Melanin in a dentigerous cyst and associated adenomatoid odontogenic tumor.

The authors report on a case of dentigerous cyst associated with odontogenic adenomatoid tumor in an 8-year-old black Nigerian boy. Both the cyst and the tumor contained melanocytes and melanin-laden epithelial cells. To their knowledge this is the first reported case of melanotic follicular cyst and adenomatoid tumor. A review of the literature revealed that melanin is rarely found in odontogenic lesions. Since the neural crest influence on the development of odontogenic tissues is well established, the occurrence of melanocytes in these tissues is not surprising. A racial predisposition may be present; black patients predominated in the 15 reported cases of melanotic odontogenic lesions.

Cytokeratin expression of the odontogenic epithelia in dental follicles and developmental cysts.

The patterns of cytokeratin expression in the epithelium of 5 dental follicles, 7 dentigerous cysts, 5 odontogenic keratocysts, 3 nasopalatine cysts and an epidermoid cyst have been studies using a panel of monoclonal antibodies. The epithelium of dental follicles and of developmental odontogenic cysts strongly expressed keratins 5 and 19 and showed weaker expression of keratins typical of stratified non-cornified and of simple epithelia. Staining with mAbs against the latter keratins varied with the degree of epithelial differentiation. Nasopalatine cysts strongly expressed simple epithelial keratins and the epidermoid cyst strongly expressed a marker of cornification. Odontogenic cysts thus appear to differ in their pattern of keratin expression from other oral developmental cysts and all derivatives of odontogenic epithelia appear to share similar basic patterns of cytokeratin expression.

Quantitation of lactoferrin in odontogenic cyst fluids.

A competitive enzyme linked immunosorbent assay (ELISA) method was used to measure the concentration of lactoferrin in fluids from 36 odontogenic keratocysts, 15 dentigerous cysts, and 30 radicular/residual cysts. Keratocyst fluids contained significantly higher concentrations of lactoferrin than fluids from the other two types of cyst (p less than 0.001); but the range of values obtained within each group was large. Although lactoferrin represents a larger proportion of the total protein in keratocyst fluids than in dentigerous or radicular cyst fluids, lactoferrin concentration is not an absolute diagnostic marker for keratocysts. Lactoferrin concentration correlated strongly with the numbers of neutrophils present in keratocyst fluids (p less than 0.001), less so for dentigerous cyst fluids (p less than 0.05, and not at all in the case of radicular cyst fluids. It is suggested that neutrophils are the source of lactoferrin in the three categories of cyst studied but that the relatively impermeable nature of the keratocyst lining probably accounts for the particularly high concentrations of lactoferrin found in their fluids. Given that most keratocysts were asymptomatic, acute inflammation itself does not explain the reason for the high numbers of neutrophils in many of the fluids.

Lactoferrin in aspirates of odontogenic cyst fluid.

The possibility that the presence of lactoferrin in aspirates of odontogenic cyst fluid might be a useful preoperative diagnostic marker for odontogenic keratocyst was investigated. Using qualitative and quantitative immunodiffusion methods fluid from 29 of 29 dental (radicular) cysts, 12 of 14 dentigerous cysts and 27 of 31 keratocysts were found to contain lactoferrin. Although some of the highest concentrations of lactoferrin were detected in fluids from keratocysts, there was no significant difference between lactoferrin concentrations among the three groups. Neutrophil elastase was detected in 20 of 24 samples tested, 22 of which also contained lactoferrin. Immunocytochemical localisation of both lactoferrin and elastase was confined to neutrophils infiltrating cyst walls. These results suggest that lactoferrin in fluid from odontogenic cysts is derived from infiltrating neutrophils and that its presence in aspirated fluids is not a useful diagnostic marker for odontogenic keratocyst.

Quantification and analysis of the glycosaminoglycans in human odontogenic cyst linings.

Glycosaminoglycans (GAG) were extracted from the connective tissue of 15 dental cysts, 2 dentigerous cysts and 7 keratocysts, and separated electrophoretically and chromatographically. Hyaluronic acid (dental, 2.38; dentigerous, 3.98; keratocyst, 3.19 micrograms uronic acid/mg lyophilized tissue) was the major GAG detected, with lesser amounts of heparin (dental, 1.70; dentigerous, 1.95; keratocyst, 1.80 micrograms uronic acid/mg lyophilized tissue) and chrondroitin-4-sulphate (dental, 1.33; dentigerous, 2.85; keratocyst, 1.37 micrograms uronic acid/mg lyophilized tissue). It is suggested that enzymic release of these GAGs allows their diffusion into the luminal fluid where they may contribute to expansile cyst growth.

Glycosaminoglycans in fluid aspirates from odontogenic cysts.

Glycosaminoglycans and proteoglycans were analysed in keratinizing and nonkeratinizing odontogenic cyst fluids. Hyaluronic acid showed the highest incidence and abundance amongst the glycosaminoglycans detected. Appreciable amounts of chondroitin-4-sulphate were also observed, particularly in the dental cysts, with lesser amounts of the other glycosaminoglycans. Heparan sulphate showed a higher incidence and abundance in the keratocyst than the other cysts, whilst chondroitin-6-sulphate could not be detected in any of the cysts. A considerable proportion of the glycosaminoglycans of the fluids appeared to be complexed with protein and was released only after proteolytic digestion. The origin of these macromolecules is uncertain although it is likely that they are derived from both the connective tissue and the epithelium of the cyst wall.

Amoxicillin concentrations in serum, jaw cyst, and jawbone following a single oral administration.

Forty-four patient who underwent enucleation of jaw cysts were administered amoxicillin preoperatively. Specimens of venous blood (44), walls and fluids from periodontal (31) and dentigerous (13) cysts, and jawbone (26) were obtained during the operation and assayed for amoxicillin content. Measurable concentrations were found in all specimens. The levels were higher in periodontal cysts than in dentigerous cysts, and higher in maxillary bone than in mandibular bone. Since amoxicillin can easily and rapidly pass through the epithelial lining according to the change in concentration, the penetration by amoxicillin of blood/cyst wall/cyst fluid probably depends on simple diffusion.

Some observations on the fluids of odontogenic cysts.

The fluids of 44 dental cysts, 19 dentigerous cysts, 36 odontogenic keratocysts, and 12 ameloblastomas have been investigated. The incidence of epithelial cells, inflammatory cells, cholesterol crystals and bacteria was recorded in smears. There was a high incidence of epithelial cells in odontogenic keratocysts and not in other lesions. Cholesterol crystals had a similar incidence in all lesions. The proportion of the soluble proteins and total protein content was determined from cellulose acetate electrophoresis. Dental cysts contained an average of 51.19% albumin, 17.52% beta globulin, 22.04 % gamma globulin, and 6.30 g/100 ml protein. Dentigerous cysts contained an average of 61.35% albumin, 13.98% beta globulin, 12.70% gamma globulin and 5.40 g/100 ml protein. Odontogenic keratocysts contained an average of 78.03% albumin, 7.51% beta globulin, 7.91% gamma globulin, and 2.09 g/100 ml protein. Ameloblastomas contained an average of 67.38% albumin, 12.83% beta globulin, 12.60% gamma globulin and 4.86 g/100 ml protein. The immunoglobulin content was determined by single radial immunodiffusion. Dental cysts contained an average of 488.9 mg/100 ml IgA, 2535.4 mg/100 ml IgG, and 135.6 mg/100 ml IgM. Dentigerous cysts contained an average of 308.4 mg/100 ml IgA, 1618.2 mg/100 ml IgG, and 155.6 mg/100 ml IgM. Odontogenic keratocysts contained an average of 135.6 mg/100 ml IgA, 491.9 mg/100 ml IgG, and 54.1 mg/100 ml IgM. The significance of these findings in the pathogenesis and diagnosis of these lesions is discussed.