontogenic tumours.1 Previously to this, OKCs have been called variously as odontogenic cysts and odontogenic keratocysts. The designation was reverted to by consensus back to odontogenic keratocyst in 2017, justified on the grounds that the PTCH mutation found in OKC can also be found in non-neoplastic lesions and resolution of the cyst after marsupialisation does not correlate with a neoplastic process.1,4 The authors have attempted to address this by including pre-2017 terms in the literature review.
The protoconid: a key cusp in lower molars. Evidence from a recent modern human population
Published in Annals of Human Biology, 2022
José María Bermúdez de Castro, Cecilia García-Campos, Susana Sarmiento, María Martinón-Torres
In order to try to understand the final morphology of human Ms, let us give a brief overview of the morphogenesis of teeth. Mammalian tooth formation occurs through several stages of molecular interaction (e.g. Balic 2019; Chen et al. 2009; Ferguson et al. 1998; Zhang et al. 2005). Growth factors induce proliferation of the epithelium to form a dental lamina. After thickening of the epithelium, invagination occurs to form a tooth bud. The next stage is the folding of the epithelial layers to form the cap and bell stages, in which the primary enamel knot and the secondary enamel knots are differentiated (e.g. Li et al. 2013). The role of the primary enamel knot that forms at the end of the bud stage became known during the second half of the 1990s (Jernvall et al. 1994; Jernvall and Thesleff 2000; Thesleff et al. 2001). The primary enamel knot was first identified in the 1920s in cap stage tooth germs. It was recognised as a group or transitory cluster of non-dividing epithelial cells placed at the tip of the tooth bud (Orban 1928), and whose formation would be regulated by signals from the mesenchyme (Jernvall et al. 1998; Thesleff et al. 2001). The primary enamel knot becomes fully developed in the cap-stage dental epithelium and expresses at least ten different signalling molecules belonging to the BMP, FGF, SHH, and WNT families (Thesleff et al. 2001). Most of the cells of the enamel knots disappear by apoptosis once their function has been carried out (Thesleff et al. 2001). The primary enamel knot acts as a signalling centre that provides positional information for tooth morphogenesis and regulates the growth of tooth cusps by inducing secondary enamel knots (e.g. Cho et al. 2007; Matalova et al. 2005; Pispa et al. 1999; Tucker et al. 2004).