Oral manifestations in patients with gastro-oesophageal reflux disease: a single-center case–control study

Objective:  To assess the occurrence of oral pathological changes and symptoms in patients affected by gastro-oesophageal reflux disease (GERD).
Patients and methods:  200 patients with GERD and 100 matched healthy controls were studied. Thorough visual examination of the dental and oral mucosal tissues was performed and medical history relevant to oral symptoms was collected. The primary outcome was defined as a statistically significant difference, between the study group and controls, in the presence of the following indicators: soft/hard palate and uvula erythema, tooth wear, xerostomia, oral acid/burning sensation, subjective halitosis and dental sensitivity. Statistical analysis included chi-squared test, and crude odds ratio with 95% CI.
Results:  Univariate analysis showed that xerostomia, oral acid/burning sensation, subjective halitosis, and soft and hard palate mucosa and uvula erythema were more common in patients with GERD than matched controls ( P  < 0.05).
Conclusions:  This study failed to find any significant association between GERD and dental erosions, whereas some symptoms and other objective oral mucosal changes were found to be significantly associated with GERD.     

Physiotherapeutic treatment improves oral opening in oral submucous fibrosis

Background:  In oral submucous fibrosis (OSF) fibrous bands and burning mucosal pain restrict oral opening to limit speech and eating. The pathogenesis of OSF remains unclear, while surgical and pharmacological treatments have limited success, and are often inaccessible in communities using areca nut where OSF is prevalent. Improved outcomes are reported for surgical treatment when followed by physiotherapy. We tested the hypothesis that physiotherapy alone can modify tissue remodelling in OSF to increase oral opening.
Materials and methods:  Fifty-four Nepali OSF patients were managed for 4 months in three randomly assigned groups receiving either: five times daily physiotherapy by inter-positioning tongue spatulas between teeth and adding a new spatula every 5–10 days; local injection of hyaluronidase with steroids; or no active treatment.
Results:  More males presented with OSF than females ( p  < 0.05). All patients reported reduced opening and 47% had mucosal pain. Progressive mucosal involvement was always in the same order, starting with the soft palate, and then progressing to the fauces, unilateral buccal mucosa, bilateral buccal mucosa, floor of mouth and finally lip mucosa ( p  < 0.006). Physiotherapy improved oral opening ( p  < 0.0005), but not oral pain, while no clear improvement was seen in untreated patients as well as patients managed by injection.
Conclusions:  We conclude OSF in the Nepali population progresses in a predictable pattern, and that physiotherapy is effective for increasing the oral opening. We further suggest physiotherapy can be readily used to improve OSF in communities with otherwise limited health resources.     

Helicobacter pylori in the oral cavity is associated with gastroesophageal disease

Background:  In Mexico, more than 80% of the population is infected with Helicobacter pylori . The frequency of H. pylori detection in the oral cavity is unknown, as its relationship with gastroesophageal pathology.
Aim:  To detect the presence of H. pylori in the oral cavity in Mexican population by PCR and to determine its association with gastroesophageal disease.
Methods:  Patients were divided into two groups with different clinic conditions from whom gastric biopsy, dental plaque, and saliva samples were taken and analyzed. The first group comprised of hospitalized patients, the majority of whom were diagnosed with gastroesophageal disease, while the second group was selected from a dental clinic (ambulatory population) the majority of whom appeared to be healthy subjects.
Results:  H. pylori was detected in gastric biopsy, dental plaque and saliva samples by PCR using a set of specific primers for the signal sequence of the vacuolating cytotoxin gene; detection of H. pylori in general was higher in gastric biopsy and dental plaque samples than in saliva samples. Detection of H. pylori in the oral cavity is significantly ( P  = 0.0001) associated with patients presenting gastroesophageal disease, while healthy subjects and those with other non-gastric disease do not present with H. pylori in their oral cavity.
Conclusions:  H. pylori detection in the oral cavity is associated to gastroesophageal disease. In addition, it is suggested that all patients presenting gastric symptoms and H. pylori detection in the oral cavity would begin bacterial treatment immediately.     

In vitro and in vivo cytokeratin patterns of expression in bioengineered human periodontal mucosa

Background and Objective:  Development of human oral mucosa substitutes by tissue engineering may provide new therapeutic tools for the management of periodontal diseases. In this study we evaluated a fibrin–agarose human oral mucosa substitute both in vitro and in vivo .
Material and Methods:  In vitro bioengineered oral mucosa substitutes were developed from irrelevant biopsy samples of human oral gingiva. In vivo evaluation of the constructed tissues was performed by implantation into athymic nude mice. The expression of several epithelial markers was assessed by microarray analysis and immunohistochemistry.
Results:  Bioengineered oral mucosa samples kept in vitro developed a multilayered epithelium that expressed several cytokeratins, including some markers of simple epithelia (cytokeratins 7, 8 and 18), along with markers of stratified epithelia (cytokeratins 5 and 13) and of cell proliferation (proliferating cell nuclear antigen). Bioengineered tissues grafted in vivo onto nude mice exhibited very good biointegration with the host, showing a cytokeratin expression pattern that was very similar to that of normal native oral mucosa controls. Histological analysis of the artificial tissues demonstrated that oral mucosa substitutes evaluated in vivo were structurally mature, showing some typical structures of human native oral mucosa such as rete ridges and chorial papillae, along with numerous blood vessels at the fibrin–agarose stromal substitute. These structures were absent in samples evaluated in vitro .
Conclusion:  The results indicate that this model of human oral mucosa, constructed using fibrin–agarose scaffolds, shows similarities to native oral mucosa controls and imply that bioengineered oral mucosa substitutes could eventually be used clinically.     

Non-surgical periodontal treatment of cyclosporin A-induced gingival overgrowth: immunohistochemical results

Aim:  The present study was planned to analyze the effects of a 12-month non-surgical periodontal treatment on histologic and immunohistochemical features of cyclosporin A (CsA)-induced gingival overgrowth (GO).
Materials and methods:  Gingival samples were collected from 21 liver transplant subjects exhibiting CsA-induced GO prior to, and 12 months after non-surgical periodontal therapy including oral hygiene instructions, scaling and 2-month recall appointments, and also from 18 healthy control subjects. Gingival biopsy specimens were stained with hematoxylin–eosin and monoclonal antibodies for vimentin, CD3 (T-lymphocytes), CD20 (B-lymphocytes), CD34 (endothelium) and Ki-67 (fibroblasts proliferation rate), using a streptavidin-biotin-peroxidase complex method.
Results:  Total inflammatory cells, gingival vessels and fibroblast proliferation rate demonstrated significant reduction after non-surgical periodontal treatment ( P  < 0.0001) in overgrown gingiva, while B- and T-lymphocytes remained nearly unchanged ( P  = 0.61 and 0.33, respectively). At the 12-month evaluation no significant differences were found when comparing the gingival biopsies from CsA-treated patients and those from healthy controls ( P  > 0.05).
Conclusions:  Control of clinical inflammation by means of non-surgical periodontal treatment results both in lowering of inflammatory infiltrate and in changes in connective tissue composition. Thus, plaque-induced inflammation would seem to modulate the drug-gingival tissue interaction.
Clinical relevance:  A strict plaque control program play a pivotal role in the management of transplant patients exhibiting cyclosporin A-GO.     

Quantitative analysis of Langerhans' cells in oral chronic graft-vs.-host disease

Background:  The Langerhans cells (LCs) are scattered throughout the epithelium of skin and mucosa and have been associated with the graft-vs.-host disease (GVHD), which is the highest cause of morbidity and mortality in patients who underwent bone marrow transplant (BMT). This study aims at quantifying the LCs in the oral chronic GVHD (cGVHD).
Methods:  Microscopic sections from biopsies carried out in the buccal mucosa of 40 patients who underwent allogenic BMT and developed (20) or not (20) oral cGVHD (Groups 1 and 2, respectively) were utilised. For the control group, free surgical margins of 20 biopsies of non-inflammatory lesions in the buccal mucosa (Group 3) were used. The sections were studied in routine colouration and immunostained for CD1a.
Results:  Group 1 (with cGVHD) presented a greater number of Langerhans' cells/mm² (50.6 ± 37.2) when compared with the other groups (Group 2, 23.11 ± 19.7; Group 3, 16.6 ± 17.3).
Conclusion:  Our results suggest a greater recruitment of LCs in patients transplanted with cGVHD, probably as a result of cytokines secreted by the inflammatory cells.     

Progressive increase of human papillomavirus carriage rates in potentially malignant and malignant oral disorders with increasing malignant potential

Introduction:  We investigated the potential role of human papillomaviruses (HPVs) in potentially malignant oral disorders, oral leukoplakia (OL) and oral lichen planus (OLP), and in oral squamous cell cancer (OSCC) in an Eastern Hungarian population with a high incidence of OSCC.
Methods:  Excised tumor samples (65 OSCC patients) and exfoliated cells from potentially malignant lesions (from 44 and 119 patients with OL and OLP, respectively) as well as from healthy controls (72 individuals) were analysed. OLPs were classified based on clinical appearance, 61 patients had erosive–atrophic lesions (associated with higher malignancy risk, EA-OLP) and 58 had non-erosive non-atrophic lesions (with lower risk of becoming malignant, non-EA-OLP), respectively. Exfoliated cells collected from apparently healthy mucosa accompanied each lesion sample. HPV was detected by MY/GP polymerase chain reaction (PCR) and genotyped by restriction analysis of amplimers. Copy numbers in lesions were determined using real-time PCR. Prevalence rates, copy number distributions, and association with risk factors and diseases were analysed using chi-square test, t -test, and logistic regression, respectively.
Results:  We detected HPVs significantly more frequently in lesions than in controls ( P  ≤ 0.001 in all comparisons). HPV prevalence increased gradually with increasing severity of lesions (32.8, 40.9, and 47.7% in OLP, OL, and OSCC, respectively). Copy number distribution patterns roughly corresponded to prevalence rates, but OLP and OL were comparable. HPV prevalence differed significantly between EA-OLP and non-EA-OLP groups (42.6 vs. 22.4%); EA-OLP group showed a prevalence similar to that found in OL.
Conclusion:  HPVs may be involved in the development or progression of not only OSCC but also of potentially malignant oral lesions.     

Longitudinal study of TP53 mutations in eight patients with potentially malignant oral mucosal disorders

Objectives:  In a previous cross-sectional study, the authors found a higher rate of TP53 mutation in oral lichen planus (OLP) than in hyperkeratosis. By analysing for TP53 mutations in serial samples from patients on long-term follow-up of their oral lesions, it was hoped to determine if these mutations were related to disease progression.
Methods:  Eight patients presenting with lesions diagnosed clinically as oral leukoplakia or lichen planus were followed from 2 to 12 years. Two to five samples of archival biopsy tissue were analysed from each patient by constant denaturant gradient gel electrophoresis for hotspots A, B, C, D and exon 6.
Results:  Four patients were diagnosed clinically as OLP: two of these were confirmed histopathologically, one was diagnosed as non-specific hyperkeratosis and one as cancer. Four patients had leukoplakia only, with a histopathological diagnosis of hyperkeratosis. Seven patients had TP53 mutations, three of them on repeated occasions. All five patients who developed squamous-cell carcinoma had mutations. Two of them had mutated pre-malignant lesions, and one of these previously had a non-mutated cancer. Three patients had two different primary cancers, only one of them mutated. One patient developed a mutated cancer 5 years after the last mutation-free biopsy. Of the cancer-free patients, a lesion regarded clinically as cancer-suspicious in one case was mutated, in another patient two OLP lesions were mutated, the third had five biopsies taken during 8 years, all non-mutated.
Conclusions:  TP53 mutations may occur early or late in the development of oral squamous-cell carcinoma.     

Immune-expression of HSP27 and IL-10 in recurrent aphthous ulceration

Background:  Recently, abnormal cellular immune response has been considered responsible for the oral lesion in the recurrent aphthous ulceration (RAU). For reasons not yet defined, antigens of the oral microbiota would trigger abnormal Th1 immune response against epithelial cells. On the other hand, studies have demonstrated that heat shock proteins (HSP) can block the production of proinflammatory cytokine through inhibition of NF-κB and mitogen-activated protein kinase pathways or activate anti-inflammatory cytokines and therefore control the magnitude of the immune response. HSP27 has been considered a powerful inductor of IL-10, a major inhibitor of Th1 response.
Methods:  Using immunohistochemistry, we studied the expression and location of HSP27 and IL-10 in ulcerated lesions clinically diagnosed as RAU ( n  = 27) and to compare it with that of oral clinically normal mucosa (CT; n  = 6) and of other inflammatory chronic diseases such as oral fibrous inflammatory hyperplasia (FIH; n  = 18), Crohn's disease (CD; n  = 10) and ulcerative colitis (UC; n  = 9).
Results:  A lower proportion of HSP27-positive epithelial cells in RAU and CD were observed when compared with CT and FIH ( P  < 0.001**; P  = 0.013**). A lower proportion of IL-10-positive interstitial cells in RAU was observed when compared with FIH, UC, CT and CD ( P  < 0.001**; P  < 0.001**; P  < 0.001**; P  = 0.034*).
Conclusion:  Altogether the data suggest that a reduced cellular expression of HSP27 and IL-10 in RAU might be related with the aetiopathogenesis of the ulcerated oral lesions.     

Oral ulcers in HIV-positive Peruvian patients: an immunohistochemical and in situ hybridization study

Background:  This study describes the histopathological, immunohistochemical (IHC) and in situ hybridization (ISH) data of 25 cases of oral ulcers in HIV-positive patients, with clinical and microscopical features similar to ulcers not otherwise specified (NOS)/necrotizing ulcerative stomatitis (NUS).
Methods:  Sex, age and clinical history were obtained from the clinical records. Histological analysis for H&E, Gomori–Grocott and Ziehl–Neelsen stains, IHC analysis to detect infectious agents and to characterize inflammatory cellular infiltrate, and ISH for cytomegalovirus (CMV) and EBER1/2 were performed.
Results:  Twenty-one patients were men and four were women (mean age of 34.6 years). The tongue was preferentially affected. Microscopically, the lesions showed extensive necrosis, leukocytoclasia, vasculitis with luminal fibrin clots and an intense inflammatory cellular infiltrate predominated by CD68⁺ atypical large cells, normal-sized and crescent-shaped nuclei macrophages, interspersed by CD8⁺ T lymphocytes. Mast cells were also observed in all samples studied. CD4⁺ T lymphocytes, CD20⁺ B lymphocytes and VS38c⁺ plasma cells were practically absent. CMV and EBER1/2 were identified in scarce cells of 3 and 16 of 25 cases respectively.
Conclusion:  These results show that CD68⁺ macrophages, followed by CD8⁺ T lymphocytes, were the predominant inflammatory cells, indicating they are relevant to the pathogenesis of the ulcers, possibly reflecting an abnormal immune response in the oral mucosa. The clinicopathological and immunoprofile features of the present cases are similar to NOS ulcers/NUS in HIV-positive patients.     

Role of TP53 in the progression of pre-malignant and malignant oral mucosal lesions. A follow-up study of 144 patients

Background:  Prediction of progression from pre-malignant oral mucosal lesions to malignancy, or recurrence of an existing oral squamous cell carcinoma (OSCC), is an important clinical problem in oral medicine.
Methods:  This study presents a follow-up of a study published in 2002. Samples from 54 patients with OSCC, 45 with oral lichen planus (OLP) and 45 with hyperkeratosis (clinically leukoplakia), diagnosed between 1987 and 1996, were analysed for TP53 protein expression and TP53 mutation. Follow-up was 11–17 years for OSCC (mean 13.3), 12–22 years for OLP (mean 15.9) and 12–17 years for hyperkeratosis (mean 14.5).
Results:  Of the 54 OSCC patients, 28 experienced recurrent disease, 21 died of OSCC, 22 died of other causes. Of the 14 OSCC patients with mutated TP53 ( n  = 11), the cancer recurred in eight (57%) and in 20/39 (51%) without mutation. Expression of TP53 protein was significantly associated with reduced overall survival. Among OLP patients, nine were TP53- mutated out of 31 tested. One TP53- mutated OLP patient developed OSCC in a different site. Of the hyperkeratosis patients, three were mutated of 22 tested. One hyperkeratosis patient (non-mutated) developed OSCC in the same site.
Conclusion:  TP53 mutations can exist in benign oral mucosal lesions for many years without progression to malignancy. No association was found between TP53 protein expression or TP53 mutation and recurrence of OSCC or disease-related survival. Overall survival was reduced in patients with positive TP53 protein expression.     

Serum soluble CD44v6 levels in patients with oral and maxillofacial malignancy

Objective:  To determine the levels of serum sCD44v6 in patients with oral cancer and evaluate the value of serum sCD44v6 in adjuvant diagnosis, staging and monitoring treatment response in these patients.
Materials and Methods:  A total of 112 hospitalized patients with oral and maxillofacial malignancy and 28 healthy individuals were examined for serum sCD44v6 levels. Venous blood was collected from these patients and the healthy individuals. One week after treatment, venous blood was collected once again in 60 patients with oral and maxillofacial squamous cell carcinoma (OSCC).
Results:  The sCD44v6 concentration was not significantly different between patients with oral and maxillofacial malignancy and control group ( P  > 0.05). The levels of serum sCD44v6 in patients with OSCC and salivary carcinoma showed no difference with those in control group ( P  > 0.05). The sCD44v6 level in patients with stage III and IV disease was higher than that of patients with stage I and II and that of the control group, but the difference was not significant ( P  > 0.05).  Serum sCD44v6 levels in patients with OSCC after treatment became lower than that prevailed during pretreatment ( P  < 0.05).
Conclusion:  The possible roles of CD44v6 in the diagnosis of oral and maxillofacial malignancy deserve further elucidation and evaluation. Serum sCD44v6 may be a valuable marker in monitoring treatment response in patients with OSCC.     

Estimation of serum leptin in oral squamous cell carcinoma

J Oral Pathol Med (2010) 39 : 69–73
Background:  Cachexia contributes significantly to mortality in cancer patients; role of cytokines in inducing cachexia is an emerging view. Leptin, a homologous protein of cytokine family, is found to be decreased in serum with cachexia. The purpose of this study was to compare serum leptin levels of oral squamous cell carcinoma patients with that of control group and correlate it with body mass index.
Method:  Serum samples of 31 oral squamous cell carcinoma patients and that of 28 healthy individuals were subjected to evaluation of serum leptin levels (ng/ml) using enzyme-linked immunosorbent assay.
Results:  A significant reduction in leptin level of oral squamous cell carcinoma patients was observed. Definite correlation between body mass index and serum leptin and also between serum leptin levels of various histopathological variants of oral squamous cell carcinoma was observed.
Conclusion:  The results of this study suggest that evaluation of serum leptin level can provide status of cachexia in oral squamous cell carcinoma patients.     

Five-year evaluation of the influence of keratinized mucosa on peri-implant soft-tissue health and stability around implants supporting full-arch mandibular fixed prostheses

Background: The question of the importance of keratinized mucosa around dental implants for the prevention of peri-implant disease could not be answered in the relevant literature so far.
Objective: To investigate the influence of peri-implant keratinized mucosa on long-term peri-implant soft-tissue health and stability over a period of 5 years.
Material and methods: A total of 386 mandibular dental implants were placed in 73 completely edentulous patients, and subsequently restored with fixed full-arch prostheses. At prosthesis delivery (baseline) and after 3, 6, 12, 18, 24, 36, 48 and 60 months, modified plaque index (mPlI), modified sulcus bleeding index (mBI), distance between implant shoulder and mucosal margin (DIM) and width of peri-implant keratinized mucosa (KM) were recorded. Statistical analysis included multivariate logistic regression, multivariate ordinal logistic regression, generalized estimating equations and Bonferroni's correction.
Results: Fifty-eight patients with 307 implants completed the 5-year study. Statistically significantly higher plaque accumulation on lingual sites (mean mPlI 0.67, SD 0.85), bleeding tendencies on lingual sites (mean mBI 0.22, SD 0.53) and larger soft-tissue recession on buccal sites (mean DIM −0.69 mm, SD 1.11 mm) were found when the width of KM was <2 mm, compared to sites with≥2 mm of KM (mean mPlI 0.40, SD 0.68, P =0.001; mean mBI 0.13, SD 0.41, P <0.01; mean DIM −0.08 mm, SD 0.86 mm, P <0.001). The width of keratinized mucosa had no effect on bleeding tendency or plaque accumulation on buccal sites ( P >0.05).
Conclusion: In patients exercising good oral hygiene and receiving regular implant maintenance therapy, implants with a reduced width of <2 mm of peri-implant keratinized mucosa were more prone to lingual plaque accumulation and bleeding as well as buccal soft-tissue recession over a period of 5 years.     

Oral distribution of Candida species and presence of oral lesions in Brazilian leprosy patients under multidrug therapy

Objective:  The aim of this study was to evaluate the prevalence of Candida spp. and presence of oral lesions in Brazilian leprosy patients under multidrug therapy (MDT).
Methods:  Thirty-eight individuals (18 males and 20 females, median age 53 years) clinically and microbiologically diagnosed as leprosy (lepromatous variant), and under MDT for at least 45 days were studied. The control group constituted by 38 healthy individuals (median age 53.5), matched to the test group in relation to age, gender and oral conditions. Oral rinses were collected and the Candida identification was performed by phenotypic tests. The existence of Candida dubliniensis among the isolates was analyzed using a validated multiplex PCR assay. Twenty-nine leprosy patients were examined intra-orally for the presence of lesions. Data were analyzed by z- and Mann–Whitney tests (α = 5%).
Results:  Yeast carriage rate between leprosy patients (65.8%) and controls (47.4%) was similar ( P  = 0.099), and no significant difference between yeast counts was observed ( P  = 0.1004). Candida albicans was the most frequently isolated species in both groups. In the leprosy group, Candida tropicalis and Candida parapsilosis were also identified. In the control group, we additionally identified Candida tropicalis , Candida glabrata and Candida kefyr. Candida dubliniensis was not detected. No leprosy-related oral lesion was registered.
Conclusion:  Within the limits of the study, we concluded that Brazilian leprosy patients under MDT showed similar levels of carriage and Candida species distribution in relation to the controls.     

Graph models for phenotype and genotype association between oral mucosa and submandibular gland tumorigenesis in rat

Background:  In recent years, success of statistics in field of genetics has been the identification of genes that affect the process of disease. Experimental models using animals enable early stages of tumor development to be studied. The aim of this study was to apply graph models to assess the association between the observed phenotypic changes in rat oral mucosa and induced tumorigenesis in the submandibular gland (SMG).
Materials and methods:  We studied changes in oncogenes TP53 and bcl-2, histopathological and immunomarker variables in samples of oral mucosa and SMG of Wistar male rats, 60 days old and 180 g in weight, in which tumorigenesis was induced in their SMG by a 0.5% solution of 9,10-dimethyl-1,2-benzanthracene in acetone. A set of linear structural equations were defined, with each formula indicating the response variables and the direct influences. In graph models, saliva was considered as a latent variable. The association was analyzed using Graphical Gaussian Markov models and odd ratios.
Results:  About 40% of animals treated with 9, 10-dimethyl-1, 2-benzanthracene showed histological alterations in the epithelial basal strata of their oral mucosa only at 150 days. Statistical models indicated a relationship between gene alteration in gene bcl-2 in the SMG and histological changes observed in the oral mucosa ( P  = 0.04).
Conclusion:  Graph statistical model with one latent variable allows to conclude that these results associated with other clinical parameters may be useful in detecting early changes in SMG tumorigenesis. Furthermore, the design of randomized sampling of oral mucosa allows to validate these results and establish a reliable methodology for presumptive diagnosis or screening in the future.     

RNA from brush oral cytology to measure squamous cell carcinoma gene expression

Background:  RNA expression analysis of oral keratinocytes can be used to detect early stages of disease such as oral cancer or to monitor on-going treatment responses of the same or other oral diseases. A limitation is the inability to obtain high quality RNA from oral tissue without using biopsies. While oral cytology cell samples can be obtained from patients in a minimally invasive manner they have not been validated for quantitative analysis of RNA expression.
Methods:  As a starting point in the analysis of tumor markers in oral squamous cell carcinoma (OSCC), we examined RNA in brush cytology samples from hamsters treated with dibenzo[a,l]pyrene to induce oral carcinoma. Three separate samples from each animal were assessed for expression of candidate marker genes and control genes measured with real-time RT-PCR.
Results:  Brush oral cytology samples from normal mucosa were shown to consist almost exclusively of epithelial cells. Remarkably, ß-2 microglobulin and cytochrome p450, 1B1 (CYP1B1) RNA showed potential utility as markers of OSCC in samples obtained in this rapid and non-surgical manner.
Conclusion:  Brush oral cytology may prove useful as a source of RNA for gene expression analysis during the progression of diseases of the oral epithelium such as OSCC.     

Periodontal disease in mothers indicates risk in their children

Introduction.  It is well established that severe periodontitis clusters in families, but there are no data about the relationship between mothers with chronic periodontitis and their children's periodontal status.
Objective.  To evaluate a risk for periodontal diseases in children of periodontally diseased and healthy mothers.
Methods.  Four study groups were included: (I) 20 female patients with untreated generalized severe chronic periodontitis, (II) their children (34), (III) 13 periodontally healthy mothers and (IV) their children (13). Material was collected from years 2004–2006. The clinical examination included registration of visible plaque index, modified gingival index and, bleeding sites on probing. Periodontal microbiological samples were obtained from all study subjects and the isolates were identified according to morphology and biochemical profiles; similar interfamilial pathogens were compared by PCR-technique.
Results.  The children of diseased mothers more frequently had periodontal diseases, especially gingivitis. In addition, clinical parameters of gingival inflammation were more expressed and oral hygiene was worse in this group of children. VPI and VPI% of the diseased and healthy mothers differed significantly. The most common oral pathogens were P. intermedia/nigrescens and A. actinomycetemcomitans . The children of healthy mothers harboured pathogens less frequently than the children of diseased mothers. The sharing of P. intermedia/nigrescens was more frequent (5 families) than A. actinomycetemcomitans (2 families).
Conclusion.  Maternal indicators, such as periodontitis, hygiene habits, and periodontal microflora are risk factors for childhood periodontal diseases, and might be predictive of future childhood and adolescent periodontitis.     

Oral Candida infection and colonization in solid organ transplant recipients

Introduction:  Oral Candida carriage and infection have been reported to be associated with a greater risk for systemic infection in transplant recipients; however, a systematic analysis of the oral Candida titers and species has not been previously conducted. The objectives of this study were to determine the prevalence of oropharyngeal candidiasis, the oral carrier status, Candida titers and species in this population.
Methods:  Ninety kidney and heart transplant subjects and 72 age-matched healthy controls were included. Swabs from the oral mucosa and a standardized amount of unstimulated saliva were plated on Chromagar™ Candida , and colony-forming units per millilitre were calculated. Initial speciation was based on colony color and was confirmed by standard germ tube, biotyping, or polymerase chain reaction assays.
Results:  Infection with C. albicans was detected in seven transplant subjects and none of the controls. The transplant group had significantly higher oral Candida titers than the control group. There were no statistically significant relationships between the dose or type of immunosuppressants and oral Candida titers or infection. A significantly higher percentage of transplant subjects were colonized by more than one species, compared with control subjects. The most frequent species combination in transplant subjects was C. albicans and C. glabrata . C. glabrata was isolated from 13.5% of transplant carriers and none of the controls.
Conclusions:  Increased oral Candida infection and carriage titers were found in the transplant population. Although the majority of transplant patients were colonized by C. albicans , C. glabrata appears to emerge as the second most prevalent species.     

Evaluation of myofibroblasts in oral epithelial dysplasia and squamous cell carcinoma

Background:  Carcinogenesis is accompanied by a number of changes in the adjacent stroma including the appearance of myofibroblasts. The purpose of this study was to evaluate and compare the presence of myofibroblasts in normal mucosa, oral epithelial dysplasia, and different grades of oral squamous cell carcinoma.
Methods:  The study sample consisted of three groups, including 40 oral squamous cell carcinomas, 15 dysplasias, and 15 sections of normal oral epithelium. Vimentin, desmin, and alpha-smooth muscle actin were used to identify myofibroblasts.
Results:  The percentage and intensity of alpha-smooth muscle actin were examined, and positive immunostaining was observed in the myofibroblasts of all squamous cell carcinomas; however these cells did not stain in the dysplasias or normal epithelium specimens. The presence of myofibroblasts was significantly higher in oral squamous cell carcinomas compared to both, dysplasias and normal mucosa cases ( P  < 0.001). A significant difference was not observed between the different grades of oral squamous cell carcinoma ( P  = 0.2).
Conclusions:  These findings show the presence of myofibroblasts in the stroma of oral squamous cell carcinoma but not dysplasia and normal mucosa, suggesting further investigation to clarify the role of myofibroblasts in the carcinogenesis of this tumor.