Characterization of initial/early histologic features of proliferative leukoplakia and correlation with malignant transformation: a multicenter study.

The aim of this multicenter retrospective study is to characterize the histopathologic features of initial/early biopsies of proliferative leukoplakia (PL; also known as proliferative verrucous leukoplakia), and to analyze the correlation between histopathologic features and malignant transformation (MT). Patients with a clinical diagnosis of PL who have at least one biopsy and one follow-up visit were included in this study. Initial/early biopsy specimens were reviewed. The biopsies were evaluated for the presence of squamous cell carcinoma (SCCa), oral epithelial dysplasia (OED), and atypical verrucous hyperplasia (AVH). Cases that lacked unequivocal features of dysplasia were termed "hyperkeratosis/parakeratosis not reactive (HkNR)". Pearson chi-square test and Wilcoxon test were used for statistical analysis. There were 86 early/initial biopsies from 59 patients; 74.6% were females. Most of the cases had a smooth/homogenous (34.8%) or fissured appearance (32.6%), and only 13.0% had a verrucous appearance. The most common biopsy site was the gingiva/alveolar mucosa (40.8%) and buccal mucosa (25.0%). The most common histologic diagnosis was OED (53.5%) followed by HkNR (31.4%). Of note, two-thirds of HkNR cases showed only hyperkeratosis and epithelial atrophy. A lymphocytic band was seen in 34.8% of OED cases and 29.6% of HkNR cases, mostly associated with epithelial atrophy. Twenty-eight patients (47.5%) developed carcinoma and 28.9% of early/initial biopsy sites underwent MT. The mortality rate was 11.9%. Our findings show that one-third of cases of PL do not show OED with most exhibiting hyperkeratosis and epithelial atrophy, but MT nevertheless occurred at such sites in 3.7% of cases.

Neuronal-immune axis alters pain and sensory afferent damage during dental pulp injury.

ABSTRACT: Dental pulp tissue is densely innervated by afferent fibers of the trigeminal ganglion. When bacteria cause dental decay near the pulpal tissue, a strong neuronal and immune response occurs, creating pulpitis, which is associated with severe pain and pulp tissue damage. Neuroimmune interactions have the potential to modulate both the pain and pathological outcome of pulpitis. We first investigated the role of the neuropeptide calcitonin gene-related peptide (CGRP), released from peptidergic sensory afferents, in dental pain and immune responses by using Calca knockout (Calca -/- ) and wild-type (Calca +/+ ) mice, in a model of pulpitis by creating a mechanical exposure of the dental pulp horn. We found that the neuropeptide CGRP, facilitated the recruitment of myeloid cells into the pulp while also increasing spontaneous pain-like behavior 20% to 25% at an early time point. Moreover, when we depleted neutrophils and monocytes, we found that there was 20% to 30% more sensory afferent loss and increased presence of bacteria in deeper parts of the tissue, whereas there was a significant reduction in mechanical pain response scores compared with the control group at a later time point. Overall, we showed that there is a crosstalk between peptidergic neurons and neutrophils in the pulp, modulating the pain and inflammatory outcomes of the disease.

Gingival Leukoplakia: Hyperkeratosis with Epithelial Atrophy Is A Frequent Histopathologic Finding.

White lesions on the gingiva and palatal mucosa may represent reactive keratoses, including specific diseases such as benign alveolar ridge keratosis, or nonreactive keratoses, such as true leukoplakia, the latter being associated with a high recurrence rate at this site. The aim of this study is to determine the histopathologic features of gingival keratoses. Hyperkeratotic lesions from the gingiva, palatal mucosa, and alveolar ridge mucosa were available for evaluation after excluding specific keratotic lesions such as candidiasis. There were 321 biopsies from 296 patients and approximately half of the cases (159/321, 49.5%) were reactive keratoses. The rest of the 162 biopsies from 149 patients (76 females; 51.0%) represented true leukoaplakias. The most common location was the gingiva (73.2%) followed by the palatal mucosa (17.0%). Hyperkeratosis/parakeratosis not reactive (HkNR) represented 43.8% of cases; 45.7% were dysplasia or carcinoma, and the rest were not readily classifiable as reactive or non-reactive keratoses. Histopathologic features commonly noted in the HkNR lesions include sharp demarcation (72.7%), corrugated surface (53.5%), and epithelial atrophy (48.1%). A lymphocytic band was noted in 8.5% of the cases, mostly associated with epithelial atrophy (5/6 cases). Seven patients with 17 biopsies from noncontiguous sites likely had proliferative leukoplakia; the most common location was the gingiva (88.2%) and the most common diagnosis was HkNR (52.9%). HkNR is a common histopathologic diagnosis for leukoplakias on the gingiva, and these lesions frequently exhibit thick hyperkeratosis, epithelial atrophy and a lymphocytic band at the interface.

Calcifying synovial sarcoma of the tongue with SS18 rearrangement: a rare variant in a rare location.

Synovial sarcoma is a soft tissue malignancy harboring t(X;18) resulting in fusion of two genes SS8 (at 18q11) and SSX (1, 2 or 4 at Xp11) forming the gene fusion product SS18-SSX. It affects adults in their 3rd-4th decades, most frequently in the para-articular regions of the extremities. Less than 10% of the cases occur within the head and neck region and of these, 60% occur in the neck and only 10% occur in the oral cavity. We report a synovial sarcoma of the tongue in a 14-year-old female patient with unusual histology. The patient presented with a mass occupying most of the tongue with extension into the floor of mouth and the lingual gingiva of the anterior mandibular teeth. The tumor was composed of a highly cellular proliferation of spindle cells in a herringbone pattern with many small vessels but without glandular structures, and with extensive calcifications throughout the tumor. Tumor cells were positive for epithelial membrane antigen and transducin-like enhancer of split-1, and fluorescence in situ hybridization studies identified SS18 gene rearrangement. The patient was managed with two debulking procedures followed by chemoradiation and is currently alive with disease.

Comparative analysis of prevalence of apical periodontitis in smokers and non-smokers using cone-beam computed tomography.

OBJECTIVE: The aim of this study was to compare the prevalence and size of periapical lesions among smokers and non-smokers using cone-beam computed tomography (CBCT). MATERIALS AND METHODS: Retrievable CBCT datasets for 46 male patients ≥18 years during a consecutive period from 2008 to 2016 were examined. The medical, smoking history and other clinical findings (signs of previous dental trauma; Decayed Missing Filled Teeth (DMFT) scores; the percentage of root filled teeth; and oral hygiene status) were obtained. Periapical status of all included teeth was assessed by CBCT images. Statistical analysis was conducted using t-test, Pearson correlation and multiple regression. RESULTS: The prevalence of apical periodontitis was 13.93% in smokers and 14.26% in non-smokers with no significant difference (p = 0.936). The mean of the average size of lesions between the two groups were almost comparable, 3.50 mm in smokers and 2.89 mm in non-smokers (p = 0.567). Pearson correlation and multiple regression analysis showed that the percentage of lesion present and the average lesion size were not correlated to any independent variable. CONCLUSIONS: While smoking is considered a risk factor for marginal periodontitis, there was no difference between smokers and non-smokers in terms of apical periodontitis.