Genital ulcers as diagnostic clue for acute myeloid leukaemia.

Acute myeloid leukaemia is a myeloid neoplasm with an extremely varying clinical appearance. Skin lesions are common for specific subtypes of acute myeloid leukaemia but are often misinterpreted. Here, we present a case of acute myeloid leukaemia in a young woman exhibiting genital ulcerations and gingival erosions.

Localized juvenile spongiotic gingival hyperplasia: a report of 3 cases.

Localized juvenile spongiotic gingival hyperplasia (LJSGH) is a recently described benign condition that affects the gingiva of children and young adults. Clinically distinctive, LJSGH presents as a localized area of erythema on the attached gingiva, with a subtly papillary surface architecture. The lesions are generally biopsied because of the lack of resolution with conservative oral hygiene therapeutic measures and esthetic concerns. The histopathology has a characteristic appearance of subtle papillary epithelial hyperplasia, acute inflammation, and numerous engorged capillary vascular spaces in the lamina propria, although clinical correlation is necessary to make the diagnosis. The purposes of this paper were to: introduce localized juvenile spongiotic gingival hyperplasia to the pediatric dental community; document its clinical and histologic features and treatment and the follow-up of three cases; and discuss the most common clinical differential diagnoses.

Inflammatory environment induces gingival tissue-specific mesenchymal stem cells to differentiate towards a pro-fibrotic phenotype.

BACKGROUND INFORMATION: Human gingival tissues are prone to hyperplasia under inflammatory stimuli. We have identified gingival tissue-specific mesenchymal stem cells (GMSCs) and found their functional change being correlated with drug-induced gingival hyperplasia. However, whether these cells exhibit characteristics of pro-fibrotic phenotype under inflammatory condition remains unknown. RESULTS: GMSCs isolated from human normal gingival tissues (N-GMSC) and inflammatory gingival tissues (I-GMSC) were cultured in vitro, representative cytokines were added to simulate the in vivo inflammatory environment. Under the influence of the inflammatory cytokines, GMSCs exhibited higher rate of proliferation than those under normal condition, while their potential for osteogenic and adipogenic differentiation was suppressed. The expression of matrix metalloproteinases (MMP)-1, MMP-2, IL-1, IL-6, TNF-α and type 1 collagen was significantly higher in I-GMSCs than in N-GMSCs. Furthermore, compared with dental pulp stem cells, GMSCs showed different pattern of gene expression and extracellular matrix formation in inflammatory environment. CONCLUSIONS: Inflammatory microenvironment induces GMSCs to differentiate towards a pro-fibrotic phenotype, which could underlie the hyperplastic appearance of inflammatory gingiva.

The role of pathophysiological explanations in clinical case representations of dental students and experts.

INTRODUCTION: Teaching of biomedical knowledge lays the foundations for the understanding and treatment of diseases. However, the representation of pathophysiological explanations in the management of clinical cases differs for various levels of medical expertise and different theories have been proposed to explain this phenomenon. The present study investigated for the first time how biomedical knowledge is used in clinical reasoning in dental medicine. MATERIALS AND METHODS: In an experimental study 20 experts in the field of Periodontology and 61 students of different levels of training produced written pathophysiological explanations after having studied three different clinical cases. By comparing the written protocols to a visualised expert-made 'canonical' explanation the concepts used in the pathophysiological explanation were counted and classified as well as the links between concepts. RESULTS: The statistical analysis by MANOVA showed significant differences between third- and fourth-year students, students of intermediate expertise level (fifth-year) and experts for various parameters qualifying concepts or links of the written pathophysiological explanations. The participants of intermediate expertise level produced a high rate of concepts and links; however, characteristic findings for knowledge encapsulation in the different levels of expertise were not evident. The analysis showed that the design of the clinical cases and of the canonical explanations significantly influenced the outcomes. CONCLUSION: The present study demonstrated the pathophysiological representations of clinical cases in dental students and experts to be different from other medical disciplines. It could be assumed that this observation is based on different contents for teaching of practical skills and diagnostic procedures in dental compared with medical education.

A painful gum.

CASE STUDY: This middle aged Malaysian man presented complaining of painful gums for a few months. He is known to have had epilepsy since childhood.

On the relation of nitric oxide to nifedipine-induced gingival hyperplasia and impaired submandibular glands function in rats in vivo.

Calcium-channel blockers such as nifedipine could be associated with gingival overgrowth. The aim of this study was to examine the role of nitric oxide (NO) on nifedipine-induced gingival hyperplasia along with submandibular secretory function in rats. Animals in divided groups received nifedipine (250 mg/kg diet) alone and in combination with L-arginine (2.25% w/v) or N(omega)-nitro-L-arginine methyl ester (L-NAME) (0.7% w/v) in drinking water for 20 days. Controls received only tap water. Pure submandibular saliva was collected intraorally by micropolyethylene cannula and the mandibular gingiva was examined by means of dissecting microscope for signs of redness, thickness, inflammation and exuda. Twenty-day nifedipine treatment induced gingival hyperplasia accompanied with reduced salivary flow rate and concentrations of total protein, epidermal growth factor (EGF) and calcium in comparison with controls. Co-treatment of animals with nifedipine and L-arginine protected from gingival hyperplasia and retained flow rate, and concentrations of total protein, EGF and calcium in normal levels. Co-treatment of animals with nifedipine and L-NAME potentiated nifedipine-induced gingival hyperplasia and reductions in flow rate and concentrations of total protein, EGF, and calcium. It is concluded that nifedipine-induced gingival hyperplasia is associated with salivary dysfunction. Activation of cGMP-dependent positive signal-transduction mechanisms in salivary glands might be the mechanism for protective effects of NO against nifedipine-induced gingival hyperplasia.

Heparan sulfate interacting protein (HIP/L29) negatively regulates growth responses to basic fibroblast growth factor in gingival fibroblasts.

Basic fibroblast growth factor (bFGF) modulates gingival growth, and its release from heparan sulfate (HS) in the extracellular matrix (ECM) governs local tissue bioavailability. We identified a heparin/HS interacting protein (HIP/L29) that recognizes specific HS sequences. We hypothesize that HIP/L29, by modulating the interactions of bFGF with HS chains on proteoglycans, could regulate bFGF bioavailability. To investigate interactions between bFGF and HIP/L29, we isolated and cultured fibroblasts from normal gingiva and overgrown gingiva from patients on cyclosporine (CSA). bFGF significantly stimulated gingival fibroblast proliferation with or without heparin. Recombinant human HIP/L29 dramatically decreased bFGF-induced proliferation, but did not alter responses to insulin-like growth factor-1 (IGF-1). Analysis of mitogen-activated protein kinase (MAPK) phosphorylation patterns showed that bFGF stimulation of p44 (Erk-1), but not p42 (Erk-2), also was inhibited by HIP/L29 in a dose-dependent manner. Together, these results support our hypothesis that HIP/L29 modulates the bioavailability and action of bFGF.

Hiperplasia gingival inducida por medicamentos antihipertensivos e inmunosupresores / Gingival hyperplasia induced by antihypertensive and immunosupressor drugs

El agrandamiento o hiperplasia gingival es uno de los hallazgos más frecuente en las patologías gingivales, debido principalmente a la exposición crónica de los tejidos a los factores irritantes de la placa bacteriana, y se asocia comunmente a la ingesta de medicamentos como los antihipertensivos, inmunosupresores y anticonvulsivos. En este artículo se revisará principalmente la hiperplasia inducida por el consumo de antihipertensivos e inmunosupresores, pues actualmente son drogas muy usadas, por las altas tasas de hipertensión encontradas en la población, el auge de los trasplantes de órganos y el tratamiento de múltiples enfermedades relacionadas con problemas inmunológicos. Los medicamentos más usados en esas patologías son la ciclosporina A (CsA) y la Nifedipina (NIF)

Pathophysiology of acquired dental diseases of the horse.

Periodontitis, infundibular necrosis, and periapical infection are dental diseases commonly affecting adult horses. Routine dental examinations and care may help to prevent these diseases. Further investigation of the treatment of horses with these diseases using local antimicrobial therapy, restorative dentistry, and endodontic therapy is needed. An understanding of the pathogenesis of these diseases aids in diagnosis and treatment. Gingival hyperplasia and odontogenic tumors are uncommon but should remain in a list of differential diagnoses when examining a horse with pertinent clinical signs. Recognition of odontogenic tumors as early as possible may facilitate surgery. Examination of the oral cavity of foals beyond the neonatal period should allow identification of brachygnathia and timely treatment when indicated.

Pre-transplant gingival hyperplasia predicts severe cyclosporin-induced gingival overgrowth in renal transplant patients.

The relationship between the pre-transplant periodontal status and the development of post-transplant gingival overgrowth was investigated in a longitudinal study. The periodontal condition of 35 patients was examined on 2 occasions while they were on the transplant waiting list and then at 4-6, 10-12, 16 and 20 weeks post-transplant. At each visit the plaque index, the bleeding index and a pocket index (CPITN) were measured. Dental impressions were taken of the pre- and post-transplant gingival condition and used to make stone models which were used to score the gingival overgrowth index (GOI). The patients divided into 3 distinct groups having severe (n=13), mild (n=16) or no post-transplant gingival overgrowth (n=6). Only 1 of the patients had taken cyclosporin prior to inclusion into the study. All the patients who developed severe overgrowth had evidence of gingival hyperplasia before the transplant. There was no difference in the serum cyclosporin levels between the three groups (chi2<2.28, p>0.319). Furthermore, there was no statistical difference for any of the periodontal indices. This study indicates that the hyperplastic gingival inflammatory response of some individuals appears to be potentiated by cyclosporin resulting in severe post-transplant overgrowth. In other patients the same reaction may allow the fibroblastic activity to occur to an extent where it produces a mild clinically apparent overgrowth.

Hiperplasia gengival induzida pela ciclosporina: estudo clínico e histopatológico / Cyclosporine-induced gingival hyperplasia: clinical and histopathologic study

A hiperplasia gengival é a manifestaçäo bucal mais frequente associada à terapia com Ciclosporina (CsA). O objetivo do presente estudo foi avaliar os aspectos clínicos e histopatológicos da hiperplasia gengival induzida pela CsA em 10 pacientes pós-transplante de órgäos. Os resultados mostraram que a interaçäo de outras drogas com a CsA, assim como o grau de higiene bucal e a idade do paciente estäo relacionados com o desenvolvimento dessa lesäo

Age dependency of cyclosporin A-induced gingival overgrowth in rats.

Effects of age on cyclosporin A- (CsA) induced gingival overgrowth were investigated in Fischer rats. Rats 15, 30, 45, and 60 days old were fed a diet containing cyclosporin A (120-200 micrograms/g) for 40 days. Gingival overgrowth was estimated by measuring the gingival sulcus depth with a thin color slide probe under a stereoscopic dissecting microscope. The youngest group (15 days old) of rats developed the most significant gingival overgrowth (buccal sulcus depth of mandibular first molar, CsA-treated rat/untreated rat: 875 +/- 78/275 +/- 25 micron, mean +/- SD, P < 0.001), followed by those in which CsA treatment was initiated at age 30 days (505 +/- 29/267 +/- 56, P < 0.001) and 45 days (400 +/- 45/267 +/- 25, P < 0.001). Significant gingival overgrowth was not induced in rats when CsA treatment had been started at age 60 days (310 +/- 38/292 +/- 18). Average body weight gain of CsA-treated rats during this experiment period was not different from untreated rats of the same age group. These results suggest that CsA-induced gingival overgrowth in rats is age dependent.

On the mechanism of drug-induced gingival hyperplasia.

Proposed mechanisms of the side effect of drug-induced gingival hyperplasia are reviewed. Hypotheses with regard to inflammation from bacterial plaque, increased sulfated glycosaminoglycans, immunoglobulins, gingival fibroblast phenotype population differences, epithelial growth factor, pharmacokinetics and tissuebinding, collagenase activation, disruption of fibroblast cellular sodium/calcium flux, folic acid and a combination hypothesis are evaluated.