Enhanced cortical bone expansion in Lgals3-deficient mice during aging

Aging and hormonal changes disrupt the balance between bone formation and resorption, leading to reduced bone mass and higher fracture risk. Previous studies have explored galectin-3's role in bone remodeling, but its specific impact on cortical and trabecular bone during aging remains unclear. While it is known that galectin-3 influences cellular processes, its function in bone mass preservation has not been fully established. Researchers have identified galectin-3 as a β-galactoside binding lectin, but its role in anabolic bone processes is still under investigation. No prior work had resolved how galectin-3 deficiency might affect bone mass in both sexes. This uncertainty drove the need to examine the effects of Lgals3 deficiency on bone parameters. The gap in knowledge regarding galectin-3's role in bone anabolism motivated this study. Understanding these mechanisms could provide insights into preventing age-related bone loss.

This study aimed to investigate the effects of galectin-3 deficiency on bone parameters in aging mice. The researchers sought to determine whether Lgals3 deficiency influences cortical and trabecular bone mass. They focused on comparing bone parameters between Lgals3-KO mice and wild-type littermates. The study aimed to clarify whether galectin-3 acts as a negative regulator of bone formation. Researchers hypothesized that galectin-3 deficiency might preserve bone mass during aging. The study also aimed to assess sex-specific differences in bone preservation. By examining osteoblast and osteoclast activity, the team intended to identify the mechanisms behind increased bone mass. Their goal was to determine if galectin-3 disruption could be useful in preventing age-related bone loss.

The researchers used mice with null alleles of the Lgals3 gene and their wild-type littermates. Bone parameters were analyzed at 36 weeks of age to assess aging effects. Histomorphometry was performed to evaluate bone remodeling dynamics. Ex vivo primary cell differentiation assays were conducted to study osteoblast and osteoclast activity. The team measured cortical bone expansion and trabecular bone preservation. They compared male and female Lgals3-KO mice to assess sex-specific effects. Bone mass was evaluated using microcomputed tomography and histological techniques. The study focused on identifying anabolic contributions to increased bone mass.

At 36 weeks, Lgals3-KO mice showed increased cortical bone expansion compared to wild-type controls. Both male and female mutant mice preserved or enhanced bone mass. Female Lgals3-KO mice were protected from age-related trabecular bone loss. Histomorphometry revealed increased osteoblastogenesis in mutant mice. Osteoclastogenesis showed little to no change in Lgals3-KO mice. The increased bone mass was primarily attributed to anabolic processes. Galectin-3 deficiency appeared to enhance bone formation without significant resorption. These findings suggest galectin-3 functions as a negative regulator of bone formation.

The study suggests that galectin-3 acts as a negative regulator of bone formation. Lgals3 deficiency enhances cortical bone expansion during aging. The increased bone mass in mutant mice is primarily due to increased anabolism. Female Lgals3-KO mice show protection from trabecular bone loss. The findings indicate that galectin-3 disruption may help prevent age-related bone loss. The results support the idea that galectin-3 influences osteoblastogenesis. The study does not propose galectin-3 as essential for bone homeostasis. The authors suggest further research to explore galectin-3's role in bone health.