Relação entre o tratamento periodontal e o controle metabólico do diabetes mellitus: revisão de literatura / The relationship between periodontal treatment and metabolic control of diabetes mellitus: a review of literature

Diabetes Mellitus (DM) é uma doença metabólica devido a alterações na produção de insulina ou resistência tecidual à mesma, levando a alteração no metabolismo de lipídeos, de açúcares e de proteína. A hiperglicemia resultante pode induzir diversas patologias de sistemas orgânicos. Por sua vez, a Doença Periodontal (DP) promove um desafio bacteriano constante, o que gera maior atividade de monócitos/macrófagos, aumentando a secreção de citocinas pró-inflamatórias. Em estados hiperglicêmicos, existe a formação de produtos finais de glicação avançada (AGEs). O acúmulo nos tecidos de AGEs em diabéticos gera uma resposta hiperinflamatória. Esses fatores, em conjunto, levam a uma alteração na resposta imuno-inflamatóriado hospedeiro, gerando uma menor resistência à infecção e capacidade reparadora. Sendo assim, a terapia periodontal, através do controle do biofilme dental a níveis compatíveis com saúde, reduz a carga microbiana local e,conseqüentemente, diminui os desafios metabólicos nestes indivíduos. Assim, o objetivo deste trabalho, foi revisar os mecanismos pelos quais a DP, bem como a sua terapia associada ou não ao uso de antimicrobianos sistêmicos, podem atuar sobre o controle sistêmico do DM. Conclui-se que, apesar de existir discordância na literatura, os periodontistas deveriam atuar de forma educativa com seus pacientes e seus médicos alertando para a relação entre DP e DM.

Diabetes Mellitus (DM) is a metabolic disease due to alterations in the production of insulin or tissue resistance to it, leading to abnormal fat, sugar, and protein metabolism. Resultant hyperglycemia can induce diverse multiple systems pathologies. On the other hand, periodontal disease (PD)promotes a constant bacterial challenge, which increases monocyte/macrophage activity, and pro-inflammatory cytokines secretion. In hyperglycemic states, there is advanced glycation end-products (AGEs) production. In diabetic subjects, the AGEs accumulation in the tissue leads to a hyper-inflammatory response, generating po or resistance to infections and impaired wound healing. There fore, periodontal therapy, through dental biofilm control, decreases the microbial load and, as a consequence, reduces the metabolic challenges in those subjects. The present paper aims to review the mechanisms through what periodontal disease and its treatment, associated or not to systemic antibiotics, can affect systemic control of DM. It was concluded that despite the existing lack of agreement in the studied literature, periodontists should warn their patients and their doctors about the relationship between PD and DM.

Lack of association between the TNF-alpha -308 (G/A) genetic polymorphism and periodontal disease in Brazilians.

This study evaluated the frequency of the tumor necrosis factor-alpha (TNF-alpha) -308 G/A polymorphism in Brazilians with periodontal health (PH = 51), chronic periodontitis (CP = 74) and generalized aggressive periodontitis (GAgP = 38). Human DNA was obtained from mouthwash samples and TNF-alpha genotyping was performed by PCR and RFLP analyses. Differences in clinical and genetic parameters among groups were sought by Kruskal-Wallis, chi(2) and Fisher's exact tests. The allele -308G was detected in 91.7%, whereas the allele -308A was found in 35.4% of all subjects. No significant differences were observed in the frequency of these alleles (chi(2) = 2.610, p > 0.05) and the genotypes G/G, G/A, and A/A (chi(2) = 2.547, p = 0.636) among groups. The data suggest that the TNF-alpha -308 G/A polymorphism is not associated with periodontitis in this Brazilian population.

Lack of association between the TNF-α -308 (G/A) genetic polymorphism and periodontal disease in Brazilians

This study evaluated the frequency of the tumor necrosis factor-alpha (TNF-α) -308 G/A polymorphism in Brazilians with periodontal health (PH = 51), chronic periodontitis (CP = 74) and generalized aggressive periodontitis (GAgP = 38). Human DNA was obtained from mouthwash samples and TNF-α genotyping was performed by PCR and RFLP analyses. Differences in clinical and genetic parameters among groups were sought by Kruskal-Wallis, χ² and Fisher's exact tests. The allele -308G was detected in 91.7 percent, whereas the allele -308A was found in 35.4 percent of all subjects. No significant differences were observed in the frequency of these alleles (χ² = 2.610, p > 0.05) and the genotypes G/G, G/A, and A/A (χ² = 2.547, p = 0.636) among groups. The data suggest that the TNF-α -308 G/A polymorphism is not associated with periodontitis in this Brazilian population.