Resumen Introducción: La hipertrofia gingival (HG) es el aumento del volumen de la encía asociado a ciertas enfermedades sistémicas, hereditarias (idiopático), ingesta de algunos medicamentos o a factores locales como el tratamiento ortodóntico, capaz de provocar cambios histológicos en el tejido conectivo gingival. Objetivo: Describir las características histológicas e identificar el colágeno tipo I y tipo III en tejidos gingivales de sujetos con hipertrofia gingival portadores de ortodoncia. Materiales y método: Se diseñó un estudio de casos y controles que incluyó el análisis de biopsias de tejido gingival de 12 pacientes sometidos a cirugías periodontales. La muestra se dividió en dos grupos: individuos sanos (control; n= 6) y pacientes con HG portadores de ortodoncia (pacientes; n= 6). Las muestras fueron procesadas e incluidas en parafina. Las tinciones Masson-Goldner y rojo sirius/verde rápido fueron empleadas. El colágeno tipo I y tipo III fueron identificados mediante inmunohistoquímica con anticuerpos monoclonales. Resultado: En los pacientes con HG portadores de ortodoncia se observó un epitelio hiperplásico y tejido conectivo denso con abundantes fibras de colágeno distribuidos aleatoriamente. La inmunodetención de colágeno tipo I indicó la presencia de abundantes fibras desorganizadas y el colágeno tipo III fue inmunolocalizado subyacente a la membrana basal, vasos sanguíneos y toda la extensión del tejido conectivo de los pacientes con HG con tratamiento ortodóntico. Conclusión: La acumulación de fibras de colágeno, particularmente del colágeno tipo I y tipo III, son hallazgos histológicos que caracterizan la HG en pacientes portadores de ortodoncia. Futuros estudios son necesarios para dilucidar el fenotipo de los fibroblastos gingivales y la probable pérdida homeostática entre la producción y degradación de colágeno en esta patología.

Abstract Introduction: Gingival hypertrophy (GH) is the increase in the volume of the gingiva associated with certain systemic, hereditary (idiopathic) diseases, the intake of some medications or local factors such as orthodontic treatment, capable of causing histological changes in the gingival connective tissue. Objective: To describe the histological characteristics and identify type I and type III collagen in gingival tissues of subjects with gingival hypertrophy wearing orthodontics. Method: A case-control study was designed that included the analysis of gingival tissue biopsies from 12 patients submitted to periodontal surgeries. The sample was divided into two groups: healthy individuals (Control; n= 6) and patients with GH wearing orthodontics (Patients; n= 6). The samples were processed and embedded in paraffin. Masson-goldner and sirius red/fast green stains were used. Type I and type III collagen were identified by immunohistochemistry with monoclonal antibodies. Result: A hyperplastic epithelium and dense connective tissue with abundant randomly distributed collagen fibers were observed in patients with orthodontic GH. Immunodetention of type I collagen indicated the presence of abundant disorganized fibers and type III collagen was inmunolocalized underlying the basement membrane, blood vessels and the entire extension of the connective tissue of patients with GH orthodontic. Conclusion: The accumulation of collagen fibers, particularly type I and type III collagen, are histological findings that characterize GH in orthodontic wearers. Future studies are necessary to elucidate the phenotype of gingival fibroblasts and the probable homeostatic loss between collagen production and degradation in this pathology.

ABSTRACT: The objective of the study was to compare, through a systematic review, the clinical results of periodontal / peri-implant plastic surgery (CP) procedures with autogenous soft tissue graft (ITB) obtained from the lateral palate area (ALP) versus the tuberosity area (AT). We conducted an electronic search of clinical trials in the Medline/Pubmed, Cochrane database and the journals of Periodontics and Implants with the greatest impact according to the Web of Science, to find articles published until April 2020. The risk of bias of the articles added was assessed according to the Cochrane Manual Version 5.1.0 for randomized clinical trials and the Newcastle-Ottawa scale for controlled clinical trials. From the initial sample of 930 articles, four clinical trials were included (three randomized) in the present study, where a total of 87 PC were performed around dental pieces and implants, of which 42 surgeries were performed with ITB of the ALP and 45 surgeries with ITB of the AT, the results were evaluated from the 8 weeks to 12 months. No statistically significant differences were found in the clinical results between the two groups, the gingival phenotype in the receiving area was improved for the group that obtained the ITB of the AT and the level of pain at the donor site was lower in the first two weeks than the ALP donor site. The studies showed a lowrisk of bias on average. Both soft tissue graft donor areas provide similar clinical results, grafting the tuberosity area improves the gingival phenotype of the recipient area and reduces post-operative pain of the donor site in the first few weeks.

RESUMEN: Comparar mediante una revisión sistemática los resultados clínicos de los procedimientos de cirugía plástica periodontal/periimplantar (CP) con injerto de tejido blando autógeno (ITB) obtenido del área lateral del paladar (ALP) versus del área de la tuberosidad (AT). Se realizó una búsqueda electrónica de ensayos clínicos en la base de datos Medline/Pubmed, Cochrane y las revistas de Periodoncia e Implantes de mayor impacto según la Web of Science, para hallar artículos publicados hasta abril del 2020. Se valoró el riesgo de sesgo de los artículos añadidos según el manual Cochrane Versión 5.1.0 para ensayos clínicos aleatorizados y la escala Newcastle-Ottawa para ensayos clínicos controlados. De una muestra inicial de 930 artículos, cuatro ensayos clínicos (tres aleatorizados) fueron incluidos en el presente estudio, donde se realizaron un total de 87 CP alrededor de piezas e implantes dentales, de las cuales 42 cirugías fueron realizadas con ITB del ALP y 45 cirugías con ITB del AT, se evaluó los resultados desde las 8 semanas hasta los 12 meses. No se hallaron diferencias estadísticamente significativas en los resultados clínicos entre ambos grupos, se mejoró el fenotipo gingival en la zona receptora para el grupo que obtuvo el ITB del AT y el nivel del dolor del sitio donador del AT fue menor en las dos primeras semanas que el sitio donante del ALP. Los estudios incluidos manifestaron un bajo riesgo de sesgo en promedio. Ambas áreas donantes de injerto de tejido blando proporcionan resultados clínicos similares, el injerto del área de la tuberosidad mejora el fenotipo gingival de la zona receptora y reduce el dolor post operatorio en las primeras semanas del sitio donador.

Resumo Introdução A determinação do fenótipo gengival possibilita compreender melhor as variações e diferenças clínicas intra e interindividuais dos tecidos periodontais saudáveis. Objetivo O objetivo deste estudo foi determinar os perfis do fenótipo gengival e compará-los em diferentes regiões da cavidade oral, levando em consideração parâmetros clínicos relacionados aos tecidos moles circunjacentes nos dentes anteriores superiores e inferiores. Material e método Noventa e um pacientes com saúde periodontal foram examinados e os parâmetros clínicos profundidade de sondagem (PS), largura de mucosa ceratinizada (MC), espessura gengival em ambos incisivos centrais superiores (EG) e fenótipo gengival (FG) foram coletados nos dentes anteriores superiores e inferiores. Os dados foram analisados estatisticamente pelos testes t-Student pareado e independente, Correlação de Pearson e Qui-quadrado, com um nível de significância de 5%. Resultado O fenótipo gengival espesso predominou nos dentes anteriores superiores (60,5%), enquanto o fenótipo fino foi mais prevalente nos dentes anteriores inferiores (84,6%). Diferenças estatisticamente significativas foram encontradas para os parâmetros largura de mucosa ceratinizada e espessura gengival em relação aos fenótipos gengivais superiores e inferiores (p<0,05). Não houve diferença estatística entre profundidade de sondagem e o fenótipo gengival nos dentes superiores e inferiores. Conclusão Concluiu-se que o fenótipo gengival espesso é mais frequente nos dentes anteriores superiores e que o fenótipo fino é mais comum nos dentes anteriores inferiores, sendo mais frequente em indivíduos do sexo masculino. Os parâmetros largura de mucosa ceratinizada e espessura gengival mostraram-se adequados à determinação do fenótipo gengival.

Abstract Introduction Gingival phenotype determination enables a better understanding of intra and interindividual clinical variations in healthy periodontal tissues. Objective The aim of this study was to determine gingival phenotype profiles and compare these in different regions of the oral cavity, considering clinical parameters related to the surrounding soft tissue in the upper and lower front teeth. Material and method Ninety-one periodontally-healthy patients were examined and clinical parameters such as probing depth (PD), keratinized tissue width (KW), gingival thickness at both maxillary central incisors (GT) and gingival phenotype (GP) were determined for the upper and lower front teeth. Data were statistically analyzed by paired and independent t-Student tests, Pearson Correlation and the Chi-square test, using a significance level of 5%. Result The thick gingival phenotype predominated in the upper anterior teeth (60.5%), while the thin phenotype was more prevalent in the lower anterior teeth (84.6%). Statistically significant differences were found for keratinized tissue and gingival thickness parameters, in relation to the upper and lower gingival phenotypes (p<0.05). There were no statistical significances for probing depth and gingival phenotype in the upper and lower teeth. Conclusion It was concluded that the thick phenotype is more frequent in the upper anterior teeth and that the thin phenotype is more common in the lower anterior teeth, and more frequent in males. The keratinized tissue and gingival thickness parameters proved to be suitable for the determination of gingival phenotype.

O linfoma de células natural killers (NK)/T extranodal é um tumor maligno agressivo com características clinicopatológicas distintas, caracterizadas por invasão e destruição vasculares, necrose proeminente, fenótipo linfocítico citotóxico e uma forte associação com o vírus Epstein-Barr. Relatamos aqui um caso de linfoma de células NK/T nasal extranodal, envolvendo o seio maxilar, assoalho de órbita, e interessantemente estendendo-se para a cavidade oral através do osso alveolar e mucosa vestibular, preservando o palato, levando a um diagnóstico inicial equivocado de doença periodontal agressiva. Ainda, nós investigamos pela primeira vez a expressão imunoistoquímica das proteínas Fatty acid sinthase (FASN) e glucose transporter 1 (GLUT-1) nesta neoplasia. FASN revelou uma forte expressão citoplasmática nas células neoplásicas, enquanto GLUT-1 e CD44 foram negativas. Estes achados sugerem que a expressão de FASN e a perda de CD44 podem estar envolvidas na patogênese do linfoma de células NK/T nasal extranodal, e que GLUT-1 não deve participar da adaptação das células tumorais ao ambiente de hipóxia. Estudos adicionais com séries maiores são necessários para confirmar nossos resultados iniciais.

Extranodal natural killer (NK)/T-cell lymphoma is an aggressive malignant tumor with distinctive clinicopathological features, characterized by vascular invasion and destruction, prominent necrosis, cytotoxic lymphocyte phenotype and a strong association with Epstein-Barr virus. Here is reported an extranodal nasal NK/T-cell lymphoma case, involving the maxillary sinus, floor of the orbit, and interestingly extending to the oral cavity through the alveolar bone and buccal mucosa, preserving the palate, leading to a primary misdiagnosis of aggressive periodontal disease. Moreover, this work investigated for the first time the immunohistochemical expression of fatty acid synthase (FASN) and glucose transporter 1 (GLUT-1) proteins in this neoplasia. FASN showed strong cytoplasmatic expression in the neoplastic cells, whereas GLUT-1 and CD44 were negative. These findings suggest that the expression of FASN and the loss of CD44 might be involved in the pathogenesis of the extranodal nasal NK/T-cell lymphoma, and that GLUT-1 may not participate in the survival adaptation of the tumor cells to the hypoxic environment. Further studies with larger series are required to confirm these initial results.

Os hábitos tabágicos constituem um factor de risco para patologias crónicas que envolvem o tecido ósseo como a osteoporose e a perda óssea alveolar associada à doença periodontal. O processo de formação óssea envolve a diferenciação de células osteoprogenitoras em osteoblastos e a formação de uma matrix colagenosa mineralizada. Assim, o objectivo deste trabalho foi caracterizar o comportamento de células osteoblásticas provenientes de medula óssea humana na presença de concentrações de nicotina representativas dos níveis sanguíneos e salivares presentes nos indivíduos com hábitos tabágicos. As culturas celulares foram mantidas durante 28 dias em condições experimentais que favorecem a diferenciação do fenótipo osteoblástico e cultivadas na ausência (situação controlo) e na presença de nicotina (10 ng/ml - 1 mg/ml). A exposição a 10 ng/ml (concentração representativa dos níveis plasmáticos) não afectou significativamente a proliferação e actividade funcional. A presença de concentrações superiores (0,01 - 1 mg/ml, representativas dos níveis salivares) influenciou o comportamento celular, de modo dependente da dose. As culturas expostas a 0,01 - 0,2 mg/ ml apresentaram estimulação da proliferação celular e da actividade de fosfatase alcalina, associada a uma antecipação do processo de mineralização da matriz extracelular. A exposição a 0,3 mg/ml causou um efeito inibitório inicial, seguido de recuperação dos parâmetros de crescimento e função. Na presença de concentrações superiores, observaram-se efeitos negativos no comportamento celular durante todo o período de incubação; as culturas apresentaram uma diminuição do número de células aderentes, níveis de fosfatase alcalina baixos e extensa vacuolização citoplasmática. Os resultados sugerem a possibilidade de modulação local da actividade osteoblástica pela nicotina, a nível da cavidade oral.

The use of tobacco has been implicated in bone pathologies like osteoporosis and alveolar bone loss associated to periodontal disease. Bone formation involves the differentiation of osteoprogenitor cells into osteoblasts and the formation of a mineralised colagenous matrix. Therefore, the aim of this work was to characterise the behaviour of human bone marrow derived osteoblastic cells in the presence of nicotine at concentrations representatives of those present in plasma and saliva of tobacco users. Cell cultures were maintained for 28 days in experimental conditions that favour the differentiation of the osteoblastic phenotype and cultured in the absence (control) and in the presence of nicotine (10 ng/ml - 1 mg/ml). Results showed that nicotine, at 10 ng/ml (representative of plasmatic levels), did not affect significantly cell proliferation and functional activity. The presence of higher levels, 0.01 - 1mg/ml (representative of the salivary levels), affected cell behaviour in a dose dependent manner. Cultures exposed to 0.01 - 0.2 mg/ml presented increased cell proliferation and alkaline phosphatase activity, associated to an anticipation of the matrix mineralization. Treatment with 0.3 mg/ml caused an initial inhibitory effect followed by a recovery of the cell growth and functional parameters. In the presence of higher concentrations, negative effects on cell behaviour were observed throughout the incubation time; cultures presented decreased numbers of adherent cells, low alkaline phosphatase levels and cytoplasm vacuolation. Results suggest the possibility of local modulation of the osteoblastic activity by nicotine, at the oral cavity.

Periodontitis is nowadays accepted as a multi-factorial disease with microbial agent as the initiator ,necessary but not enough , and a wide variety of determinants and factors that influence the manifestation and progression of the disease. The potencial importance of genetics and heredity to the knowledge about the pathogenesis and the clinic dental practice of periodontal diseases has been recognized since the earliest days of dentistry and medicine, but the relative complexity resulting from the interaction among the exposure to oral bacteria and the host response promote the dificulty of the genetics factors role clarification. Even so, genetic factors influence in periodontal diseases are suggest for several forms of periodontitis. In general, it’s considered the existence of sufficient scientific basis in favour of the genetic factors presence in Aggressive Periodontitis, whereas, the evidence of the genetic participation in Chronic Periodontitis isn’t so manifest. A multitude of host factors are involved in responses to microbial challenge and in the subsequent immune responses of the periodontal diseases, so, genetics polymorphisms probably exist in many of if not most of the inflammatory and immune mediators such as demonstrated by the IL-1,IL-4, IL-10,TNF, PGE2, specific HLA antigens (Human Leukocite Antigen), Vitamine D receptor, fMLP receptor, IgG Fc receptors (FcIIIb and FcgRII) and the N-acetyltransferase (NAT2) receptor. Correlation of these genetic polymorphisms with phenotypic characteristics of periodontitis patients groups may provide the frame work for identification of individual risk profiles.

Hoy en día y tras numerosos estudios epidemiológicos, se acepta el concepto de la existencia de determinados factores de riesgo que van a modular la susceptibilidad o resistencia del hospedador a padecer enfermedad periodontal, por lo tanto, en el desarrollo van a intervenir varias causas considerándose dicha patología de etiología multifactorial. De este modo, las enfermedades periodontales son producidas por una interacción de un agente microbiano único o múltiple considerado como el factor etiológico primario necesario pero no suficiente, un huésped más o menos susceptible y unos factores ambientales que influyen sobre ambos. La importancia de la herencia y la genética para el conocimiento de la etiopatogenia de la enfermedad periodontal y para la práctica clínica en general fueron destacadas desde muy temprano, pero las complejas interacciones que ocurren entre los mecanismos de respuesta del hospedador y la acción de los microorganismos patógenos han hecho que las aclaraciones sobre el papel de los factores genéticos en la enfermedad periodontal sean más difíciles. Aun así, la influencia de los factores genéticos en la periodontitis parece ser diferente para los distintos tipos de enfermedad periodontal y ha sido estudiada en cada una de las periodontitis definidas. En general, se considera que hay suficiente base científica a favor de la presencia de factores genéticos en la aparición de periodontitis agresivas. En las periodontitis crónicas, en cambio, la evidencia de la participación genética es menos manifiesta. Numerosos estudios ponen en evidencia que existe una asociación entre las periodontitis y una variación genética de determinados genes (polimorfismos) que codifican diferentes citoquinas proinflamatorias y mediadores involucrados en la etiopatogénia de la enfermedad periodontal como la IL-1,IL- 4, IL-10,TNF, PGE2. El fenotipo HLA (Human Leukocite Antigen), también ha sido investigado como posible factor de resistencia y susceptibilidad de la enfermedad periodontal así como los polimorfismos del gen de la vitamina D, del receptor fMLP , del receptor FcIIIb de los neutrófilos, del receptor FcgRII y de la N-acetyltransferasa (NAT2).

The periodontal disease brings about the destruction of the protective and supporting tissues of the teeth, therefore, the role of enzymes capable of degrading connective tissue matrix is of great importance. There are evidences of the possible involvement of the matrix metalloproteinases, leukocyte proteases and bacterial proteases in the pathogenesis of such disease. Their action is controlled by specific inhibitors in the tissues. This means that any protease-inhibitor imbalance favouring the presence of proteases may lead to the destruction of matrix connective tissue. In turn, proteolytic activity is influenced by different factors that globally induce a degradative or formative phenotype, and thus, may be involved in the pathogenesis of the periodontal disease.

La enfermedad periodontal inflamatoria ocasiona la destrucción de los tejidos que protegen y soportan al diente; es por eso de gran importancia el papel que pueden desempeñar las enzimas que sean capaces de degradar la matriz del tejido conectivo, como las enzimas proteolíticas. Existen evidencias de que las metaloproteinasas de la matriz, las proteasas leucocitarias y las bacterianas, pueden participar en la etiopatogenia de esta enfermedad. Su acción es regulada en los tejidos, por la presencia de inhibidores específicos, de manera que un desbalance proteasas-inhibidores a favor de los primeros, conduciría a la destrucción de las proteínas de la matriz del tejido conectivo. A su vez, en la actividad proteolítica influyen diferentes factores, que de manera global, inducen un fenotipo degradativo o formativo, y que por lo tanto, podrían estar involucrados en la etiopatogenia de la enfermedad periodontal inflamatoria.