Postmenopausal osteoporosis is characterized as an osteometabolic disease, of multifactorial etiology and is highly prevalent in women (Salari et al., 2021, Yong and Logan, 2021). According to a systematic review and meta-analysis by Salari et al. (2021), 23.1% of women are affected by the disease, totaling a prevalence of 18.3% among men and women worldwide. Due to the decrease in postmenopausal estrogen levels, there is an imbalance between the activity of osteoblasts and osteoclasts, leading to an increased and disproportionate process of bone remodeling (Maeda et al., 2019, Tanaka and Matsumoto, 2021). Clinically, the main observed disease signals are a reduction in bone mass and density of long bones and vertebrae of patients (Yong & Logan, 2021).

For many years, the most used drugs to treat postmenopausal osteoporosis have been antiresorptive medications, with emphasis on bisphosphonates (Ominsky et al., 2011). Acting by inhibiting osteoclasts or osteoclasts precursors, antiresorptive drugs inhibit bone resorption, stabilizing bone loss caused by metabolic diseases (Carpenter & Ross, 2020). Bisphosphonates, however, are also related to serious adverse effects that might occur during or after osteoporosis treatment (Mbese & Aderibigbe, 2021). Osteonecrosis of the jaw, atypical femoral fractures, and atrial fibrillation are some of the most described adverse effects related to the use of bisphosphonates in the literature (Mbese and Aderibigbe, 2021, Thirunavukarasu et al., 2015).

Recently, studies have described a new anti-resorptive drug, the anti-sclerostin monoclonal antibody (Scl-Ab) – Romosozumab, for the treatment of osteoporosis in postmenopausal women at high risk of bone fractures (Liu et al., 2018, Tamplen et al., 2018, Tanaka and Matsumoto, 2021, Xu et al., 2016). Sclerostin is a glycoprotein encoded by the SOST gene that is expressed mainly in osteocytes (Tanaka & Matsumoto, 2021) and is an antagonist of the Wnt signaling pathway – one of the key elements for bone formation (Maeda et al., 2019, Marini et al., 2023). Sclerostin functions as a potent antagonist of the Wnt signaling pathway by binding to the LRP5/6 receptor complex, which typically facilitates Wnt protein signaling. This interaction inhibits the engagement of Wnt ligands with the receptor complex, thereby disrupting downstream signaling cascades crucial for bone formation. Consequently, sclerostin's antagonistic action on LRP5/6 leads to the downregulation of osteoblast activity and subsequent inhibition of bone formation, thereby intricately modulating bone metabolism and homeostasis (Duan and Bonewald, 2016, Maeda et al., 2019, Marini et al., 2023). Therefore, dysregulated sclerostin expression can promote reduced bone formation and increased bone resorption (Wang et al., 2021). Besides, several factors can modulate the expression of sclerostin by osteocytes, such as mechanical stress, parathyroid hormone, or the presence of cytokines (Delgado-Calle et al., 2017, Tanaka and Matsumoto, 2021).

Based on the aforementioned, the change in sclerostin expression and bone repair after treatment with Scl-Ab has demonstrated that sclerostin inhibition might be a viable approach for the development of different anti-resorptive agents in the treatment of diseases characterized by bone loss (Carpenter and Ross, 2020, Piccoli et al., 2020, Tanaka and Matsumoto, 2021).

Studies have also demonstrated that, locally, sclerostin inhibition plays an important role in reducing the osseointegration period of implants installed on femurs of ovariectomized rats and providing bone regeneration around implants of non-ovariectomized rats (Virdi et al., 2015, Yu et al., 2018). Moreover, it is also reported that systemic use of anti-sclerostin antibodies is capable of promoting bone and cementum regeneration in large alveolar bone defects, such as reduction of alveolar bone loss in periodontitis models (Liu et al., 2018, Taut et al., 2013, Xu et al., 2016, Yao et al., 2020). Furthermore, a recent review by Couto et al. (2023) also highlights important findings regarding the anti-sclerostin effect on osseointegration and bone remodeling in different pre-clinical and clinical studies.

Given the current scarcity of studies that evaluate the behavior of new drugs based on anti-sclerostin monoclonal antibodies in the repair of post-extraction sockets, this study aimed to evaluate the effects of an anti-sclerostin monoclonal antibody medication on the repair of post-extraction sockets of ovariectomized rats.