cysts and cystic lesions

�9 D] [:Ir162 Ii [ I P A T H O L O G Y

Cysts and cystic lesions of the jaws

P. R. Morgan

In this article, some recent findings on benign cysts and cystic neoplasms of odontogenic origin are reviewed with special regard to their diagnostic relevance. Emphasis is given to less common lesions and those which present diagnostic difficulty or which may involve more complex management. Some recent applied research contributions in this area will also be included.

Introduction

The jaws are unique in the skeleton in the amount and variety of epithelial residues contained within them and in the range of cystic lesions to which they give rise. Management of such lesions is a significant proportion of the work-load of oral and maxillofacial surgeons and relies on good pre-operative interpretation of radiographs and computerised tomography (CT) scans and accurate histopathological diagnosis of biopsy and surgical specimens. To some extent, it is artificial to separate the histopathological features from clinical and radio- logical appearances when considering these lesions, as in other, longer reviews in this area 1,2 and therefore descrip- tions will not always be confined to histopathology. For the purposes of this account, cysts will be divided into benign cysts of odontogenic and non-odontogenic origin and cystic neoplasms (benign and malignant). Non-epithelial lined cysts will be mentioned briefly.

odontogenic cysts and tumours. Whilst all cysts lined by stratified epithelium contain the primary keratins of keratinocytes, 5 and 14, keratocysts express keratins 1 and 10 (markers of cornification) as well as 4 and 13 (markers of non-cornified epithelium). Dentigerous and radicular cysts also express keratins 4 and 13. Keratin 19 is expressed in odontogenic epithelia under all cir- cumstances, normal development, adult vestiges, cysts and neoplasms (Fig. 1). Indeed, its presence is so consistent that it could be considered an obligatory keratin of odontogenic epithelium and has the potential to be of diagnostic value. 5 Keratins 8 and 18, found in abun- dance in simple epithelia, are expressed at low but vari-

General characteristics of odontogenic epithelium

From the range and complexity of normal structures and pathological lesions to which it gives rise, odontogenic epithelium must be regarded as pluripotent? This is borne out by the repertoire of keratin proteins which are expressed in the developing normal tooth germ 4 and in

P. R. Morgan, BSc, BDS, PhD, MRCPath, Department of Oral Medicine & Pathology, UMDS, Floor 28, Guy's Tower, Guy's Hospital, London SE1 9RT, UK

Fig. 1- -A frozen section of an odontogenic keratocyst stained with a monoclonal antibody to demonstrate keratin 19, present in all odontogenic epithelia. Streptavidin-biotin peroxidase reaction,

Current Diagnostic Pathology (1995) 2, 86-93 �9 1995 Pearson Professional Ltd 86

CYSTS AND CYSTIC LESIONS OF THE JAWS 87

Fig. 2- -Hya l ine bodies in the l ining of a radicular cyst. These structures are probably a secretion product, unique to odontogen ic epithel ia and s imi lar to enamel cuticle, which may be deposi ted concentr ical ly on a ' template ' layer. H&E.

able levels in keratinocytes of odontogenic cysts, apart from keratocysts, and of course in zones of mucous metaplasia.

Hyaline bodies (Rushton bodies) are highly eosinophilic, laminated, circular or folded elongate structures (Fig. 2) which lie in the epithelium of about 10 per cent of all forms of odontogenic cyst but do not occur in other cyst types. There is considerable evidence now that they represent a secretion product, probably similar to dental cuticle which is deposited in variable amounts on tooth enamel at the completion of its formation. The available histological, histochemical and ultrastructural evidence supports the view that it is a product of odontogenic epithelium secreted on to a template of endogenous or exogenous origin e.g. cholesterol crystal, root fragment or root filling mater ia l )When present, hyaline bodies may therefore be considered a marker of odontogenic cysts.

Cyst growth

There is a considerable literature on possible mecha- nisms of cyst initiation and subsequent enlargement. 7 Theories have ranged from the osmotic/hydrostatic pressure concept of Toiler s to differential growth 9 and inflammatory mediators such as prostaglandins m and, more recently, interleukins. ~ There is little doubt that fluid-filled cysts are under positive hydrostatic pressure but it may be doubtful whether this is transmitted as a resorptive force to the surrounding bone, especially as the cell population of most cyst walls includes myofibroblasts which may serve to contain the pressure generated. ~2

A simple classification of jaw cysts 1,2 groups them broadly according to pathogenesis, with odontogenic cysts making up the largest proportion (Table).

Odontogenic cysts

These are derived from residues of odontogenic epithelium which otherwise gradually involute following

Table-~Simplified classification of jaw cysts

ODONTOGENIC CYSTS Developmental Dentigerous cyst

Eruption cyst Odontogenic keratocyst Lateral periodontal cyst Botryoid odontogenic cyst Glandular odontogenic cyst Inflammatory Radicular cyst, lateral radicular cyst, residual cyst, paradental cyst NON-ODONTOGENIC CYSTS Nasopalatine duct cyst 'Fissural' cyst

CYSTIC NEOPLASMS Ameloblastoma Unicystic ameloblastoma Calcifying odontogenic cyst

completion of tooth development and eruption. A major division into developmental 13 and inflammatory catego- ries is usual.

Dentigerous cyst (follicular cyst)

This cyst is diagnosed by its precise relationship with the crown of an unerupted tooth, commonly the lower third molar or upper permanent canine. Being derived from the reduced enamel epithelium, the remnant of the enamel organ, it is attached to the tooth at the enamel- cementum junction (Fig. 3A). It is therefore important for diagnosis that the tooth is supplied with the soft tissue specimen, or at least that accurate clinical inlor- marion is supplied by the operator. Radiographically, they are unitocular but the illusion of a dentigcrous cyst on a radiograph can be given by other radiolucent lesions which may secondarily involve or displace an unerupted looth, such as an ameloblastoma (see below).

Histologically, the cyst lining is characterised by uniform, non-keratinised epithelium, either stratified squamous about 4 10 cells thick or with a cuboidal basal layer, thus often resembling reduced enamel epithelium. Mucous metaplasia is frequently encotmtered (Fig. 3B). In the young patient, the wall is myxoid and contains clusters of odontogenic epithelial rests and in more mature follicles these often show cementicle-like miner- alisation. The immature, myxoid follicle has been vari- ously misdiagnosed as odontogenic cyst, myxoma, odontogenic fibroma, odontome and even ameloblastoma.~4 Rests of odontogenic epithelium in the wall may also form squamous pearls such as are found in greater profusion in the squamous odontogenic tumour. In such pearls basal cells are inconspicuous and mitoses exceed- ingly rare. It is not always possible to establish the point at which an enlarged follicle becomes a dentigerous cyst. Although there is rarely unanimity, a practical guide to the diagnosis of a cyst is a follicular space of 5 mm or more on a radiograph and a lining of stratified squamous epithelium as well as, or instead of, reduced enamel epithelium.

As developmental jaw cysts are usually symptomless, secondary inflammatory changes often provoke initial

88 CURRENT DIAGNOSTIC PATHOLOGY

(A) (A)

(B)

Fig. 3--A dentigerous cyst on a lower third molar tooth. (A) The cyst wall, attached at the enamel-cementum junction, has been partial ly removed after f ixation to reveal the crown of the tooth. (B) Part of the vascular fibrous wall of a dentigerous cyst lined by non-keratinised stratified squamous epithel ium which shows a zone of mucous metaplasia. Such an appearance is characteristic in the absence of inf lammation. H&E.

presentation and a high proportion of surgical specimens of dentigerous cysts show lymphoplasmacytic infiltrates in the wall and neutrophils in the epithelial lining. Accu- mulations of cholesterol clefts, foreign body giant cells and haemosiderin-laden macrophages may greatly en- large the wall and locally herniate into the cyst lumen. Thus, at cut-up, disrupted cysts may glisten with discharging semi-fluid contents which are rich in cholesterol.

Odontogenic keratocyst (primordial cyst)

More has been written in recent years on the odontogenic keratocyst than on any other jaw cyst. Radiographically it has a multilocular, or apparently multilocular, appearance and is sometimes multiple, especially when it represents a manifestation of the naevoid basal cell carcinoma syndrome (Gorlin's syndrome). Rather than expanding the jaw, the cyst tends to grow mesiodistally at the expense of the medullary bone and extends between the roots of the teeth.

Macroscopically, the opened cyst reveals a white,

(B)

Fig. 4--Part of an odontogenic keratocyst which has formed alongside an unerupted tooth. (A) The white, folded lining reveals the presence of keratinising epithelium. Proximity to a tooth is an incidental but not uncommon feature and on a radiograph may simulate a dentigerous relationship. (B) Characteristic histological appearance of an odontogenic keratocyst epithelium: uniform thickness and with a flat basal surface, elongate basal cells, a thin prickle cell zone and corrugated parakeratin surface layer. The fibrous wall is usually thin, delicate and vascular. H&E.

folded inner surface (Fig. 4A) following discharge of stacked keratin, as with an epidermoid cyst. In most cases, there should be little difficulty in establishing the diagnosis histologically. Typically, the wall is thin and rarely removed intact. It is lined by uniform, para- keratinised epithelium, some 10-12 cells thick, with a flat basal surface (Fig. 4B). Key features are a narrow, folded (corrugated) zone of keratin, prickle cells which retain their long axes at right angles to the basement membrane until close to the keratinised layer and elongate, often palisaded, basal cells which show reversed polarity in at least some areas. It was established many years ago that keratocysts show a higher frequency of mitoses than is found in other odontogenic cysts. 15 Mitotic figures may be found in both basal and parabasal layers. A study using PCNA as a marker of cell proliferation has shown higher indices for keratocysts than for

16 other odontogenic cysts. Odontogenic keratocysts have a higher recurrence rate too, due in part to their physical fragility leading to disruption during removal, the epithelium separating easily from the fibrous wall. A


further possible reason is the presence of daughter cysts in the wall which may remain after cyst enucleation.

Differences in proliferation rates and in the frequency of basal epithelial" cell budding between solitary, multiple and recurrent odontogenic keratocysts and those associated with naevoid basal cell carcinoma syndrome have been the subject of a number of recent studies. 17 Significantly higher rates of mitosis occur in keratocysts in patients with Gorlin's syndrome. Satellite cysts have been detected in about 50% of syndrome patients and in the walls of 25% of multiple or recurrent cysts whereas they are found in less than 10% of solitary keratocysts. In practical terms, the possible diagnosis of naevoid basal cell carcinoma syndrome should be investigated for all patients with odontogenic keratocysts. The syndrome is an autosomal dominant condition with numer- ous defects, many involving the axial skeleton.

It is important not to diagnose as a keratocyst every odontogenic cyst which shows some keratinisation. Parts of (probably) long-standing dentigerous or radicular cysts may show ortho- or parakeratinisation but without the other features of odontogenic keratocysts. Also, soft tissue removed together with impacted, partially erupted third molar teeth may include some keratinised gingival mucosa which may unwittingly be mistaken for keratocyst wall. It is of interest that, whilst all odontogenic keratocysts keratinise, only a minority are orthokera- tinised; moreover, these recur less frequently than parakeratinising cysts. 18,19

Although inflammatory infiltrates in odontogenic keratocysts are usually well-localised and mild, diagnostic problems may result from an ~xtensive inflammatory infiltrate which suppresses keratinisation (Fig. 5). This could give rise to misdiagnosis of a dentigerous or residual cyst with the consequence that, in the absence of follow-up, the patient may develop a recurrence which is unrecognised until well advanced. If, in a similar context, the basal cells are markedly columnar the keratocyst might be misdiagnosed as an ameloblastoma, particularly since the radiographic appearance of these two lesions are sinfilar. One should be wary of over-

diagnosis in such cases, especially if the biopsy sample is small.

Lateral periodontal, botryoid, and glandular odontogenic cysts

The lateral periodontal cyst is usually unilocular and lies alongside a vital tooth and therefore, like the radicular cyst, is presumed to originate from cell rests of Malassez in the periodontal ligament or possibly from part of the developing follicle, z~ The stimulus to its formation is unknown, and it is usually detected as a symptomless radiolucency on routine radiography. Its epithelial lining is about 2-6 cells thick, non-keratinised, stratified squamous and with a flat basal surface. There may be a narrow zone of subepithelial hyalinisation, a feature occasionally encountered in other odontogenic cysts and neoplasms. The fibrous wall is usually uninflamed, cellular and delicate, lacking daughter cysts. A characteristic feature is the presence of periodic, plaqueqike thickenings in the epithelium (unrelated to inflamma- tion) which may bulge into the cyst lumen or wall or both (Fig. 6). These contain glycogen and may be composed predominantly of clear cells but there is no evidence that they represent centres of proliferation. Indeed, mitotic figures, epithelial budding and daughter cyst formation are unusual in the lateral periodontal cyst. A proportion of cysts which radiographically suggest a diagnosis of lateral periodontal cyst turn out to be odontogenic keratocysts on histological examination, despite their unilocular profile.

Botryoid and glandular odontogenic cysts are rare entities with features in common with each other and with the lateral periodontal cyst. The former is so called because the low magnification appearance or macro- scopic cut surface sometimes resembles a bunch of grapes. Radiographically, most have been multilocular and located in the mandible. In their more detailed features, botryoid cysts resemble lateral periodontal cysts, the thin, non-keratinised epithelial lining with thickened plaques being a consistent feature. A number of recent

Fig. 5--A keratocyst which has become secondarily inflamed. Note the loss of keratinisation in the zone showing an arcading pattern of epithelial hyperplasia. If the biopsy is small or inf lammatory change extensive, this may lead to a mistaken diagnosis of an inf lammatory cyst. H&E.

4~

Fig, 6--Wall of a lateral periodontal cyst with a Iocalised thickening of the uniform, non-keratinising epithelium. Several such thickenings may be encountered in a given plane of section. H&E.


publications point to a high recurrence rate for this multicystic lesion.

Greater difficulty attaches to the status of the glandular (sialo- or mucoepidermoid-) odontogenic cyst. It is sur- prising that this cyst has been recognised only recently as a distinct entity 21,22 and less than 20 cases have been reported in the world literature. It has an appearance of multilocularity on radiographic examination. Its histological features include multiple thickened epithelial plaques, like those of the lateral periodontal cyst, and multicystic growth, like the botryoid cyst. Intriguing additional features are present in the epithelium: papil- lary 'outgrowths' into the cyst lumen with apocrine-like 'decapitation' secretion of surface cells, ductal structures, mucin-producing goblet cells and occasionally acini (Fig. 7). The nomenclature for this cyst has not yet been established and interpretations of the histological features range widely. Mucous metaplasia may be present in the lining of any odontogenic cyst and to some commentators, the glandular odontogenic cyst is an ex- treme example of this change. An opposing view is that the lesion is in fact a low-grade central mucoepidermoid carcinoma. When more cases become available for study and when a wider range of markers of odontogenic epithelium have been developed, the histogenesis of this group of cysts should become clearer.

Inflammatory odontogenic cysts

Radicular cyst

By far the most common jaw cyst is the radicular cyst, an odontogenic cyst which forms from epithelial rests of Malassez in the periodontal ligament consequent upon activation from the products of necrotic dental pulp in an adjacent tooth. The wall is relatively thick and usually contains a dense inflammatory infiltrate towards the inner aspect, consisting of plasma cells and lymphocytes. Neutrophils tend to accumulate in the epithelium which is of non-keratinised, stratified squamous type and varies greatly in thickness (Fig. 8). Sometimes the arcading

Fig. 8--Radicular cyst: a frequent presentation with a dense, mixed inflammatory infiltrate adjacent to variably hyperplastic, non-keratinised epithelim. The upper part of the field shows part of the wall apparently devoid of epithelium, also a common finding. H&E.

pattern of hyperplasia (Fig. 5) can be so striking that the unwary may suspect the presence of an ameloblastoma. 23 It is essential that the condition of the related tooth be known for the correct diagnosis to be made: the histological features of a radicular cyst may be identical to those of a secondarily inflamed dentigerous cyst. Similarly, a long-standing radicular cyst may come to resemble a developmental cyst when the inflammatory infiltrate fades. A cyst which forms alongside a non-vital tooth is termed a lateral radicular cyst and one which is retained following removal of the offending tooth or root is referred to as a residual cyst, the histological features being identical to those just described.

Paradental cyst

The paradental cyst is an inflammatory cyst which lies on the disto-buccal aspect of fully or partially erupted third molar teeth, near the bifurcation of the roots (Fig. 9). There is a male preponderance, a history of pericoronitis is common and sometimes a predisposing

Fig. 7--Parts of two Iocules of a glandular (sialo-) odontogenic cyst with thickened epithelial plaques, similar to those found in lateral periodontal and botryoid cysts but also showing ductal structure, and extensive mucus- secreting cells. H&E.

Fig. 9--A paradental cyst attached to the enamel-cementum junction of a lower molar tooth on the disto-buccal aspect. Although slightly disrupted, it lies alongside the tooth and does not enclose the crown.


factor is an extension of enamel down to where the roots separate and a bilateral presentation is not u n u s u a l . 24 The associated tooth is therefore usually vital and such cysts are often removed still attached after extraction of the erupting or partially erupted tooth due to impaction. Whether the source of epithelium is the reduced enamel epithelium, periodontal pocket epithelium or cell rests of Malassez, the aetiological mechanism appears to be epithelial activation by inflammatory infiltrate which is induced by bacterial plaque.

A related cyst, the mandibular infected buccal cyst, has a similar association with first or second lower permanent molar teeth 25 but in younger patients than the paradental cyst. As Shear 2 argues, the two entities are probably related but are worth while recognising as distinct for reasons of management.

Both these cysts have the same histological appearance as the radicular cyst: hyperplastic, non-cornified epithelium lining a fibrous wall containing a dense, mixed inflammatory infiltrate. Clinical information is therefore essential for an accurate diagnosis.

Malignant transformation in jaw cysts

Although rare, malignant transformation does occur in odontogenic cysts, about 60 cases having been reported in the world literature. Malignant transformation appears to arise most frequently in residual cysts, reported cases equalling those of dentigerous cysts and odontogenic keratocysts combined; 80% of such malignancies occur in the mandible (Fig. l()). 2r Not surprisingly, the age at presentation tends to be greater than that of patients with benign cysts; the 6th or 7th decade rather than the 4th or 5th. As far as can be assessed with such small numbers of cases, the prognosis appears to be better than that of mucosal carcinomas which infiltrate the .jaws, and that of primary intra-osseous carcinomas, nodal metastases being less common. This difference in prognosis might be expected when the carcinoma is removed while being retained within the confines of the fibrous cyst wall.

Differential diagnosis should include other odontogenic carcinomas: primary intra-osseous carcinomas, which are thought to arise from residues of odontogenic epithelium in the jaws, and malignant variants of ameloblastoma and other odontogenic tumours. Central mucoepidermoid carcinomas, in which the epidermoid component may predominate, should also be considered. Any of these malignancies may be cystic, at least in part. The mandible is also a well-recognised site for carcinomas metastatic to the jaws from such sites as lung, breast, prostate, thyroid and kidney which may simulate cysts radiographically.

Dysplastic change may be encountered in cyst epithelia and levels should be checked carefully for evidence of frank invasion. This is particularly the case in those odontogenic keratocysts which show basal budding (Fig. 11) and epithelial islands, since the presence of dysplasia may give the impression of a wide field of invasion.

AmelobIastoma and its unicystic variants

Ameloblastomas are the most common odontogenic neoplasms. They present usually in the mandibular third molar region and least often in the anterior maxilla. Their peak age prevalence is in the 4th or 5th decade. Histological criteria for their diagnosis were set out by Vickers and Gorlin. 27 The epithelial cells comprise two distinct populations. Firstly, peripheral, or basal, cells which are columnar and often markedly elongate and showing reversed polarity, with the nucleus occupying the part of the cell away fi-om the basement membrane; this layer thus resembles the pre-ametoblast of the developing tooth germ. The second population consists of polyhedral suprabasal cells with fewer intercellular con- tacts than conventional prickle cells; this is the stellate reticulum-like layer, similar to the stellate reticulum of the bell stage in the developing tooth. Two principal arrangements of epithelium are recognised, follicular (Fig. 12A) and plexiform (Fig. 12B), although there is

Fig. 10--Squamous cell carcinoma which has arisen in an odontogenic keratocyst. This mandibular tumour was more solid than cystic but dysplastic keratocyst lining is still evident associated with islands of well-differentiated carcinoma. A dense lymphocytic response is also present. H&E.

Fig. 11--Odotogenic keratocyst showing extensive basal budding together with bulbous rete processes and some cell disorganisation but minimal cytological features of malignancy. However, the presence of these features increase the l ikelihood of recurrence. H&E.


(A)

(B)

Fig. 12--Examples of cyst formation in conventional ameloblastomas. (A) Follicular ameloblastomas with cystic change in the stellate reticulum component of the neoplasm. The cystic area on the right is lined by cells showing 'acanthomatous' change. (B) Plexiform ameloblastomas with stromal cysts; surviving small blood vessels indicate the location of the connective tissue component. The lumen of the main cyst is shown at the top of the figure and is composed of degenerate epithelial cells. H&E.

no behavioural difference between the two. Although usually slow growing and lacking in detectable mitoses, both types tend to infiltrate the bone and to recur unless removed by local resection. The follicular form consists of round or irregular islands of tumour, the stroma being composed of vascular, cellular fibrous tissue. As its de- scriptive name suggests, in the plexiform ameloblastoma the epithelial component takes the form of interlacing strands which appear to entrap the stroma. Cystic change is common in both types, microcysts forming in the epithelial masses and stromal cysts in the connective tissue. As the ameloblastoma enlarges, the cysts coalesce and may form one or more cystic cavities containing straw-coloured fluid. Biopsy of the stretched wall of such a tumour may lead to the misdiagnosis of a non- neoplastic cyst. Fortunately, the solid or invaginated areas are likely to contain more representative ameloblastoma. Another conmaon feature of ameloblastomas is squamous metaplasia ('acanthomatous change') which only rarely consists of true keratinisation when it may

be confused with an odontogenic keratocyst. 28 An additional but rare feature of ameloblastomas is the inclusion of eosinophilic granular cells whose origin is obscure but which are befieved to arise in the epithelial compartment.

Other variants of ameloblastoma may also be predominantly cystic:

�9 Desmoplastic, in which the stroma is more densely fibrous.

�9 Basal cell, in which basaloid cells predominate. �9 Papilliferous keratoameloblastoma, a rare type in which

cystic spaces may be filled with desquamated, keratinising squames.

Some ameloblastomas are characteristically unilocular on radiographs and prove to be unicystic (Fig. 13), and sometimes in a dentigerous relation to a tooth, when examined macroscopically. They also tend to present in younger patients than do conventional ameloblastomas. Levels should be taken through the excision specimen to investigate the presence of a conventional ameloblastoma. Sometimes part of the lining expands into a plexiform pattern of ameloblastoma. On occasion, strict criteria for ameloblastoma can be hard to establish and the diagnosis has to take account of the clinical presentation as well as 'suggestive' features in the epithelial lining. Unicystic ameloblastomas are generally considered to have a lower recurrence rate than their conventional counterparts. This is true of those with a continuous epithelial lining and those with ameloblastomatous mural nodules which invaginate the lumen. They may be treated successfully by careful enucleation, but when the wall is found to be infiltrated by islands of ameloblastomatous epithelium treatment should be as radical as for the conventional solid or multi-cystic types. 13

Calcifying odontogenic cyst

This curious entity is usually classified with epithelial odontogenic tumours since it is really a neoplasm which sometimes may be as aggressive as an ameloblastoma.

Fig. 13--Unicystic ameloblastoma. This lesion shows few histological hallmarks of an ameloblastoma, Basal epithelial cells palisaded in places but with little evidence of the reversed polarity characteristic of ameloblasts and stellate reticulum cells are poorly developed. Epithelium in this field has a somewhat plexiform arrangement. H&E.


Fig. 14--Calcifying odontogenic cyst with characteristic ghost cells suprabasally. Basal and parabasal layers resemble eqivalent cells in ameloblastomas. Groups of ghost cells may find their way into the connective tissue and stimulate a foreign body reaction. H&E.

It shows a wide site and age variation 29 but is conf ined

to the too th-bear ing regions of the jaws . S o m e t i m e s the

calc i fying odon togen ic cyst is not cyst ic and often it

does not calcify. Its basal cells and parabasal epithelial

cells r e semble those o f the ame lob la s toma but more

superficial cells expand to form lightly eos inophi l ic ,

partially kerat inis ing and usually nucleate cells t e rmed

'ghos t ce l ls ' (Fig. 14). These may b e c o m e calc i f ied and

are not d iss imi lar to cells o f the p i loma t r ixoma wilh

which this lesion has often been compared . Ghos t cells

are not unique to the calc i fying odon logen ic cysl but

have been descr ibed in cases of amelob las toma, amelo-

Mastic f ib roma and ameloblas t ic f ib roodon lome . A

further feature seen in a proport ion o f cases is the depo-

sition of poorly minera l i sed dysplas t ic dent ine or

'dentinoid" in the cyst wall. Somet imes typical dental

hard t issues form, in which case one has to cons ider

whe ther ' o d o n t o m e ' should be the more appropr ia te

designat ion, a dec is ion for which the age, site and radio-

graphic appearance should be taken into account. As

these turnouts are rather rare, this material has scarcely

been tested for its authent ici ty as dentine. A diagnosis

o f calc i fying odon togen ic cyst is not a clear pointer to a

l e s ion ' s l ikely behaviour . Deta i led analysis o f 92 cases

emphas i s ed the need to subgroup them into hamar to-

matous, cyst ic and neoplas t ic variants. 29

References

1. Kramer 1, Pindborg J, Shear M. Histological typing of odontogenic tumours 2nd ed. Berlin Heidelberg: Spinger-Verlag, 1992.

2. Shear M. Cysts of the oral regions. 3rd ed. Oxford: Wright, Butterworth-Heinemann, 1992.

3. Smith A, Matthews J. Odontogenic epithelium and its residues. In:

Browne R, ed. Investigative pathology of odontogenic cysts. CRC Press, 1991:53 85.

4. Heikinheimo K, Sandberg M, Happonen R-P, Virtanen I, Bosch F. Cytoskeletal gene expression in normal and neoplastic human odontogenic epithelia. Lab Invest 1991; 65: 688-701.

5. Morgan P R, Shirlaw P J, Johnson N W, Leigh I M, Lane E B. Potential applications of anti-keratin antibodies in oral diagnosis. J Oral Pathol 1987; 16: 212-222.

6. Morgan P, Johnson N. Histological, histochemical and ultrastructural studies on the nature of hyalin bodies in odontogenic cysts. J Oral Pathol 1974; 3: 127-147.

7. Browne R, Smith A. Pathogenesis of odontogenic cysts. In: Browne R, ed. Investigative pathology of odontogenic cysts. CRC Press, 1991: 87-109.

8. Toiler P. The osinolality of fluids from cysts of the jaws. Brit Dent J 1970; 129: 275-278.

9. Kramer I R H. Changing views on oral disease. Proc Roy Soc Med 1974; 67: 271-276.

10. Harris M, Toller P. The pathogenesis of dental cysts. Brit Med Bull 1975; 31: 159-163.

11. Meghji S, Henderson B, Bando Y, Harris M. Interleukin-1: the principal osteolytic cytokine produced by keratocysts. Archs oral Biol 1992; 37: 935-943.

12. Lombardi T, Morgan P R. hnmunohistochemical characterisation of odontogenic cysts with mesenchymal and myofilament markers. J Oral Pathoi Med 1995; 24:170 176.

13. Shear M. Developmental odontogenic cysts. An update. J Oral PatholMed 1994; 23:1 11.

14. Kim J, Ellis G. Dental follicular tissue: misinterpretation as odontogenic tumors. J Oral Maxillofacial Surg 1993; 51: 762-767.

15. Browne R. The odontogenic keratocyst histological features and their correlation with clinical behaviour. Br Dent J 197 I; 131 : 249-259.

16. Li T-J, Browne R, Matthews J. Quantification of PCNA+ ceils within odontogenic jaw cyst epithelium. J Oral Pathol Med 1994; 23:184 189.

17. Woolgar J A, Rippin J W, Browne R M. A comparative histological study of odontogcnic keratocysts in basal cell naevus syndrome and control patients. J Oral Pathol 1987; 16: 75-80.

18. Brannon R. The odontogcnic keratocyst. A clinicopathologic study {71312 cases. Part 11. Histoh}gical features. Oral Surg Oral Med Oral Pathol 1977: 43:233 255.

19. Wright J. The odontogenic kcratocyst: orthokcratinizcd w,'iant. Oral Surg Oral McdOral Pathol 1981; 51: 609 618.

20. Allini M, Shear M. The lateral periodontal cyst: an update. J Oral Pathol Med 1992; 21:245 250.

21. Padayachee A, Van Wyk C W. Two cystic lesions with features of both the botyroid odontogeuic cyst and lhc central mucoepidcrmoid turnout: sialo odontogenic cyst'? J Oral Pathol 1987; 16: 499-504.

22. Gardner D G, Kessler H P, Morency R, Schaffner D L. The glandular odontogenic cyst: an apparent entity. J Oral Pathol 1988; 17:359 366.

23. Lucas R. Pathology of Tumours of the Oral Tissues. 4th ed. Edinburgh: Churchill Livingstone, 1984.

24. Craig G. The puradental cyst. A specific inflamnmtory odontogenic cyst. Br Dent J 1976; 141:9 14.

25. Stoneman D, Worth H. The mandibular bucca] infected cyst - molar area. Deut Radiol Photog 1983; 56:1 14.

26. Schwimmer A, Aydin F, Morrison S. Squamous ceil carcinoma arising in residual odontogenic cyst. Oral Surg Oral Med Oral Pathol 1991; 72: 218--221.

27. Vickers R, Gorlin R. Ameloblastoma: delineation of early histopathologic features of neoplasia. Cancer 1970; 26:699 710.

28. Siar C, Ng K. 'Combined ameloblastoma and odontogenic keratocyst' or 'keratinising ameloblastoma'. Br J Oral Maxfac Surg1993; 31:183 186.

29. Hong S, Ellis G, Hartman K. Calcifying odontogenic cyst. A review of 92 cases with reevaluation of their nature as cysts or neoplasms, the nature of ghost cells, and subclassification. Oral Surg Oral Med Oral Pathol 1991; 72:56 64.

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