Figure 3.5 Radiograph of a residual cyst. The lesion is at the site of a previously extracted tooth. The lesion must be differentiated from an odontogenic keratocyst.
Table 3.1 The relationship between the size of a lesion on radiological examination and the histological diagnosis of a cyst or granuloma. The arrow illustrates the increasing chance of a lesion being a cyst.
Source: Based on Mortenson et al. (1970 ).
Shrout et al. (1993 ) used radiometric methods to analyse the grey levels on digitised images of periapical lesions. In a pilot study of only 10 mandibular lesions, they showed that analysis of grey levels could correctly identify 4 of 6 granulomas and all 4 cysts. They concluded that it may be feasible to differentiate between radicular cysts and periapical granulomas on the basis of radiographic density. With the advent of digital radiography and powerful software to routinely analyse images, it would be interesting to see if these findings could be confirmed. Early studies examining grey levels on images from cone beam computed tomography (CBCT) suggest that this may provide an accurate diagnosis (Simon et al. 2006 ). Measurement of conventional parameters on CBCT, however, have proved to be no more accurate than conventional X‐rays (Guo et al. 2013 ).
Although teeth may be resorbed by radicular cysts, there is a poor correlation between radiological evidence of resorption and actual tooth resorption on histology. Laux et al. (2000 ) compared the radiological and histological findings in 114 periapical lesions. Ninety three (81%) showed histological evidence of tooth resorption, but only 21 (19%) showed evidence of resorption on the radiographs. It should be noted, however, that only 30 of the 93 lesions with histological resorption showed dentine involvement. In the majority (63 cases) only cementum was involved and it was acknowledged that this would not normally be visible on a plain radiograph.
The data from these studies suggest that there are no specific radiological features that can be used to distinguish between a radicular cyst and a periapical granuloma. Clinicians know that it is useful in treatment planning to have an indication, a priori, whether a periapical lesion is a cyst or a granuloma. There are a number of key features that together can identify that a lesion is odontogenic and can be highly suggestive of a cyst (Box 3.2). Both granulomas and cysts are associated with a heavily restored or carious tooth and lie within the periodontal ligament. Cysts are more often over 15 mm in diameter, more often have a corticated margin, and show a greater degree of radiopacity.
Box 3.2 Clinical and Radiological Features: Key Facts
Always associated with a non‐vital tooth
Most commonly found on upper anterior teeth
Often symptomless and found on radiological examination
Firm or hard swelling, but large lesions may show ‘egg‐shell’ crackling
Residual cysts are found at sites of a previous tooth extraction
Radiology shows well‐demarcated, corticated lesion
Rarely greater than 30 mm in diameter
Pathogenesis
For any type of cyst to develop, three elements are needed: a source of epithelium, a stimulus for epithelial proliferation, and a mechanism of growth and bone resorption. In the case of a radicular cyst, the process is driven by an inflammatory response at the apex of a tooth (Box 3.3). Although trauma, instrumentation, and irritation from filling materials may cause inflammation, in reality this is usually short lived and the chronic inflammation needed to initiate cyst formation almost always follows microbial infection in a dead pulp following caries. The presence of bacteria and their products in the root canal then leads to periapical inflammation and the formation of a periapical granuloma, which may then lead to cyst formation.
It must be noted, however, that although cysts are a direct sequela of periapical inflammation, cyst formation is not inevitable and radicular cysts are in fact quite rare relative to the prevalence of caries and periapical lesions. In an analysis of 256 periapical lesions, Nair et al. (1996 ) showed that only 15% were actually cysts, although a further 37% were granulomas with proliferating epithelium. Their criteria for diagnosis of a cyst was unusually stringent and depended on the ability to examine, in multiple serial sections, the entire specimen and to be able to visualise a distinct epithelial‐lined cavity. Few studies have undertaken such meticulous examination of lesions using serial sections, but those that have have confirmed the findings of Nair et al. (1996 ) that cysts form the minority of periapical lesions. The actual frequencies reported have been 17.1% (Simon 1980 ), 15.2% (Nair et al. 1996 ), 32.0% (Ricucci et al. 2006b ), and 24.2% (Ricucci et al. 2020 ).
Box 3.3 Pathogenesis: Key Facts
Three elements are needed:
A source of epithelium
A stimulus for epithelial proliferation
A mechanism of growth and bone resorption
The cyst develops in three phases:
Phase of initiation – rest cells of Malassez are stimulated to proliferate within a periapical granuloma
Phase of cyst formation – a cavity within the granuloma becomes lined by proliferating epithelium
Phase of growth and enlargement – growth and enlargement are driven by increased osmotic pressure, and are associated with inflammation, cell proliferation and bone resorption
It is convenient first to consider the pathology of periapical periodontitis and then to discuss the pathogenesis of radicular cysts in three phases: the phase of initiation, the phase of cyst formation, and the phase of growth and enlargement.
Pathology of Periapical Periodontitis
Radicular cysts develop within a pre‐existing periapical granuloma where proliferation of the epithelial cell rests of Malassez is initiated by inflammation caused by the necrotic debris and bacterial factors derived from the dead pulp. One can think of this process as part of normal healing, where the host response acts to prevent dissemination of bacteria and stimulates epithelial regeneration. Histologically a periapical granuloma is composed of granulation tissue at various stages of development and maturation. Early lesions may show clear evidence of acute inflammation with polymorphonuclear leukocytes (PMNs), while later lesions become dominated by lymphocytes and plasma cells and may develop a fibrous outer capsule. The process involves many cell types that give rise to a massive array of pro‐inflammatory mediators, cytokines, chemokines, and growth factors, which work together in complex interactions to pursue the final goal of elimination of the cause and healing. However, as well as being protective to the host, these immunomodulatory pathways are also destructive, especially if the bacterial insult persists, as is often the case in
