Avaliação do potencial da tanshinona para inibir a perda óssea induzida por inflamação: análise microtomográfica em modelo murino de calvária

Abstract

Introduction. Diseases characterized by bone destruction and loss, especially those associated with inflammatory processes, significantly compromise the quality of life of individuals, justifying the search for therapeutic agents capable of modulating bone resorption. In this context, tanshinone stands out as a natural bioactive compound with anti-inflammatory, antioxidant, and bone metabolism-modulating properties, showing potential action in regulating osteogenic activity. Additionally, the use of molecules derived from bacterial components has enabled a better understanding of the mechanisms involved in the host immune response and bone resorption processes. Among these molecules, Pam2CSK4, a synthetic lipopeptide, stands out as a potent inducer of inflammatory response and bone resorption. Objective. This study aimed to evaluate the effect of Pam2CSK4 on the induction of bone resorption and the effect of tanshinone IIA (TII-A) on the reduction of bone resorption in an experimental mouse calvaria model. Methodology. An experimental, in vivo laboratory study with a blinded design was conducted. Male mice were used, distributed into three groups (n=6): a control group (CONTROL), which received saline solution; a group subjected to inflammatory induction (Pam2CSK4); and a group treated with TII-A associated with inflammatory induction (TII-A). Through microtomographic analysis, parameters related to trabecular bone microarchitecture were evaluated, such as bone volume (BV), percentage of bone volume (BV/TV), number of trabeculae (Tb.N), trabecular thickness (Tb.Th), and trabecular separation (Tb.Sp). Results. A significant reduction was observed in some of the evaluated parameters. The Pam2CSK4 and TII-A groups showed a significant reduction in bone volume (BV) (p = 0.025 and p = 0.012, respectively) and percentage of bone volume (BV/TV) (p = 0.025 and p = 0.012, respectively) compared to the control group, with no significant differences between the Pam2CSK4 and TII A groups (p = 0.897). Trabecular thickness (Tb.Th) also showed significant differences compared to the control group, both in the Pam2CSK4 group (p < 0.001) and in the TII-A group (p = 0.012). However, no statistically significant differences were observed between the Pam2CSK4 and TII-A groups (p = 0.054). Conversely, the number of trabeculae (Tb.N) did not show a statistically significant difference between the groups evaluated (p = 0.059). Similarly, the trabecular separation parameter (Tb.Sp) also did not show significant differences when comparing the control, Pam2CSK4, and TII-A groups (p = 0.256). Conclusion. The experimental model induced by Pam2CSK4 was effective in promoting changes related to bone resorption in the calvaria of the animals evaluated. However, TII-A did not demonstrate a significant antiresorptive effect under the conditions established in this study. The findings identified in the microtomographic analysis regarding changes in bone microarchitecture in the study highlight the complexity of the pharmacological modulation of inflammatory bone loss and reinforce the need for future investigations to better elucidate the therapeutic potential of the substance studied