ABSTRACT
CONTEXT: Langerhans cells (LCs) are effective antigen-presenting cells that function as "custodians" of mucosa, modifying the immune system to pathogen entry, and tolerance to self-antigen and commensal microbes. A reduction in number of LCs in human immunodeficiency virus (HIV)-positive individuals may predispose to local mucosal infections. AIMS: To quantitatively determine the number of oral mucosal LCs in HIV/acquired immunodeficiency syndrome HIV/acquired immunodeficiency syndrome (AIDS) associated oral Kaposi sarcoma (KS) with/without oral candidiasis (OC) and to define in situ interrelationships between the cells, OC, and HIV infection. MATERIALS AND METHODS: Thirty-two periodic acid-Schiff. (PAS) stained histologic sections of palatal HIV/AIDS associated KS with intact oral epithelium were examined for Candida and divided into two groups: . (1) KS coinfected with Candida and. (2) KS noninfected with Candida. Sections were immunohistochemically stained with CD1a. The standard length of surface epithelium was measured and number of positively stained LCs counted per unit length. Control cases included non-Candida infected palatal mucosa overlying pleomorphic adenoma. (PA) and oral mucosa infected with Candida in otherwise healthy individuals. RESULTS: LC number per unit length of surface epithelium was statistically significantly greatest in uninfected PA mucosa and lowest in KS coinfected with Candida (P = 0.0001). A statistically significant difference was also noted between uninfected PA mucosa and non-Candida infected KS (P = 0.0014), in KS coinfected with Candida and non-infected KS (P = 0.0035), between OC and PA (P = 0.0001), and OC and KS coinfected with Candida (P = 0.0247). CONCLUSION: LC numbers are significantly reduced in oral tissues of HIV/AIDS infected patients by Candida infection when compared to oral tissues without.
Subject(s)
Candidiasis, Oral/etiology , HIV Infections/complications , Langerhans Cells/cytology , Mouth Mucosa/cytology , Mouth Neoplasms/etiology , Sarcoma, Kaposi/etiology , Adolescent , Adult , Aged , Aged, 80 and over , Antigen-Presenting Cells/cytology , Antigen-Presenting Cells/immunology , Candidiasis, Oral/diagnosis , Cell Count , Child , Child, Preschool , Female , HIV Infections/immunology , HIV Infections/virology , Humans , Langerhans Cells/immunology , Male , Middle Aged , Mouth Mucosa/immunology , Mouth Mucosa/microbiology , Mouth Mucosa/pathology , Mouth Neoplasms/pathology , Sarcoma, Kaposi/pathology , Young AdultABSTRACT
BACKGROUND: Adenomatoid odontogenic tumour (AOT) is a benign odontogenic jaw lesion. The aim of this study was to update the biological profile of AOT. MATERIAL AND METHODS: Cases published in the literature and cases in files of co-authors were included. RESULTS: 550 new cases were retrieved, and of a total of 1082 cases analysed, 87.2% were found in the second and third decades. The M:F ratio was 1:1.9. 70.8% were of the follicular variant (extrafollicular: 26.9%, peripheral: 2.3%). 64.3% occurred in the maxilla. 60% of follicular AOTs were associated with unerupted canines. Nineteen cases of AOT (2.8%, M:F ratio was 1:1.4) were associated with embedded third molars. Twenty-two peripheral AOTs (2.3%, M:F ratio was 1:5.3) were recorded. The relative frequency (RF) of AOT ranged between 0.6% and 38.5%, revealing a considerably wider AOT/RF range than hitherto reported (2.2-7.1%). CONCLUSIONS: This updated review based on the largest number of AOT cases ever presented, confirms the distinctive, although not pathognomonic clinicopathological profile of the AOT, its worldwide occurrence, and its consistently benign behaviour.
Subject(s)
Jaw Neoplasms/epidemiology , Odontogenic Tumors/epidemiology , Adolescent , Adult , Age Factors , Americas/epidemiology , Asia/epidemiology , Child , Cuspid/pathology , Female , Humans , Incidence , Male , Mandibular Neoplasms/epidemiology , Maxillary Neoplasms/epidemiology , Molar, Third/pathology , Retrospective Studies , Sex Factors , Tooth, Impacted/epidemiology , Tooth, Unerupted/epidemiologyABSTRACT
The follicular variant of the adenomatoid odontogenic tumor (AOT) is thought to originate from the reduced enamel epithelium of the dental follicle. The origin of the extra-follicular variant however, remains less clear. This paper presents a case of an extra-follicular AOT, which we believe originated from the epithelial lining of a unicystic ameloblastoma, and reviews the literature. The available evidence seems to indicate that some extra-follicular AOTs might arise as secondary phenomena within pre-existing odontogenic cysts or cystic tumors.
