Structural alterations in osteocyte dendrites and lacunar-canalicular networks of the mandible of ovariectomized mice

Postmenopausal osteoporosis (PMOP) leads to systemic bone metabolism disorders, significantly affecting oral bone health and complicating treatment. Osteocytes, the most abundant cells in bone tissue, play a crucial role in bone remodeling through cellular communication. However, the mineralized bone matrix surrounding osteocytes presents significant challenges for studying their dendritic networks.

Eight week old C57BL/6J female mice were randomly assigned to either a Sham group or an ovariectomized (OVX) group. The PMOP animal model was established via bilateral ovariectomy and analyzed after 12 weeks. Osteocyte dendrites and the lacuno-canalicular network (LCN) were examined via SEM and immunohistochemical staining. Quantification of nodes and connectomic measurements were performed for LCN and phalloidin network analyses. Furthermore, the expression levels of MMP13 and CTSK were assessed via immunohistochemical staining and real-time PCR.

Our findings revealed that both Sham and OVX mice exhibited two distinct morphological types of osteocyte lacunar structures in the mandible. In Sham mice, direct communication was observed between osteocytes, adjacent cells, and blood vessels via canaliculi. In contrast, connectivity analysis of the osteocyte dendritic network in OVX mice revealed a reduced material transport capacity between cells compared with Sham controls. OVX-induced systemic osteoporosis altered the osteocyte dendritic network and lacunar canaliculi in the mandible, potentially due to periluminal canalicular remodeling.

This study offers new insights into the changes and mechanisms affecting the dendritic network and lacunar canaliculi of mandibular osteocytes in postmenopausal osteoporosis, contributing to a deeper understanding of oral bone lesions in this condition.

After menopause, many women develop osteoporosis-a condition where bones become weak and break easily. This not only affects bones such as the spine or hips but also damages the jawbone, making dental treatments harder. We wanted to understand how osteoporosis weakens the jawbone by studying tiny bone cells called osteocytes, which act like "messengers" controlling bone health. Using advanced microscopy and special staining techniques, we mapped communication networks between osteocytes in the jawbone (like tracing telephone wires between cells). We then compared bone structures between healthy mice and mice with osteoporosis after ovary removal. Osteoporosis damaged the "wires" (dendrites) connecting osteocytes, reducing their ability to share nutrients and signals. It also widened tunnels (canaliculi) around osteocytes-like potholes in roads-disrupting their links to blood vessels and neighboring cells. These changes likely occur because osteoporosis impairs the bone's self-repair system around these tunnels. Our discovery that osteoporosis breaks bone cell networks reveals a new mechanism for jawbone weakening, paving the way for better dental treatments, protective drugs, and patient education.