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Periodontitis, which is induced by repeated bacterial invasion and the ensuing immune reactions that follow, is the leading cause of tooth loss. Periodontal tissue is comprised of four different components, each with potential role in pathogenesis, however, most studies on immune responses focus on gingival tissue. Here, we present a modified ligature-induced periodontitis model in male mice to analyze the pathogenesis, which captures the complexity of periodontal tissue. We find that the inflammatory response in the peri-root tissues and the expression of IL-6 and RANKL by Thy-1.2 − fibroblasts/stromal cells are prominent throughout the bone destruction phase, and present already at an early stage. The initiation phase is characterized by high levels of ST2 (encoded by Il1rl1 ) expression in the peri-root tissue, suggesting that the IL-33/ST2 axis is involved in the pathogenesis. Both Il1rl1 - and Il33 -deficient mice exhibit exacerbated bone loss in the acute phase of periodontitis, along with macrophage polarization towards a classically activated phenotype and increased neutrophil infiltration, indicating a protective role of the IL-33/ST2 axis in acute inflammation. Thus, our findings highlight the hidden role of the peri-root tissue and simultaneously advance our understanding of the etiology of periodontitis via implicating the IL-33/ST2 axis. Current animal models of periodontitis are biased towards sample collection from gingival tissue, while other periodontal structures may play similarly important role in the initiation and maintenance of inflammation. Here authors present a model that enables a more comprehensive and longitudinal assessment of periodontal tissues, which points to a pivotal role for the peri-root tissues and an IL-33/ST2 axis in the pathogenesis.

Periodontitis is an inflammatory disease characterized by the destruction of the periodontium. In the last decade, a new murine model of periodontitis has been widely used to simulate alveolar bone resorption and periodontal soft tissue destruction by ligation. Typically, 3-0 to 9-0 silks are selected for ligation around the molars in mice, and significant bone loss and inflammatory infiltration are observed within a week. The ligature-maintained period can vary according to specific aims. We reviewed the findings on the interaction of systemic diseases with periodontitis, periodontal tissue destruction, the immunological and bacteriological responses, and new treatments. In these studies, the activation of osteoclasts, upregulation of pro-inflammatory factors, and excessive immune response have been considered as major factors in periodontal disruption. Multiple genes identified in periodontal tissues partly reflect the complexity of the pathogenesis of periodontitis. The effects of novel treatment methods on periodontitis have also been evaluated in a ligature-induced periodontitis model in mice. This model cannot completely represent all aspects of periodontitis in humans but is considered an effective method for the exploration of its mechanisms. Through this review, we aimed to provide evidence and enlightenment for future studies planning to use this model.

Periodontal disease is a chronic inflammatory disease caused by periodontal bacteria. Recently, periodontal phototherapy, treatment using various types of lasers, has attracted attention. Photobiomodulation, the biological effect of low-power laser irradiation, has been widely studied. Although many types of lasers are applied in periodontal phototherapy, molecular biological effects of laser irradiation on cells in periodontal tissues are unclear. Here, we have summarized the molecular biological effects of diode, Nd:YAG, Er:YAG, Er,Cr:YSGG, and CO2 lasers irradiation on cells in periodontal tissues. Photobiomodulation by laser irradiation enhanced cell proliferation and calcification in osteoblasts with altering gene expression. Positive effects were observed in fibroblasts on the proliferation, migration, and secretion of chemokines/cytokines. Laser irradiation suppressed gene expression related to inflammation in osteoblasts, fibroblasts, human periodontal ligament cells (hPDLCs), and endothelial cells. Furthermore, recent studies have revealed that laser irradiation affects cell differentiation in hPDLCs and stem cells. Additionally, some studies have also investigated the effects of laser irradiation on endothelial cells, cementoblasts, epithelial cells, osteoclasts, and osteocytes. The appropriate irradiation power was different for each laser apparatus and targeted cells. Thus, through this review, we tried to shed light on basic research that would ultimately lead to clinical application of periodontal phototherapy in the future.

Periodontal disease is an inflammatory disease caused by pathogenic oral microorganisms that leads to the destruction of alveolar bone and connective tissues around the teeth. Although many studies have shown that periodontal disease is a risk factor for systemic diseases, such as type 2 diabetes and cardiovascular diseases, the relationship between nonalcoholic fatty liver disease (NAFLD) and periodontal disease has not yet been clarified. Thus, the purpose of this review was to reveal the relationship between NAFLD and periodontal disease based on epidemiological studies, basic research, and immunology. Many cross-sectional and prospective epidemiological studies have indicated that periodontal disease is a risk factor for NAFLD. An in vivo animal model revealed that infection with periodontopathic bacteria accelerates the progression of NAFLD accompanied by enhanced steatosis. Moreover, the detection of periodontopathic bacteria in the liver may demonstrate that the bacteria have a direct impact on NAFLD. Furthermore, Porphyromonas gingivalis lipopolysaccharide induces inflammation and accumulation of intracellular lipids in hepatocytes. Th17 may be a key molecule for explaining the relationship between periodontal disease and NAFLD. In this review, we attempted to establish that oral health is essential for systemic health, especially in patients with NAFLD.

ObjectivesRecently, the application of erbium-doped yttrium aluminum garnet (Er:YAG) laser has been increasing in periodontal therapy. In this retrospective study, we evaluated the safety and effectiveness of a novel pocket therapy using Er:YAG laser in combination with conventional mechanical scaling and root planing treatment (Er:YAG laser-assisted comprehensive periodontal pocket therapy).MethodsForty sites in 29 elderly patients having residual periodontal pockets of ≥ 5 mm depth were treated by curette and Er:YAG laser from 2006 to 2009. After root debridement by curette, laser irradiation was performed on the root surfaces. Then, inflamed connective tissue on the inner gingival surface and on the bone surface/within extant bone defects was thoroughly debrided by curette and laser. Furthermore, in most cases, removal of the outer epithelium and coagulation of the blood clot in the pocket entrance were additionally performed with laser. Clinical parameters were evaluated before and 3, 6, and 12 months after treatment.ResultsWith Er:YAG laser-assisted pocket therapy, debridement of pockets was thoroughly and safely performed, and favorable clinical improvements were observed in most cases, without any adverse side effects and complications. After 1 year, probing pocket depth significantly decreased from 6.4 ± 1.4 to 3.5 ± 1.3 mm (p < 0.001, 3.0 mm reduction), and clinical attachment level significantly decreased from 7.5 ± 1.6 to 5.2 ± 1.9 mm (p < 0.001, 2.3 mm gain).ConclusionThe results of this study indicate that Er:YAG laser-assisted therapy is useful for the treatment of residual pockets as a minimally invasive flapless surgery.Clinical relevanceEr:YAG laser-assisted comprehensive pocket therapy reduces the necessity of more conventional surgical therapies.

Periodontitis is an inflammatory disease caused by pathogenic oral microorganisms that induce the destruction of periodontal tissue. We sought to identify the relevant differentially expressed genes (DEGs) and clarify the mechanism underlying the rapid alveolar bone loss by using ligature-induced periodontitis in mice. A silk ligature was tied around the maxillary left second molar in 9-week-old C57BL/6 J male mice. In-vivo micro-CT analysis revealed that ligation induced severe bone loss. RNA-sequencing analysis, to examine host responses at 3 days post-ligation, detected 12,853 genes with fragments per kilobase of exon per million mapped reads ≥ 1, and 78 DEGs. Gene ontology term enrichment analysis revealed the expression profiles related to neutrophil chemotaxis and inflammatory responses were significantly enriched in the ligated gingiva. The expression levels of innate immune response-related genes, including S100a8 and S100a9 , were significantly higher in the ligated side. S100A8 was strongly detected by immunohistochemistry at the attached epithelium in ligated sites. Inhibition of S100A8 and S100A9 expression revealed that they regulated IL1B and CTSK expression in Ca9-22 cells. Thus, innate immune response-related molecules might be associated with the burst-destruction of periodontal tissue in ligature-induced periodontitis. Especially, S100A8 and S100A9 may play an important role in alveolar bone resorption.

The optimal method for decontamination of implant surfaces for peri-implantitis treatment remains controversial. In recent years, erbium-doped yttrium aluminum garnet (Er:YAG) laser irradiation and implantoplasty (IP) (i.e. mechanical modification of the implant) have been reported to be effective in decontaminating implant surfaces during the surgical treatment. Also, a lack of adequate keratinized mucosa (KM) around the implant is known to be associated with more plaque accumulation, tissue inflammation, attachment loss, and mucosal recession, increasing the risk of peri-implantitis. Therefore, free gingival graft (FGG) has been recommended for gaining adequate KM around the implant. However, the necessity of acquiring KM for the treatment of peri-implantitis using FGG remains unclear. In this report, we applied the apically positioned flap (APF) as resective surgery for peri-implantitis treatment in conjunction with IP and Er:YAG laser irradiation to polish/clean the implant surface. Furthermore, FGG was conducted simultaneously to create additional KM, which increased the tissue stability and contributed to the positive results. The two patients were 64 and 63 years old with a history of periodontitis. The removal of granulation tissue and debridement of contaminated implant surfaces were performed with Er:YAG laser irradiation post flap elevation and then modified smooth surfaces mechanically using IP. Er:YAG laser irradiation was also utilized to remove the titanium particles. In addition, we performed FGG to increase the width of KM as a vestibuloplasty. Peri-implant tissue inflammation and progressive bone resorption were not observed, and both patients maintained good oral hygiene conditions until the 1-year follow-up appointment. Bacterial analysis via high-throughput sequencing revealed proportional decreases in bacteria associated with periodontitis (Porphyromonas, Treponema, and Fusobacterium). To the best of our knowledge, this study is the first to describe peri-implantitis management and bacterial change before and after procedures by resective surgery combined with IP and Er:YAG laser irradiation for peri-implantitis treatment, accompanied by FGG for increasing KM around the implants.

Stroke is associated with multiple forms of disability, including dysphagia. Post-stroke dysphagia increases the risks of pneumonia and mortality and often results in cessation of oral feeding. However, appropriate rehabilitation methods can eventually lead to resumption of oral food intake. This study tried to clarify that re-initiating oral food intake could modify the composition of oral/gut microbial communities in patients with dysphagia. From 78 patients with sub-acute stage of stroke, 11 complete tube feeding subjects without taking antibiotics were enrolled and received rehabilitation for re-initiation of oral food intake, and 8 subjects were brought back to complete oral feeding. Oral and gut microbiota community profiles were evaluated using 16S rRNA sequencing of the saliva and feces samples before and after re-initiation of oral food intake in patients recovering from enteral nutrition under the same nutrient condition. Standard nutrition in the hospital was 1,840 kcal, including protein = 75 g, fat = 45 g, and carbohydrates = 280 g both for tube and oral feeding subjects. Oral food intake increased oral and gut microbiome diversity and altered the composition of the microbiome. Oral and gut microbiome compositions were drastically different; however, the abundance of family and genus was increased in both the oral and gut microbiome after re-initiation of oral food intake. Although oral microbiota showed more significant changes than the gut microbiota, metagenome prediction revealed the presence of more differentially enriched pathways in the gut. In addition, simpler co-occurrence networks of oral and gut microbiomes, indicating improved dysbiosis of the microbiome, were observed during oral feeding as compared to that during tube feeding. Oral food intake affects oral and gut microbiomes in patients recovering from enteral nutrition. Rehabilitation for dysphagia can modify systemic health by increasing the diversity and altering the composition and co-occurrence network structure of oral and gut microbial communities.

Improvement of obesity is important for increasing longevity. The characteristics, size, and function of adipocytes are altered in patients with obesity. Adipose tissue is not only an energy storage but also an endocrine organ. Alteration of endocrine activities in adipose tissue, among them the functional decline of brown adipose tissue (BAT), is associated with obesity. Periodontal disease is a risk factor for systemic diseases since endotoxemia is caused by periodontal bacteria. However, the effect of periodontal disease on obesity remains unclear. Thus, this study aimed to investigate the effect of endotoxemia due to Porphyromonas gingivalis , a prominent cause of periodontal disease, on the BAT. Herein, endotoxemia was induced in 12-week-old C57BL/6J mice through intravenous injection of sonicated 10 8 CFU of P. gingivalis (Pg) or saline (control [Co]) once. Eighteen hours later, despite no inflammatory M1 macrophage infiltration, inflammation-related genes were upregulated exclusively in the BAT of Pg mice compared with Co mice. Although no marked histological changes were observed in adipose tissues, expressions of genes related to lipolysis, Lipe and Pnpla2 were downregulated after P. gingivalis injection in BAT. Furthermore, expression of Pparg and Adipoq was downregulated only in the BAT but not in the white adipose tissues, along with downregulation of Ucp1 and Cidea expression, which are BAT-specific markers, in Pg mice. Microarray analysis of the BAT showed 106 differentially expressed genes between Co and Pg mice. Gene set enrichment analysis revealed that the cholesterol homeostasis gene set and PI3/Akt/mTOR signaling gene set in BAT were downregulated, whereas the TGF-β signaling gene set was enriched in Pg mice. Overall, intravenous injection of sonicated P. gingivalis altered the endocrine functions of the BAT in mice. This study indicates that endotoxemia by P. gingivalis potentially affects obesity by disrupting BAT function.

Ancient dental calculus, formed from dental plaque, is a rich source of ancient DNA and can provide information regarding the food and oral microbiology at that time. Genomic analysis of dental calculus from Neanderthals has revealed the difference in bacterial composition of oral microbiome between Neanderthals and modern humans. There are few reports investigating whether the pathogenic bacteria of periodontitis, a polymicrobial disease induced in response to the accumulation of dental plaque, were different between ancient and modern humans. This study aimed to compare the bacterial composition of the oral microbiome in ancient and modern human samples and to investigate whether lifestyle differences depending on the era have altered the bacterial composition of the oral microbiome and the causative bacteria of periodontitis. Additionally, we introduce a novel diagnostic approach for periodontitis in ancient skeletons using micro-computed tomography. Ancient 16S rDNA sequences were obtained from 12 samples at the Unko-in site (18th-19th century) of the Edo era (1603–1867), a characteristic period in Japan when immigrants were not accepted. Furthermore, modern 16S rDNA data from 53 samples were obtained from a database to compare the modern and ancient microbiome. The microbial co-occurrence network was analyzed based on 16S rDNA read abundance. Eubacterium species, Mollicutes species, and Treponema socranskii were the core species in the Edo co-occurrence network. The co-occurrence relationship between Actinomyces oricola and Eggerthella lenta appeared to have played a key role in causing periodontitis in the Edo era. However, Porphyromonas gingivalis, Fusobacterium nucleatum subsp. vincentii , and Prevotella pleuritidis were the core and highly abundant species in the co-occurrence network of modern samples. These results suggest the possibility of differences in the pathogens causing periodontitis during different eras in history.