Boric acid inhibits alveolar bone loss in rat experimental periodontitis through diminished bone resorption and enhanced osteoblast formation

Abstract

Background/purpose Inhibition of bone resorption is essential for periodontal treatment. Recently, it has been suggested that boric acid suppresses periodontitis, but the mechanism of this inhibition is still not well understood. Therefore, to analyze the cellular response to boric acid administration, we histologically evaluated alveolar bone in experimental periodontitis of rats administered boric acid. Materials and methods 5-0 silk ligatures were placed around the cervix of the second maxillary molars of 4 week-old rats treated with or without boric acid. Five and 14 days after ligature placement, the periodontal tissues between first and second molars were investigated histologically and immunohistochemically using antibodies to CD68, cathepsin K, and α-smooth muscle actin (SMA). Results Five days after the beginning of the experiment, many CD68-positive cells appeared in the periodontal tissues with ligature placement without boric acid administration. Also, the number of cathepsin K-positive osteoclasts had increased on the surface of alveolar bone. However, boric acid administration prevented severe bone resorption and reduced the number of cells positive for CD68 and cathepsin K. At day 14 post treatment, cells positive for α-SMA were seen in the periodontal tissues after boric acid administration, whereas no such cells were found around the alveolar bone without the administration of boric acid. Conclusion Boric acid inhibited the inflammation of ligature-induced periodontitis. This agent might reduce bone resorption by inhibiting osteoclastogenesis and also could accelerate osteoblastogenesis.

Synthesis of Silica-Based Boron-Incorporated Collagen/Human Hair Keratin Hybrid Cryogels with the Potential Bone Formation Capability

“…We believe that this might be due to the inorganic part of the hybrid cryogels (silicone and boron), which may provide a desirable microenvironment for the differentiation of the hAMSCs to the osteoblastic lineage. Furthermore, improving effects on the early phase bone mineralization and in vitro osteogenic differentiation of boron-based and silicon-based materials has also been previously demonstrated by several groups. Finally, these visual evaluations were also confirmed by quantitative RT-PCR analysis.…”

Nasal obstruction promotes alveolar bone destruction in the juvenile rat model

“…Chronic inflammation causes bone resorption by the activation of osteoclasts. 23 , 24 Inflammatory cytokines such as TNF-α and IL-6 and increased expression of RAGE enhances osteoclast differentiation. 25 , 26 , 27 As expected, expression of RANKL, a marker of osteoclast was increased by nasal obstruction.…”

Gremlin aggravates periodontitis via activation of the nuclear factor‐kappa B signaling pathway

“…1 Under pathological settings such as inflammation, a disturbance is induced during bone remodeling activity; either osteoblastogenesis is aberrantly suppressed to decrease bone formation or osteoclastogenesis is markedly activated to exceed bone formation and finally leading to bone loss, as seen in periodontitis. 2 Periodontitis is an inflammatory and infectious disease mainly caused by the colonization of gram negative bacteria in periodontal tissues, 3 and the pathological and clinical feature is characterized by alveolar bone loss, which eventually leads to tooth loss and seriously affects the life quality of periodontitis patients. 4 Numerous studies have unveiled the major molecules or signaling pathways responsible for the inflammationinduced alveolar bone loss, such as the nuclear factor kappa B (NF-κB).…”