An immunocytochemical study of the inflammatory cell infiltrate and epithelial expression of HLA-DR in odontogenic cysts

The presence and distribution of lymphocytes, Langerhans cells, HLA-DR' infiltrating cells and the expression of HLA-DR by lining epithelium was investigated in the walls of odonlogenic cysts using an indirect immunoperoxidase method on acetone-fixed cryostat sections. The 23 cysts studied consisted of 14 dental (radicular) cysts, 5 keratocysts, 2 dentigerous cysts, 1 surgical ciliated cyst and 1 incisive canal cyst. The cell populations detected in the walls of all cysts were similar and consisted of HLA-DR+ macrophage-type cells and a mixture of T and B lymphocytes. Analysis of the T cell subsets revealed that in all cases the CD4⁺, T_h/i subset predominated over the CD8⁺, T_s/c subset. 18/22 cyst linings contained cells expressing a Langerhans cell phenotype (CD1⁺). Cytoplasmic epithelial expression of HLA-DR was detected in 7/22 specimens. Neither the presence of HLA-DR⁺ epithelial cells nor LC were restricted to a given type of cyst. These findings indicate the occurrence of similar cellular processes irrespective of the proposed developmental or inflammatory aetiology of these lesions.     

An immunocytochemical study of the inflammatory cell infiltrate and epithelial expression of HLA-DR in odontogenic cysts

The presence and distribution of lymphocytes, Langerhans cells, HLA-DR+ infiltrating cells and the expression of HLA-DR by lining epithelium was investigated in the walls of odontogenic cysts using an indirect immunoperoxidase method on acetone-fixed cryostat sections. The 23 cysts studied consisted of 14 dental (radicular) cysts, 5 keratocysts, 2 dentigerous cysts, 1 surgical ciliated cyst and 1 incisive canal cyst. The cell populations detected in the walls of all cysts were similar and consisted of HLA-DR+ macrophage-type cells and a mixture of T and B lymphocytes. Analysis of the T cell subsets revealed that in all cases the CD4+, Th/i subset predominated over the CD8+, Ts/c subset. 18/22 cyst linings contained cells expressing a Langerhans cell phenotype (CD1+). Cytoplasmic epithelial expression of HLA-DR was detected in 7/22 specimens. Neither the presence of HLA-DR+ epithelial cells nor LC were restricted to a given type of cyst. These findings indicate the occurrence of similar cellular processes irrespective of the proposed developmental or inflammatory aetiology of these lesions.     

p53 protein and Ki-67 reactivity in epithelial odontogenic lesions. An immunohistochemical study

Forty-five examples of epithelial odontogenic lesions (9 ameloblastomas (AB): 13 odontogenic keratocysts (OKC): 15 dentigerous cysts (DC): 6 radicular cysts (RC): and 2 odontogenic carcinomas (OC)) were immunohistochemically analyzed for the presence of p53 protein (p53P) and proliferative activity as indicated by positivity for Ki-67 antigen. p53P⁺ cells, detected as dense and/or faint nuclear staining, were found in 42 of the 45 odontogenic lesions examined. Dense p53P reactivity was most commonly detected in OKC, AB and OC, with other lesions generally exhibiting only weak nuclear reactivity. Numbers of Ki-67 positive cells as well as p53P⁺ cells were scored semiquantitatively. Although the presence/absence of densely stained p53P⁺ cells was broadly related to Ki-67⁺ cell numbers, there were no differences in p53P⁺ cell numbers between lesions exhibiting differences in proliferative activity. These results suggest that overexpression of p53P, rather than increased numbers of p53P⁺ cells, is related to proliferation in odontogenic epithelial lesions.     

Ghost cell characterization in calcifying odontogenic cysts and dentinogenic ghost cell tumors: An immunohistochemical study

ObjectivesThe aim of our study was to ascertain the true nature of ghost cells (GCs) by immunolocalization of cytokeratin (CK) 6, CK19, and amelogenin in calcifying odontogenic cysts (COCs) and dentinogenic ghost cell tumors (DGCTs) in an attempt to determine the nature of this unique cell.MethodsA total of thirteen cases (six COCs and seven DGCTs) were examined immunohistochemically, in order to compare immunoreactivity for CK6, CK19, and amelogenin in odontogenic GCs.ResultsPositive expression of amelogenin (92.3%) and CK6 (77%) was chiefly found in GCs. CK19 expression was observed in the cytoplasm of odontogenic epithelial cells of the lining epithelium. GCs were devoid of CK19 expression and were positive only on the cytoplasmic periphery.ConclusionIn the current study, GCs showed accumulation of amelogenin and hard keratins in their cytoplasm during pathological transformation.     

Immunostaining of involucrin in odontogenic epithelial tumors and cysts

An immunoperoxidase method was used to detect involucrin in 47 odontogenic tumors and 35 radicular cysts. Of a total of 40 ameloblastomas, 9 cases were positive for involucrin expression and those positive cases exhibited acanthomatous or follicular patterns. Squamous odontogenic tumors were strongly positive for involucrin, whereas adenomatoid odontogenic tumors gave a negative staining reaction. Involucrin expression in odontogenic tumors was divided into three categories: single cell positive, focally positive, and squamous metaplastic cell positive. Radicular cysts showed a very irregular distribution of involucrin; nonstratified epithelium was generally negative or showed only trace staining for involucrin, whereas suprabasilar stratified squamous epithelial cells were strongly positive. Cells positive for involucrin in odontogenic tumors and in cystic epithelium are probably direct signs of epithelial differentiation; such cells were squamoid in appearance.     

An ultrastructural study of the calcifications in calcifying odontogenic cysts and odontomas.

The calcifications associated with the epithelium of the calcifying odontogenic cyst and odontoma were studied ultrastructurally and found to be of three types: (1) spherical calcifications which form on ghost cells and which therefore are dystrophic, (2) spherical calcifications which appear to be dysplastic enamel, and (3) irregularly shaped, diffuse calcifications which form on a collagenous matrix and appear to by dysplastic dentin or cementum.     

Differential expression of Cyclin D1 in keratin-producing odontogenic cysts

Objetives: The aim of the present study was to analyze the expression levels of Cyclin D1 (CCD1), a nuclear protein that plays a crucial role in cell cycle progression, in a series of keratin-producing odontogenic cysts. Study Design: A total of 58 keratin-producing odontogenic cysts, diagnosed over ten years and classified according to the WHO 2005 criteria, were immunohistochemically analyzed in terms of CCD1 expression, which was quantified in the basal, suprabasal and intermediate/superficial epithelial compartments. The extent of immunostaining was measured as a proportion of total epithelial thickness. Quantified immunohistochemical data were correlated with clinicopathological features and clinical recurrence. Results: Keratin-producing odontogenic cysts were classified as 6 syndromic keratocystic odontogenic tumors (S-KCOT), 40 sporadic or non-syndromic KCOT (NS-KCOT) and 12 orthokeratinized odontogenic cysts (OOC). Immunohistochemically, CCD1 staining was evident predominantly in the parabasal region of all cystic lesions, but among-lesion differences were apparent, showing a clear expansion of parabasal compartment especially in the S-KCOT, followed to a lesser extent in the NS-KCOT, and being much more reduced in the OOC, which had the greatest average epithelial thickness. Conclusions: The differential expression of CCD1 noted in the present study suggests that dysregulation of cell cycle progression from G1 to the S phase contributes to the different aggressiveness of these lesions. However, CCD1 expression levels did not predict NS-KCOT recurrence, which is likely influenced by factors unrelated to lesion biology. Key words:Keratin-producing odontogenic cyst, keratocyst, keratocystic odontogenic tumor, nevoid basal cell carcinoma syndrome, orthokeratinized odontogenic cyst, cyclin D1, immunohistochemistry.     

Immunohistochemical study of bcl-2 protein, Ki-67 antigen and p53 protein in epithelium of glandular odontogenic cysts and dentigerous cysts

The aim of the present study was the evaluation of the immunohistochemical expression of the apoptosis-inhibiting protein bcl-2, the cell-cycle-related antigen Ki-67 and the p53 protein, which is involved both in cell cycle and apoptosis regulation, in the lining epithelium of glandular odontogenic cysts of the jaws. Formalin-fixed and paraffin-embedded tissue sections of three glandular odontogenic cysts and six dentigerous cysts were immunostained with a standard avidin-biotin peroxidase procedure, after microwave antigen retrieval. The glandular odontogenic cysts showed immunoreactivity for bcl-2 protein in the basal and suprabasal layers, while staining in dentigerous cysts was basal or focal. Most mucous cells and superficial cuboidal cells were negative. The percentage of Ki-67- or p53-positive cells was lower in glandular odontogenic cysts compared with dentigerous cysts. The findings suggest that the biological behavior of glandular odontogenic cysts may be associated with deregulation of cell death in the lining epithelium, while cell proliferation and p53 status do not seem to play a significant role.     

Proliferation of epithelial cell rests, formation of apical cysts, and regression of apical cysts after periapical wound healing

There is continuing controversy regarding the potential for inflammatory apical cysts to heal after nonsurgical endodontic therapy. Molecular cell biology may provide answers to a series of related questions. How are the epithelial cell rests of Malassez stimulated to proliferate? How are the apical cysts formed? How does the lining epithelium of apical cysts regress after endodontic therapy? Epithelial cell rests are induced to divide and proliferate by inflammatory mediators, proinflammatory cytokines, and growth factors released from host cells during periradicular inflammation. Quiescent epithelial cell rests can behave like restricted-potential stem cells if stimulated to proliferate. Formation of apical cysts is most likely caused by the merging of proliferating epithelial strands from all directions to form a three-dimensional ball mass. After endodontic therapy, epithelial cells in epithelial strands of periapical granulomas and the lining epithelium of apical cysts may stop proliferating because of a reduction in inflammatory mediators, proinflammatory cytokines, and growth factors. Epithelial cells will also regress because of activation of apoptosis or programmed cell death through deprivation of survival factors or by receiving death signals during periapical wound healing.     

Rheumatoid nodule in the oral mucosa. A case report with immunohistochemical study

A case of rheumatoid nodule in the buccal mucosa is reported. Histologically, 3 of zones characteristic rheumatoid nodules were recognized: a central necrotic area, an intermediate zone with palisading mesenchymal cells and an outer layer composed of chronic inflammatory cells. By immunohistochemical studies, ferritin was found in some of the cells in the intermediate zone, suggesting that these cells may be of histiocytic origin. Granuloma annulare and necrobiosis lipoidica may be differential diagnoses.     

Rheumatoid nodule in the oral mucosa. A case report with immunohistochemical study

Skov, BG. Rheumatoid nodule in the oral mucosa. J Oral Pathol 1987: 16: 403–405.
A case of rheumatoid nodule in the buccal mucosa is reported. Histologically, 3 of zones characteristic rheumatoid nodules were recognized: a central necrotic area, an intermediate zone with palisading mesenchymal cells and an outer layer composed of chronic inflammatory cells. By immunohistochemical studies, ferritin was found in some of the cells in the intermediate zone, suggesting that these cells may be of histiocytic origin. Granuloma annulare and necrobiosis lipoidica may be differential diagnoses.     

Histoenzymological features of epithelial cells in lesions of oral mucosa in cysts and ameloblastomas of jaws

A histoenzymological study was carried out on 41 tissue specimens removed at biopsy and for surgical operations of the following lesions: benign hyperkeratosis, lichen planus, severe epithelial dysplasia, carcinoma in situ, epidermoid carcinoma, radicular cyst, odontogenic keratocyst and ameloblastoma. The purpose of this study was to study some possibly significant variations in levels of activities of oxidative enzymes, diaphorases, acid phosphatases and Naphthol esterases in such lesions (normal oral mucosa and epidermis serving as controls). In the lesions of the oral mucosa, these histoenzymological variations were not sufficiently characteristic to contribute to histological diagnosis. In lichen planus, some vacuolated or necrotic basal cells lacked enzyme activities, whereas in the upper layers, enzyme activities were irregularly present. Benign hyperkeratosis showed enzymatic activities similar to those of the normal epidermis, namely high oxidative activities particularly prominent in basal cells and in granular layer, and esterase activity beneath the keratinized layer. In severe epithelial dysplasia, carcinoma in situ and epidermoid carcinoma, numerous variations of activities of oxidative enzymes, esterases and acid phosphatase were seen from one cell to the other. In cystic diseases of jaws, enzymatic activities were equally nonspecific in the epithelial lining of the radicular cyst and the odontogenic keratocyst (activities similar to those of normal oral epithelium and epidermis, respectively). But in common ameloblastoma, there was diffuse uniformly low oxidative enzymatic activities in the epithelium and high widespread activity of alkaline phosphatase in the stroma. The latter may be useful in differentiating the cystic acanthomatous variety of ameloblastoma from odontogenic keratocysts of the jaws.     

Involucrin expression in epithelial tumors of oral and pharyngeal mucosa and skin

Involucrin has been recognized recently as a marker of terminal differentiation of squamous epithelial cells and also as a useful marker for keratinization; its expression in epithelial tumors of oral and pharyngeal mucosa and skin was examined. Involucrin in normal oral mucosa and skin was restricted to the granular and upper spinous layers and was absent in the basal layer. Hyperkeratosis was characterized by strong positive staining for involucrum in spinous and granular cell layers. A similar pattern was noted in seborrheic keratosis and verruca vulgaris. Condyloma acuminatum specimens revealed slight staining, whereas Paget cells were negative. Calcifying epitheliomas of Malherbe were usually unreactive. Papillomas exhibited the regular distribution of involucrin, as found in normal squamous epithelium. Basal cell carcinomas were generally negative, whereas squamous cell carcinomas showed an irregular distribution of involucrin. Immunohistochemical staining for involucrin may be useful for identification of keratinizing cells in epithelial tumor foci, just as is the use of monoclonal antibody to keratin KL1.     

Hyalin material bounding dystrophic calcification in the epithelial lining of odontogenic cysts.

Areas of dystrophic calcification present in the epithelial lining of two apical periodontal cysts have been shown to exhibit an outer layer of hyalin material. Similar calcific areas in the connective tissue walls do not show hyalin boundaries. Hyalin material has been found around muscle fibers present in the epithelial lining of a residual dental cyst. It is believed that the hyalin material is secreted by the epithelial cells and these observations are considered to be supporting evidence that hyalin bodied arise as an epithelial secretion.