Source: Courtesy of Dr Douglas W Stoneman (Previously published: Dental Radiography and Photography (1983 ) 56, 1–14. Courtesy of Eastman Kodak Co.)
With regard to the paradental cyst, the presence of a pericoronal radiolucency associated with a partially erupted third molar is not specific, since a similar radiolucency may result from an inflamed or hyperplastic dental follicle or pericoronitis (Figure 4.5). In such a case, the pathologist may be presented with fragments of inflamed tissue and a clinical diagnosis of ‘pericoronitis’, and therefore a diagnosis of paradental cyst may not be considered. In addition, some workers consider that a pericoronal radiolucency distal to a partially erupted third molar may arise as a result of lateral displacement of a dentigerous cyst during tooth eruption, or that a cyst that arises in a pericoronal relationship is a mere variant of dentigerous cyst. In this case, the final diagnosis may be of an ‘inflamed dentigerous cyst’.
Figure 4.5 Differential diagnosis of the paradental cyst. (a) The cyst is well demarcated and corticated (arrows) and is distinct from the distal follicular space (arrowhead). (b) Chronic pericoronitis on a vertically impacted and partially erupted third molar. The distal follicular space is dilated (arrowhead) and there is evidence of alveolar bone loss, but there is no cyst.
However, careful examination of radiographs will show that the paradental cyst is distinct from the pericoronal follicular tissues and the criteria for diagnosis must include the finding of a well‐demarcated cyst that is distinct from the distal aspect of the dental follicle (Figures 4.2 and 4.5a). If the follicular space is merely expanded, then the lesion may be a hyperplastic dental follicle, or bone loss associated with chronic pericoronitis. Figure 4.5b shows an expanded pericoronal space associated with a partially erupted but vertical third molar. There is also evidence of pocketing with alveolar bone loss. This appearance is consistent with chronic long‐standing pericoronitis, but without cyst formation. The relationship to the dentigerous cyst is discussed further below.
Both the paradental cyst and mandibular buccal bifurcation cyst overly the tooth roots and may resemble a periapical radicular cyst, or a radicular cyst lying lateral to the root associated with a lateral root canal. However, in the case of an inflammatory collateral cyst, the periodontal space and the lamina dura remain intact (Figures 4.2 and 4.4), a feature that excludes an inflammatory cyst of endodontic origin.
A number of other cysts may on occasion arise on the lateral aspect of a tooth, including odontogenic keratocyst and glandular odontogenic cyst. However, these do not embrace the crown of partially erupted teeth, are not associated with pericoronitis, and have characteristic features that clearly distinguish them from inflammatory collateral cysts (see Chapters 7 and 10). Developmental lateral periodontal cysts may also be considered, but the clinicopathological features are quite different (see Chapter 8). Although lateral periodontal cysts are most common in the mandible, they are found in the canine/premolar region and they lie lateral to the roots of fully erupted teeth in middle‐aged adults. They are not associated with inflammation.
A number of workers have drawn attention to the fact that the clinical and radiological features of mandibular buccal bifurcation cyst may be similar to the chronic form of osteomyelitis often referred to as Garré's osteomyelitis or periostitis ossificans (Stoneman and Worth 1983 ; Wolf and Hietanen 1990 ). This is typified by buccal expansion with laminated depositions of new subperiosteal bone – a feature that is also seen in cases of mandibular buccal bifurcation cyst (Figure 4.4). Periostitis ossificans of the mandible is most often seen in association with first molars in young people and is usually secondary to periapical infection. The mandibular buccal bifurcation cyst is of inflammatory origin and it is probable that in some cases, persistent chronic inflammation may give rise to a low‐grade osteomyelitis with periostitis. However, a diagnosis of collateral cyst can be made on the basis of a vital tooth, a well‐defined buccal radiolucency, and evidence of continuity between the buccal periodontal pocket and the cyst lumen.
Pathogenesis
There is no unanimity with regard to the pathogenesis of inflammatory collateral cysts. Craig (1976 ), however, proposed a pathogenic process that has become widely accepted. He suggested that the cyst arises within a focus of inflammation associated with pericoronitis around a partially erupted tooth. In this respect the pathogenesis is similar to the radicular cyst, in that chronic inflammation initiates the cyst and is the stimulus for proliferation of the epithelial lining. Craig (1976 ) is widely cited as having proposed that the epithelium of origin is the reduced enamel epithelium, but in fact his proposal was more nuanced than this. The reduced enamel epithelium embraces the crown of an unerupted tooth and is derived from the remnants of the inner and outer enamel epithelium. As the tooth erupts, the reduced enamel epithelium fuses with the oral epithelium and forms the dentogingival junction or the early epithelial attachment, which is composed of the junctional epithelium that binds to the tooth crown and the sulcular epithelium towards the opening of the gingival sulcus. Since inflammatory collateral cysts are associated with partially or recently erupted teeth, Craig (1976 ) actually proposed that the epithelium of origin was the early epithelial attachment that is derived from the reduced enamel epithelium. Thus the cyst is derived from the epithelium that lines the inflamed periodontal or pericoronal tissues associated with pericoronitis. Although classified as an odontogenic cyst, it probably does not arise directly from odontogenic remnants, but rather from pocket or pericoronal epithelium that is itself of odontogenic origin.
Craig (1976 ) and others (Main 1970 ; Ackermann et al. 1987 ; Fowler and Brannon 1989 ; Vedtote and Praetorius 1989 ; de Sousa et al. 2001 ; Philipsen et al. 2004 ) also considered the rest cells of Malassez as a potential source of epithelium, but this has largely been dismissed on the basis that, when seen in histological sections, the rests of Malassez always appeared inactive, and such an origin would not account for the consistent buccal distribution of the lesions (Craig 1976 ; Fowler and Brannon 1989 ).
Ackermann et al. (1987 ) agreed with Craig (1976 ) that the paradental cyst arises as a consequence of inflammatory destruction of bone that is followed by proliferation of epithelium and cyst expansion. They also discussed an origin from reduced enamel epithelium or from sulcular (or crevicular) epithelium, and suggested that cyst formation occurs as a result of unilateral expansion of the dental follicle secondary to inflammatory destruction of periodontium and alveolar bone. This, they proposed, was different from the histogenesis of a dentigerous cyst, which is not inflammatory and where expansion of the follicle is the primary event with consequent bone destruction.
Vedtofte and Praetorius (1989 ) agreed that inflammatory collateral cysts are of inflammatory origin, and are associated with pericoronitis on third molars or with a deep and inflamed periodontal pocket when found on first or second molars. While accepting that the paradental cyst was an entity, Fowler and Brannon (1989 ) suggested that it may be a variant of the dentigerous cyst, in that it is derived from a cystic expansion of follicular reduced enamel epithelium secondary to pericoronitis.
Fowler and Brannon (1989 ) also proposed that the paradental cyst may arise as a result of expansion of an occluded periodontal or pericoronal pocket. This is consistent with the proposal of Craig (1976 ) and others, if one recalls that the epithelium lining a pocket or pericoronal tissues around a partially erupted tooth