Streptococcus mutans e seu metabolismo a nível molecular no contexto ecológico da doença cárie
DOI:
https://doi.org/10.22456/2177-0018.118914Palavras-chave:
Streptococcus mutans, Metabolismo, Cárie dentária, Microbiota, Fatores de virulênciaResumo
Objetivo: Durante décadas, o Streptococcus mutans foi considerado o principal agente etiológico da doença cárie. Esta revisão apresentará seu histórico e metabolismo a nível molecular. Ao entender as vias metabólicas do S.mutans envolvidas no desenvolvimento de lesões cariosas, será possível desenvolver novos métodos de modulação de biofilmes no controle da doença cárie e elucidar a necessidade de continuar pesquisando essa bactéria. Revisão de literatura: Embora o S. mutans não constitua uma proporção significativa na colonização da microbiota bucal da dentição hígida, essa proporção aumenta quando há acidificação contínua do biofilme, associada ao excesso de carboidratos na dieta do hospedeiro. Isso ocorre devido a um conjunto de fatores de virulência, tais como, adesão, formação de biofilme, acidogenicidade, aciduricidade, atividades de proteases, produção de mutacinas e vias de transdução de sinal. Cada uma dessas propriedades, coordenadamente, alteram a ecologia do biofilme dental. Discussão: Ainda é relevante entender o metabolismo do S. mutans como microrganismo modelo em lesões cariosas devido a seus inúmeros fatores de virulência. Porém, no contexto da doença cárie como uma disbiose, estratégias terapêuticas antimicrobianas, mais especificamente anti-S.mutans, voltadas para a eliminação do microrganismo, podem não ser a chave do controle da doença cárie, enquanto a modulação do microbioma poderá se tornar o futuro das clínicas odontológicas. Conclusão: Biofilmes associados a doença cárie compreendem um ecossistema diverso, sugerindo uma etiologia polimicrobiana, porém, estudos futuros que visem à prospecção, ao desenvolvimento e à inter-relação do S. mutans com outros microrganismos e com o hospedeiro humano ainda são justificados a fim de desvendar a transição ‘homeostase-disbiose’.
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