Impacto do estresse precoce de vida sobre a progressão da periodontite apical e da doença periodontal: estudo comportamental e histológico em ratos.
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Data
2021-02-26
Autores
Botelho, Maria Clara Bertolini [UNESP]
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Universidade Estadual Paulista (Unesp)
Resumo
Estímulos estressores durante a infância afetam negativamente as funções fisiológicas, alterando as respostas inflamatórias, imunes, neuro-hormonais e comportamentais. Há evidências de que o estresse precoce de vida (EPV) pode ser um fator de risco direto ou indireto para o desenvolvimento de algumas doenças metabólicas e inflamatórias na idade adulta. No entanto, apesar de existirem evidências de que o estresse influência na progressão da periodontite apical (PA) e da doença periodontal (DP), o impacto do EPV sobre estas doenças é pouco estudado. Portanto, este estudo teve como objetivo avaliar a influência do EPV sobre a PA e DP induzidas experimentalmente em ratos. No presente estudo foram utilizados sessenta ratos machos Wistar, divididos em 6 grupos experimentais (n=10): Grupo controle: ratos não submetidos ao EPV ou a indução das doenças; Grupo EPV: ratos submetidos ao EPV; Grupo PA: ratos com PA; Grupo EPV+PA: ratos submetidos à indução da PA e do EPV; Grupo DP: ratos com DP e Grupo EPV+DP: ratos submetidos à indução da DP e do EPV. O EPV foi induzido pelo método de separação materna (SM) por um período de 3 horas durante 21 dias consecutivos. Ao completarem 90 dias, os animais dos grupos PA e EPV+PA foram submetidos à indução da PA através da exposição pulpar do primeiro e segundo molares superiores do lado direito. A indução da DP foi realizada nos grupos DP e EPV+DP através da inserção e manutenção de uma ligadura no segundo molar superior esquerdo. O protocolo de exposição pulpar para a PA e manutenção da ligadura para os animais com DP, foi de cinco semanas. O teste labirinto elevado em zero (LEZ) foi realizado em todos os animais com 37 dias após a indução das doenças para avaliar o comportamento de ansiedade. Após 3 dias do teste LEZ, os animais foram eutanasiados e as maxilas foram coletadas. Posteriormente, foi realizada análise histológica e histométrica para avaliação do infiltrado inflamatório e extensão das lesões induzidas experimentalmente. A análise histológica revelou maior intensidade do infiltrado inflamatório para os animais com PA e DP expostos ao EPV (p<0.05). A análise histométrica mostrou maior extensão das lesões periapicais nos animais com PA expostos ao EPV quando comparado aos animais com PA não estressados (p<0.05). Já para os animais com DP, não houve diferença na extensão da perda óssea alveolar entre os animais com DP submetidos ou não ao EPV (p>0.05). A análise comportamental revelou um aumento do comportamento ansioso no grupo PA em relação ao grupo controle (p<0.05). No entanto, a exposição ao EPV anulou este efeito da PA sobre o comportamento, já que os animais do grupo EPV+PA frequentaram por mais tempo os braços abertos do aparelho (p<0.05). Já para os ratos submetidos à indução de DP, foi observado aumento do tempo nos braços abertos dos grupo DP em relação ao grupo controle (p<0.05). O mesmo aconteceu com o grupo DP em relação ao grupo DP-estressado (p<0.05). Os resultados do presente estudo indicam que o EPV afeta a progressão da periodontite apical, exacerbando o processo inflamatório e a reabsorção óssea periapical. Contudo, apesar de agravar a intensidade da inflamação na doença periodontal, o EPV não afeta a reabsorção óssea alveolar.
Stress stimuli during childhood negatively affect physiological functions, altering inflammatory, immune, neuroendocrine responses and behavior. There is evidence that early life stress (ELS) can be a direct or indirect risk factor for the development of some metabolic and inflammatory diseases in adulthood. However, although there is evidence that stress influences the progression of apical periodontitis (AP) and periodontal disease (PD), the impact of ELS on these diseases is little studied. Therefore, this study aimed to evaluate the influence of ELS on experimentally induced AP and PD in rats. Sixty Wistar male rats were used in this study, divided into 6 experimental groups (n=10): Control Group: rats not subjected to ELS or to induction of diseases; ELS Group: rats subjected to ELS; PA Group: rats with PA; ELS+AP Group: rats subjected to induction of AP and ELS; PD Group: rats with PD and ELS+PD Group: rats subjected to induction of PD and ELS. ELS was induced by the method of maternal separation (MS) for a period of 3 hours for 21 consecutive days. On completing 90 days, the animals of the AP and ELS+AP groups were subjected to induction of AP through pulpal exposure of the right upper and lower first and second molars. Induction of PD was performed in the PD and ELS+PD groups through the insertion and maintenance of a ligature in the upper second left molar. The pulp exposure protocol for AP and ligation maintenance for animals with PD was five weeks. The elevated zero maze test (EZM) was performed on all animals at 37 days after diseases induction to assess anxiety-like behavior. After 3 days of the EZM test, the rats were euthanized and the jaws were collected. Subsequently, histological and histometric analysis was performed to evaluate the inflammatory infiltrate and extent of the experimentally induced lesions. Histological analysis revealed greater intensity of inflammatory infiltrate for the animals with AP and PD exposed to ELS (p<0.05). Histometric analysis showed greater extension of periapical lesions in animals with AP exposed to ELS when compared to non-stressed animals with AP (p<0.05). As for the animals with PD, there was no difference in the extent of alveolar bone loss between the animals with PD submitted or not to ELS (p>0.05). Behavioral analysis revealed an increase in anxious behavior in the AP group compared to the control group (p<0.05). However, exposure to ELS decreased this effect of AP on behavior, since the animals in the ELS+AP group frequented the open arms of the apparatus for longer. For the PD rats, an increase in time in the open arms was observed compared to the control rats (p<0.05). The same was true for the PD rats compared to the PD-stressed rats (p<0.05). The results of this study indicate that early life stress affects the progression of apical periodontitis, exacerbating the inflammatory process and periapical bone resorption. However, although it aggravates the intensity of inflammation in periodontal disease, early life stress does not affect alveolar bone resorption.
Stress stimuli during childhood negatively affect physiological functions, altering inflammatory, immune, neuroendocrine responses and behavior. There is evidence that early life stress (ELS) can be a direct or indirect risk factor for the development of some metabolic and inflammatory diseases in adulthood. However, although there is evidence that stress influences the progression of apical periodontitis (AP) and periodontal disease (PD), the impact of ELS on these diseases is little studied. Therefore, this study aimed to evaluate the influence of ELS on experimentally induced AP and PD in rats. Sixty Wistar male rats were used in this study, divided into 6 experimental groups (n=10): Control Group: rats not subjected to ELS or to induction of diseases; ELS Group: rats subjected to ELS; PA Group: rats with PA; ELS+AP Group: rats subjected to induction of AP and ELS; PD Group: rats with PD and ELS+PD Group: rats subjected to induction of PD and ELS. ELS was induced by the method of maternal separation (MS) for a period of 3 hours for 21 consecutive days. On completing 90 days, the animals of the AP and ELS+AP groups were subjected to induction of AP through pulpal exposure of the right upper and lower first and second molars. Induction of PD was performed in the PD and ELS+PD groups through the insertion and maintenance of a ligature in the upper second left molar. The pulp exposure protocol for AP and ligation maintenance for animals with PD was five weeks. The elevated zero maze test (EZM) was performed on all animals at 37 days after diseases induction to assess anxiety-like behavior. After 3 days of the EZM test, the rats were euthanized and the jaws were collected. Subsequently, histological and histometric analysis was performed to evaluate the inflammatory infiltrate and extent of the experimentally induced lesions. Histological analysis revealed greater intensity of inflammatory infiltrate for the animals with AP and PD exposed to ELS (p<0.05). Histometric analysis showed greater extension of periapical lesions in animals with AP exposed to ELS when compared to non-stressed animals with AP (p<0.05). As for the animals with PD, there was no difference in the extent of alveolar bone loss between the animals with PD submitted or not to ELS (p>0.05). Behavioral analysis revealed an increase in anxious behavior in the AP group compared to the control group (p<0.05). However, exposure to ELS decreased this effect of AP on behavior, since the animals in the ELS+AP group frequented the open arms of the apparatus for longer. For the PD rats, an increase in time in the open arms was observed compared to the control rats (p<0.05). The same was true for the PD rats compared to the PD-stressed rats (p<0.05). The results of this study indicate that early life stress affects the progression of apical periodontitis, exacerbating the inflammatory process and periapical bone resorption. However, although it aggravates the intensity of inflammation in periodontal disease, early life stress does not affect alveolar bone resorption.
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Palavras-chave
Estresse psicológico, Periodontite apical, Doença periodontal, Periodontal disease