Название | Shear's Cysts of the Oral and Maxillofacial Regions |
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Автор произведения | Paul M. Speight |
Жанр | Медицина |
Серия | |
Издательство | Медицина |
Год выпуска | 0 |
isbn | 9781119354949 |
Pocket Cyst (Bay Cyst)
With regard to the relationship between the tooth and the cyst lining, there is some evidence that there are two distinct histological types of radicular cyst. Brief mention has already been made of work by Simon (1980 ), who found that in some lesions a cavity may be present that is open to the root canal and is lined by epithelium that is attached to the root apex. Simon examined 35 extracted teeth with apical lesions still attached. Each specimen was decalcified and serial sectioned through the whole block. He found that the majority of lesions (27 cases: 75.2%) were periapical granulomas and that 8 (22.9%) of these contained strands of proliferating epithelium without evidence of cyst formation (e.g. see Figure 3.7). Only 6 cases (17.2%) were diagnosed as cysts. Three cysts showed an epithelial lining that was attached to the root apex, so that the root protruded into the cyst lumen, and the lumen was in direct continuity with the root canal, forming an open ‘pocket’ (Figure 3.18). Simon (1980 ) called these lesions bay cysts. The remaining cysts showed cavities entirely lined by epithelium with an inflamed fibrous wall, with no epithelial connection to the root apex. These were regarded as true cysts. Simon's data also suggest that cysts only comprise about 17% of periapical lesions and that bay cysts and true cysts have an equal frequency. This has been confirmed in a number of more recent studies that have shown that pocket cysts comprise about 50% of all periapical cysts. The actual frequencies reported have been 50.0% (Simon 1980 ), 38.5% (Nair et al. 1996 ), 56.3% (Ricucci et al. 2006b ), and 52.2% (Ricucci et al. 2020 ).
Figure 3.18 A low‐power view of a pocket cyst. The cyst lining is attached to the apex of the tooth (inset). Although in this plane of section the apical foramen is not visible, it can be seen that the tooth apex protrudes into the cyst lumen.
In the largest study, Nair et al. (1996 ) undertook meticulous serial sectioning of 256 periapical lesions and found that only 39 (15%) were radicular cysts. They also confirmed Simon's observations and showed that of the 39 cysts, 24 (61.5%) were true cysts and 15 (38.5%) were pocket cysts. In further detailed examination of these lesions, Nair (1998 , 2003 ) showed that in pocket cysts the epithelium was attached at the root apex, so that the lumen formed an extension of the root canal, and the intact epithelium acted as a barrier to seal off the contents of the infected root canal from the adjacent tissues (Figure 3.18). The cyst grows through accumulation of debris and necrotic tissue in the thus‐formed ‘bay’ or ‘pocket’. Simon (1980 ) and Nair (1998 , 2003 ) attached considerable clinical significance to the distinction of the two cyst types and suggested that pocket cysts were likely to heal after tooth extraction or endodontic treatment, whereas a true cyst may be self‐sustaining and can persist after treatment. From his data, Nair (1998 ) suggested that apical true cysts only account for about 10% of all periapical lesions, and this may explain the frequency of about 10% of persistent periapical lesions after conventional root canal treatment, and the low prevalence of residual cysts. Ricucci and Bergonholtz (2004 ) consider that the pocket cyst may be problematic for the endodontist, because the cyst fluid may be under pressure and may continuously wet the root canal, making instrumentation and filling difficult.
Box 3.4 Histopathology: Key Features
The cyst is lined by proliferating non‐keratinised stratified squamous epithelium
In long‐standing and residual cysts, the epithelium may become thin and regular
The cyst wall is composed of inflamed fibrous and granulation tissue
Cholesterol clefts and deposits of haemosiderin are often seen
Hyaline bodies are characteristic, but only seen in about 10% of lesions
Other features include mucous cells, cilia, focal keratinisation, and accumulation of foamy histiocytes
More recently, however, it has been suggested that true cysts and pocket cysts do not differ in any clinically significant way, and that the management can be the same. Ricucci et al. (2020 ) undertook a detailed clinicopathological analysis of 11 true cysts and 12 pocket cysts and found no significant differences in any of the clinical or histological features studied, including signs and symptoms, sex, location, size, or degree of acute inflammation. They also examined the presence of bacteria in the root canal or the cyst lumen and found no differences. The authors concluded that there are no clinically important differences between the two cyst types and that there is no real need to draw a diagnostic distinction between true cysts and pocket (bay) cysts. Furthermore, they also found that both pocket cysts and true cysts were infected, and suggested that there is little evidence for the idea that true cysts may be self‐sustainable independent of the infected root canal.
Malignant Change in Radicular Cysts
Primary intraosseous squamous cell carcinoma is defined as a central lesion in the jaw bones, which cannot be categorised as any other type of carcinoma (Koutlas and Sloan 2022 ). To establish the diagnosis, an oral lesion that has invaded the jaws, or metastatic lesions to the jaw bones, must be excluded. Intraosseous carcinomas are derived from odontogenic epithelium and may arise de novo, with no identifiable precursor lesion, or may be preceded by an odontogenic cyst or a benign odontogenic tumour. In a review of the world literature, Thomas et al. (2001 ) were only able to identify 35 cases of de novo lesions, suggesting that the majority of intraosseous squamous carcinomas arise in a pre‐existing lesion and most probably arise in odontogenic cysts. Eversole et al. (1975 ) reviewed series of cases of central squamous cell carcinoma and found that 75% were associated with a cyst lining. In a detailed review of the literature, Gardner (1969 ) examined the evidence presented with each of 63 cases reported during the period 1889–1967 and concluded that 25 (39.7%) fulfilled the criteria for an origin from odontogenic cyst.
Bodner et al. (2011 ) reviewed 116 cases of primary intraosseous squamous cell carcinomas that had arisen in odontogenic cysts. Of these, 70 cases (60.3%) were associated with radicular or residual cysts, 19 (16.4%) with dentigerous cysts, and 16 (13.8%) with an odontogenic keratocyst. Only 1 lesion was found to be associated with a lateral periodontal cyst and 10 could not be classified. The majority of cases (92, 79.3%) were found in the mandible and there was a male : female ratio of 2 : 1.
Before the diagnosis of carcinoma arising from a cyst lining can be established, a number of alternative possibilities must be excluded (Bodner et al. 2011 ; Woolgar et al. 2013 ; Koutlas and Sloan 2021 ). It is possible that a benign cyst and the carcinoma may have developed independently adjacent to one another and ultimately fused in some parts. Careful questioning of the patient and clinical examination are necessary to exclude the possibility that the neoplasm arose primarily from the oral mucosa, or that it is a metastatic deposit in the jaw. A further possibility to be considered is that the lesion was initially an epithelial neoplasm that underwent secondary cystic change. To be certain of the diagnosis, histological evidence of frank squamous cell carcinoma directly in transition from a typical odontogenic cyst lining is regarded as the gold standard diagnostic criterion, but in some cases the malignancy may have overgrown and effaced the precursor lesion. It is also important not to overinterpret an inflamed or proliferating cyst lining as malignant. On occasions, the arcading epithelium of a radicular cyst may give a pseudoepitheliomatous appearance and islands of odontogenic epithelium in the wall are not uncommon. Attention to the cytology of the islands is helpful. Often the epithelium is bland and resembles squamous odontogenic tumour rather than the atypical epithelium of malignancy (Parmar et al. 2011 ; Chrcanovic and Gomez 2018a ).
Despite the undoubted