Aetiology and pathogenesis

The epithelial lining of inflammatory cysts is derived from the rests of Malassez, which proliferate to produce thick, irregular, often incomplete squamous epithelium, with granulation tissue forming the cyst wall in the denuded areas (Fig. 45.3). Depending on the nature of the inflammatory response, there may be areas of chronic inflammation, or acute inflammation with abscess formation. Cholesterol crystal clefts are often present and mucous cells may be found. The cyst fluid is usually watery, but may be thick and viscid with cholesterol crystal clefts giving it a shimmering appearance. The cysts have capsules of collagenous fibrous connective tissue and cause bone resorption and may become quite large.

Bacterial endotoxins may initiate epithelial proliferation together with complement activation and T lymphocyte infiltration, T cells releasing contributory inflammatory cytokines-interleukins, IL-1 and IL-6, in particular. Osmosis plays a role in cyst expansion. Prostaglandins, collagenases and matrix metalloproteinases plus gene products NF-κB ligand (RANKL) and osteoprotegerin (OPG) appear to be associated with the bone destruction both in periapical cysts and periapical granulomas. The Runx2 (core-binding protein (cbfa)1/polyoma enhancer-binding protein (pebp)2alphaA) a DNA-binding transcriptional molecule expressed in osteoprogenitor cells, and transforming growth factor (TGF-β2) are involved in the new bone formation.

Clinical features

They include the following:

Diagnosis

The diagnosis is based on history, clinical examination and appropriate investigations, such as pulp vitality testing and radiographs (both intraoral and extraoral) of associated teeth, aspiration and analysis of cyst fluids, and histopathology. Protein p63 expression may be useful to identify cyst types with a more aggressive and invasive phenotype.

Treatment (see also Chs 4 and 5)

The treatment of inflammatory cysts depends on whether or not the involved non-vital tooth is to be retained. Conventional intra-canal endodontic treatment will often lead to the resolution of very small radicular cysts, but regular radiographic review is necessary until there has been complete resolution of the cyst. If, when the tooth has been root-filled, the cyst does not resolve, or if the cyst is of such a size that it is unlikely to resolve with endodontic treatment alone, surgery is indicated – either enucleation or marsupialization.

Follow-up

This is mainly in primary care.

CLINICAL FEATURES

The dentigerous cyst is most frequently found in areas where unerupted teeth are found – mandibular third molars, maxillary third molars and maxillary canines, in decreasing order of frequency. These cysts may grow to a large size, displace the tooth with which they are associated, or rarely cause resorption of adjacent tooth roots

DIAGNOSIS

Diagnosis is usually made by clinical and radiographic assessment – when the follicular space exceeds 5 mm from the crown it is likely that a cyst is present. However, odontogenic keratocysts and ameloblastomas may occasionally mimic the radiological appearances of follicular cysts. Aspiration may be helpful in differentiating the lesions

TREATMENT (see also Chs 4 and 5)

Treatment may be either marsupialization, allowing the tooth to erupt, or enucleation, with removal of the associated tooth. Rarely squamous cell carcinoma or ameloblastomas arise within a dentigerous cyst.

Eruption cysts

Eruption cysts are considered as minor soft tissue forms of dentigerous cysts. In these cases, the involved teeth are usually prevented from eruption by dense fibrous tissue overlying them. They often burst spontaneously before eruption of the associated tooth, and only require excision if impeding normal eruption. Then, a narrow window can be excised over the erupting tooth.

Clinical features

The KCOT is a great mimic; it may have many clinical appearances, and may be seen over a wide age range. Most involve the mandibular angle and may expand to occupy the major part of the ramus as a radiolucent lesion. They may sometimes be multilocular. They may resorb the cortical plates and expand into the soft tissues, envelop unerupted teeth giving a dentigerous appearance or displace teeth but not resorb them. KCOTs are generally painless, and often grow to a large size before giving rise to symptoms, unless they become secondarily infected.

Diagnosis

Diagnosis may be suggested by clinical features supported by imaging, and aspiration and estimation of soluble protein level in aspirated cyst fluid may be an aid to the diagnosis, since a protein level of <4 g/100 mL suggests KCOT, whereas a value >5 g/100 mL suggests a radicular or dentigerous cyst, or rarely a cystic ameloblastoma. The demonstration of keratin squames in an aspirate is virtually diagnostic of a KCOT. The diagnosis of KCOT is confirmed on histological grounds.

The cyst lining usually has a characteristic appearance of a regular keratinized stratified squamous epithelium, commonly five to eight cell layers thick and without rete pegs (Figs 45.4 and 45.5). There is a well-defined basal layer predominantly of columnar, but occasionally cuboidal, cells. Desquamated keratin is often present within the cyst lumen and the fibrous wall is usually thin.

Treatment (see also Chs 4 and 5)

Gorlin syndrome should be excluded – especially if the lesions are bilateral and/or in young people. Although there is some dispute over the most appropriate treatment for keratocysts, all authors agree that the cyst lining should be meticulously removed. Small unilocular lesions should be thoroughly enucleated. Large or multiloculated cysts should be excised with a margin of surrounding bone. KCOTs tend to recur following removal; recurrence rates can be as high as 60%.

Follow-up