ABSTRACT
OBJECTIVE: The aim of this Technical note is to present a new assessment method of alveolar bone grafts after secondary alveolar bone grafting using automatic registration and artificial intelligence (AI)-based segmentation. METHODS: A total of 7 Japanese patients (4 men and 3 women) with a unilateral cleft lip, alveolus, and/or palate, who underwent secondary alveolar bone grafting between March 2021 and August 2022 were evaluated. Computed tomography (CT) analyses were performed about 1 month before the surgery, and 1 day and 6 months after the surgery. All CT images were imported into a 3-dimensional analysis workstation. CT images from after the surgery were superimposed onto CT images from before the surgery, by automatic rigid image registration. The segmentation of bone tissues was automatically performed by the AI-based function. Grafted bone was extracted by subtraction of the bone tissue after the surgery from the bone tissue before the surgery. The volumes and Hounsfield units (HUs) of the grafted bones were calculated. The intraclass correlation coefficient (ICC) was reviewed to assess inter-rater reliability. RESULTS: The ICCs (2,1) of the volumes and HUs measured by the observers immediately after the surgery were 0.95 and 0.99, respectively. On the other hand, the ICCs (2,1) of the volumes and HUs measured by the observers 6 months after the surgery were 0.81 and 0.57, respectively. CONCLUSIONS: Our new assessment method enables simple and quick evaluation of residual grafted bone after secondary alveolar bone grafting and demonstrated relatively high inter-rater reliability.
ABSTRACT
Nitric oxide and reactive oxygen species regulate bone remodeling, which occurs via bone formation and resorption by osteoblasts and osteoclasts, respectively. Recently, we found that 8-nitro-cGMP, a second messenger of nitric oxide and reactive oxygen species, promotes osteoclastogenesis. Here, we investigated the formation and function of 8-nitro-cGMP in osteoblasts. Mouse calvarial osteoblasts were found to produce 8-nitro-cGMP, which was augmented by tumor necrosis factor-α (10â ng/ml) and interleukin-1ß (1â ng/ml). These cytokines suppressed osteoblastic differentiation in a NO synthase activity-dependent manner. Exogenous 8-nitro-cGMP (30â µmol/L) suppressed expression of osteoblastic phenotypes, including mineralization, in clear contrast to the enhancement of mineralization by osteoblasts induced by 8-bromo-cGMP, a cell membrane-permeable analog of cGMP. It is known that reactive sulfur species denitrates and degrades 8-nitro-cGMP. Mitochondrial cysteinyl-tRNA synthetase plays a crucial role in the endogenous production of RSS. The expression of osteoblastic phenotypes was suppressed by not only exogenous 8-nitro-cGMP but also by silencing of the Cars2 gene, indicating a role of endogenous 8-nitro-cGMP in suppressing the expression of osteoblastic phenotypes. These results suggest that 8-nitro-cGMP is a negative regulator of osteoblastic differentiation.
ABSTRACT
Osteoblasts produce the receptor activator of nuclear factor-kappa B ligand (RANKL) and osteoprotegerin, the inducer and the suppressor of osteoclast differentiation and activation. We previously proposed that the degradation of osteoprotegerin by lysine-specific gingipain of Porphyromonas gingivalis and neutrophil elastase is one of the mechanisms of bone resorption associated with infection and inflammation. In the present study, we found that cathepsin K (CTSK) also degraded osteoprotegerin in an acidic milieu and the buffer with a pH of 7.4. The 37 k fragment of osteoprotegerin produced by the reaction with CTSK was further degraded into low molecular weight fragments, including a 13 k fragment, depending on the reaction time. The N-terminal amino acid sequence of the 37 k fragment matched that of the intact osteoprotegerin, indicating that CTSK preferentially hydrolyzes the death domain-like region of osteoprotegerin, not its RANKL-binding region. The 13 k fragment of osteoprotegerin was the C-terminal 13 k portion within the RANKL-binding region of the 37 k fragment. Finally, CTSK restored RANKL-dependent osteoclast differentiation that was suppressed by the addition of osteoprotegerin. Collectively, CTSK is a possible positive regulator of osteoclastogenesis.
Subject(s)
Osteogenesis , Osteoprotegerin , Animals , Osteoprotegerin/metabolism , Cathepsin K/metabolism , Glycoproteins/metabolism , Osteoclasts/metabolism , Receptor Activator of Nuclear Factor-kappa B/metabolism , Membrane Glycoproteins/metabolism , Receptors, Cytoplasmic and Nuclear/metabolism , Carrier Proteins/metabolism , RANK Ligand/metabolism , Cell DifferentiationABSTRACT
Sagittal split ramus osteotomy (SSRO) sometimes induces an irregular split pattern referred to as a bad split. We investigated the risk factors for bad splits in the buccal plate of the ramus during SSRO. Ramus morphology and bad splits in the buccal plate of the ramus were assessed using preoperative and postoperative computed tomography images. Of the 53 rami analyzed, 45 had a successful split, and 8 had a bad split in the buccal plate. Horizontal images at the height of the mandibular foramen showed that there were significant differences in the ratio of the forward thickness to the backward thickness of the ramus between patients with a successful split and those with a bad split. In addition, the distal region of the cortical bone tended to be thicker and the curve of the lateral region of the cortical bone tended to be smaller in the bad split group than in the good split group. These results indicated that a ramus shape in which the width becomes thinner towards the back frequently induces bad splits in the buccal plate of the ramus during SSRO, and more attention should be paid to patients who have rami of these shapes in future surgeries.
Subject(s)
Cortical Bone , Osteotomy, Sagittal Split Ramus , Humans , Osteotomy, Sagittal Split Ramus/adverse effects , Risk Factors , Bone Plates , Polymers , Tomography, X-Ray ComputedABSTRACT
Neutrophils are one of the most abundant leukocytes in the sites of lesion of inflammatory diseases such as periodontitis and rheumatoid arthritis. These diseases are accompanied by bone loss, which worsens the quality of life of the patients. However, the role of neutrophils in the inflammatory bone loss has not been fully investigated. In the present study, we found that human neutrophils enhanced osteoclast differentiation from mouse bone marrow cells co-cultured with mouse osteoblasts in the presence of active vitamin D3. The enhanced osteoclast differentiation was significantly suppressed by elastatinal, a synthetic inhibitor of neutrophil elastase. Also, we found that human neutrophils degraded human recombinant osteoprotegerin (OPG), a decoy receptor for nuclear factor κB (RANK) ligand (RANKL), the essential osteoclast differentiation-inducing factor, expressed by osteoblasts. Degradation of OPG by neutrophils was suppressed by human α1-protease inhibitor, the major endogenous inhibitor of neutrophil elastase. Recombinant human neutrophil elastase degraded human OPG in its death domain-like region. These results indicated that the degradation of OPG by elastase contributed at least in part to the enhanced osteoclast differentiation by neutrophils. There is a possibility that neutrophils play an important role in inflammatory bone loss.