Abstract
The aim of this study was to evaluate the expression of MMP2 and MMP9 during apical periodontitis (AP) progression in TLR2 (TLR2 KO) and in MyD88 (MyD88 KO) knockout mice compared to wild type (WT) mice. AP was induced in mandibular first molars of TLR2 KO (n= 18), MyD88 KO (n= 18), and WT mice (n= 18). After 7, 21, and 42 days, the animals were euthanized and the jaws were dissected and subjected to histotechnical processing. Subsequent sections were stained by immunohistochemistry and evaluated for detection of MMP2 and MMP9. Statistical analysis of the semi-quantitative analysis of immunohistochemistry was performed using chi-square test (α = 0.05). In the initial periods of AP progression, an increased expression of MMP9 in the TLR2 KO and MyD88 KO mice was observed. In the final periods of AP progression, a reduction of MMP2 expression and an increase of MMP9 expression in the TLR2 KO mice were observed. MMP2 and MMP9 production was modulated for TLR2 and MyD88 during apical periodontitis progression.
Highlights
Apical periodontitis (AP) is an inflammatory alteration of periradicular tissue [1] that results in bone resorption
Immunostaining was analyzed in the AP and, coincidentally, immunostaining of both MMP2 and MMP9 were present throughout the AP extent independent of diaminobenzidine tetrahydrochloride hydrate (DAB) chromogen intensity
Knocking out the activity of Toll-like receptor 2 (TLR2) and Myeloid differentiation factor 88 (MyD88) allowed us to understand the interaction between MMP9 and MMP2 with these proteins providing valuable clues regarding AP progression
Summary
Apical periodontitis (AP) is an inflammatory alteration of periradicular tissue [1] that results in bone resorption. The association of persistent microbial tooth infection within the root canal system [1], the progression of these microorganisms from the dental pulp to the apical foramen, and the lack of local host immune response leads to AP. During AP, host cells in the periapical tissue release many inflammatory mediators, proinflammatory cytokines, and growth factors through innate and adaptive responses [2]. Toll-like receptors (TLRs) are a Type I transmembrane receptor that present a key role in the innate immune system. TLRs recognize pathogen-associated molecular patterns (PAMPs), such as bacterial or viral components, and endogenous mediators, such as proteins and proinflammatory cytokines [3]. Previous studies in experimental animals [4,5,6] and in humans [7] have demonstrated that TLRs play an important role in the AP pathogenesis
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