Diabetes and its effects on dental pulp

Abstract

Uncontrolled or poorly controlled diabetes mellitus may be a risk factor for the development of oral complications. The objective of this investigation was to determine the effect of diabetes mellitus progression on inflammatory and structural components of dental pulp. Male Wistar rats were given a single injection of Streptozotocin (STZ), and induction of diabetes was confirmed 24 h later. Dental pulp tissue samples were taken from central incisors and molars of diabetic rats 30 and 90 days after the STZ treatment. Plasma glucose levels in diabetic rats 30 and 90 days after STZ treatment were significantly increased when compared to control rats (P < 0.001). Nitrite and kallikrein levels in dental pulp tissue were higher in diabetic rats 30 days after STZ treatment than in controls, while only nitrite were decreased 90 after of STZ treatment. Myeloperoxidase activity showed changes 30 and 90 days after STZ injection when compared to controls. The activity of alkaline phosphatase showed significant changes 30 and 90 days after STZ treatment. On the other hand the concentration of collagen was decreased in diabetic rats 30 and 90 days after STZ injection. These results suggest that diabetes is a critical factor that has profound effects upon oral tissues, resulting in expression of inflammatory mediators and modifications of structural components of dental pulp.

Diabetes Induces Metabolic Alterations in Dental Pulp

“…Kallikrein-kinin system and myeloperoxidase (MPO) activity are altered in the dental pulp of STZ-induced diabetic rats (23). Moreover, a longer period of diabetes causes a reduction in the collagen concentration and an increase in alkaline phosphatase activity, which could be related to irreversible damages in the dental pulp leading to necrosis (23). In this study, the biochemical parameters studied were the sialic acid concentration and catalase and peroxidase activities.…”

“…Diabetes induces the expression of inflammatory mediators and can cause modifications in the structural components of dental pulp. Kallikrein-kinin system and myeloperoxidase (MPO) activity are altered in the dental pulp of STZ-induced diabetic rats (23). Moreover, a longer period of diabetes causes a reduction in the collagen concentration and an increase in alkaline phosphatase activity, which could be related to irreversible damages in the dental pulp leading to necrosis (23).…”

“…*Indicate statically significant differences compared with control group (p Յ 0.05). than the antioxidant system (23). The role of antioxidant enzymes in the wound healing process and its therapeutic potential has been the subject of interest in medical sciences.…”

Diabetes Mellitus e sua Influência no Sucesso do Tratamento Endodôntico: Um Estudo Clínico Retrospetivo

“…2,5,6,9,12,15,16,22 Assim, quando há a instalação de processos patológicos, a presença desta doença intensifica o processo de desenvolvimento da infeção, acelerando os fenómenos de necrose e suas consequências quer nos tecidos pulpares quer nos tecidos perirradiculares. 7,9,11,15,16 Embora vários estudos comprovem a inter-relação entre as infeções pulpares e a diabetes mellitus, existem ainda várias lacunas na literatura atual, como o esclarecimento dos diferentes fatores de virulência na via inflamatória do hospedeiro e os efeitos causados pelos diferentes agentes patogénicos pulpares.…”

“…[4][5][6] A evidência científica é consistente quanto ao impacto da diabetes na prevalência e gravidade da doença periodontal, essencialmente em doentes sem controlo dos níveis de glicémia. [5][6][7][8] A periodontite apical consiste numa lesão inflamatória crónica com origem pulpar, que se desenvolve nos tecidos periapicais do dente afetado. [8][9][10] A doença periodontal e a periodontite apical possuem alguns aspetos semelhantes, entre os quais o facto de serem infeções de caráter crónico, as bactérias envolvidas serem maioritariamente bactérias anaeróbias, Gram negativas, e em ambas as patologias haver um aumento significativo dos níveis dos mediadores inflamatórios.…”