Shear's Cysts of the Oral and Maxillofacial Regions. Paul M. Speight

13.1) Nasolabial cyst Nasolacrimal duct The nasolacrimal duct forms after 6 weeks of intrauterine life and drains tears from the lacrimal sac to the lower aspect of the lateral nasal wall. Residual epithelial remnants may persist at the inferior portion of the duct (Chapter 14) Mid‐palatal raphe cyst (Epstein pearls) Epithelial inclusions The palatal shelves fuse at about 7–8 weeks of intrauterine life. The epithelial coverings fuse and then break down into many small islands, many of which form small ‘microcysts’ (Figure 9.7). Most involute before birth, but up to 80% of newborns may have cysts up to 3 months of age (Chapter 9). There is some evidence that inclusions may arise in the bone and give rise to an intraosseous ‘median palatal cyst’ (discussed in Chapter 13) Surgical ciliated cyst Remnants of respiratory epithelium Fragments of sinus epithelium become implanted into a wound following surgery involving the maxillary sinus (Chapter 16) Cysts of the salivary and minor mucous glands Mucous retention cysts Ducts of minor mucous glands The ducts of minor mucous glands become blocked and dilated, most often as a result of trauma (Figures 15.5, 15.6, and 15.10) Salivary duct cyst Lymphoepithelial cysts Intraparotid ducts The pathogenesis is uncertain, but blockage of ducts associated with sialadenitis may cause cystic dilatation (Figure 15.12) Intraoral lymphoepithelial cysts Tonsillar crypt epithelium The opening of intraoral tonsils may become blocked, causing cystic dilatation of the crypt. Some intraoral lymphoepithelial cysts may be retention cysts arising from a superficial duct of minor salivary glands Developmental cysts of the head and neck Intraoral dermoid and epidermoid cysts Epithelial inclusions Epithelial remnants are sequestered into the tissues during fusion of facial processes. Oral dermoid and epidermoid cysts are found in the anterior oral cavity at sites of fusion of the mandibular processes (Box 18.1) Intraoral cysts of foregut origin Epithelial inclusions Oral foregut cysts arise from epithelial remnants following fusion of the tuberculum impar (first branchial arch) and the posterior one‐third of the tongue (second to fourth arches) (Box 18.2) Branchial cleft cysts Epithelial inclusions Branchial cleft cysts arise from epithelial remnants that become entrapped or persist due to incomplete obliteration of the branchial clefts or pharyngeal pouches (Box 18.3) Thyroglossal duct cyst Remnants of the thyroglossal duct The thyroid gland develops at about 4 weeks of intrauterine life in the dorsum of the tongue. The developing gland descends downwards into the upper neck forming the thyroglossal duct, which then disintegrates. However, residual epithelial remnants are found in the midline of the upper neck and tongue in about 40% of people (Box 18.4)

      In the majority of odontogenic cysts, the epithelial lining is derived from epithelial remnants of the dental lamina (Table 2.1). Early in the development of the jaws, the surface epithelium thickens and grows downwards into the mesenchyme of the future dental arches to form the dental lamina. This extends around the arch as a band that maps the future sites of tooth bud formation for both primary and secondary dentitions. The teeth develop as a result of complex epithelial–mesenchymal interactions that result in epithelial thickenings or placodes, which then form the enamel organs that pass through the well‐described bud, cap, and bell stages during formation of the fully developed tooth (Nanci 2017 ). The dental lamina remains as a thin band that joins the surface oral epithelium to the enamel organ and only disintegrates at the late bell stage of tooth development. Disintegration of the dental lamina results in the formation of small epithelial islands that lie over unerupted teeth, but also remain in the tissues adjacent to the teeth after eruption. The disintegrating vdental lamina is illustrated in Figure 9.9. The epithelial cell rests of the dental lamina give rise to most of the odontogenic cysts (Table 2.1) as well as to most odontogenic tumours. Dental lamina rests are particularly numerous at the posterior aspect of the dental arches and in the tissues overlying unerupted teeth and in the dental follicle. This accounts for the fact that the angle of the mandible is a common site for many cyst types, and that many cysts (and tumours) may arise in the dental follicle and embrace or surround an unerupted tooth and lie in a dentigerous relationship. This especially affects the mandibular third molars, since these are the most commonly impacted teeth (Brown et al. 1982 ).

      Although most types of odontogenic cyst arise from dental lamina, the most common cyst (radicular cyst) takes its origin from the rest cells of Malassez that lie in the periodontal ligament as remnants of Hertwig's root sheath (see Figure 3.6). The second most common cyst, the dentigerous cyst, arises from the reduced enamel epithelium that embraces the fully formed crown of a tooth prior to eruption. In the case of the radicular cyst, the phases of cyst formation and growth are well understood and are driven by inflammation that is initiated by bacterial factors emanating from a non‐vital pulp. This process is described in detail in Chapter 3. In developmental cysts, however, the processes are less clear, but are almost certainly driven by epithelial–mesenchymal interactions that initiate the molecular signalling pathways that underpin normal tooth development, morphogenesis, and eruption. Thus, the mechanisms of formation of developmental cysts can be regarded as the aberrant expression of normal processes.

Normal tooth eruption provides a good model of the epithelial–mesenchymal interactions that regulate tissue remodelling, including cell proliferation and bone resorption, and involve complex cascades and networks of cytokines, chemokines, and growth factors (Wise et al. 2002 ; Nel et al. 2015 ; Bastos et al. 2021 ). These biological factors are discussed in detail in the context of the radicular cyst (Table 3.2), where the cascade is started by bacterial infection, but the same factors are involved in normal development and tooth eruption and contribute to the pathogenesis of developmental cysts. For example, Il‐1α is a pivotal pro‐inflammatory cytokine that can be activated by bacterial endotoxins, but it also has an important role as a paracrine signalling molecule in the dental follicle where, along with other factors (e.g. parathyroid hormone–related protein) it mediates tissue remodelling and bone resorption during tooth eruption via its role as an activator of osteoclasts.

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