Journal articles: 'Mice – Aging; Periodontal ligament – Aging'

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Foster, B. L., Y. Soenjaya, F. H. Nociti, E. Holm, P. M. Zerfas, H. F. Wimer, D. W. Holdsworth, et al. "Deficiency in Acellular Cementum and Periodontal Attachment in Bsp Null Mice." Journal of Dental Research 92, no. 2 (November 26, 2012): 166–72. http://dx.doi.org/10.1177/0022034512469026.

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Bone sialoprotein (BSP) is an extracellular matrix protein found in mineralized tissues of the skeleton and dentition. BSP is multifunctional, affecting cell attachment and signaling through an RGD integrin-binding region, and acting as a positive regulator for mineral precipitation by nucleating hydroxyapatite crystals. BSP is present in cementum, the hard tissue covering the tooth root that anchors periodontal ligament (PDL) attachment. To test our hypothesis that BSP plays an important role in cementogenesis, we analyzed tooth development in a Bsp null (-/-) mouse model. Developmental analysis by histology, histochemistry, and SEM revealed a significant reduction in acellular cementum formation on Bsp-/- mouse molar and incisor roots, and the cementum deposited appeared hypomineralized. Structural defects in cementum-PDL interfaces in Bsp-/- mice caused PDL detachment, likely contributing to the high incidence of incisor malocclusion. Loss of BSP caused progressively disorganized PDL and significantly increased epithelial down-growth with aging. Bsp-/- mice displayed extensive root and alveolar bone resorption, mediated by increased RANKL and the presence of osteoclasts. Results collected here suggest that BSP plays a non-redundant role in acellular cementum formation, likely involved in initiating mineralization on the root surface. Through its importance to cementum integrity, BSP is essential for periodontal function.

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Kim, Yu Gyung, Sang Min Lee, Sungeun Bae, Taejun Park, Hyeonjin Kim, Yujeong Jang, Keonwoo Moon, et al. "Effect of Aging on Homeostasis in the Soft Tissue of the Periodontium: A Narrative Review." Journal of Personalized Medicine 11, no. 1 (January 18, 2021): 58. http://dx.doi.org/10.3390/jpm11010058.

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Aging is characterized by a progressive decline or loss of physiological functions, leading to increased susceptibility to disease or death. Several aging hallmarks, including genomic instability, cellular senescence, and mitochondrial dysfunction, have been suggested, which often lead to the numerous aging disorders. The periodontium, a complex structure surrounding and supporting the teeth, is composed of the gingiva, periodontal ligament, cementum, and alveolar bone. Supportive and protective roles of the periodontium are very critical to sustain life, but the periodontium undergoes morphological and physiological changes with age. In this review, we summarize the current knowledge of molecular and cellular physiological changes in the periodontium, by focusing on soft tissues including gingiva and periodontal ligament.

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Benatti, Bruno Braga, Karina Gonzales Silvério, Márcio Zaffalon Casati, Enilson Antônio Sallum, and Francisco Humberto Nociti. "Influence of Aging on Biological Properties of Periodontal Ligament Cells." Connective Tissue Research 49, no. 6 (January 2008): 401–8. http://dx.doi.org/10.1080/03008200802171159.

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Moxham, B. J., and I. L. Evans. "The Effects of Aging upon the Connective Tissues of the Periodontal Ligament." Connective Tissue Research 33, no. 1-3 (January 1995): 31–35. http://dx.doi.org/10.3109/03008209509016978.

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Zanoni, Jacqueline N., Nathalia M. Lucas, Aline R. Trevizan, and Ivan D. S. Souza. "Histological evaluation of the periodontal ligament from aged wistar rats supplemented with ascorbic acid." Anais da Academia Brasileira de Ciências 85, no. 1 (March 1, 2013): 327–35. http://dx.doi.org/10.1590/s0001-37652013005000003.

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Ascorbic acid (AA) is able to neutralize reactive oxygen species and is essential for collagen synthesis. In aging process oxidative stress is elevated. This study aims to investigate the effects of AA supplementation on the periodontal ligament (PL) of rats during aging. Twenty five rats were used and divided into groups: J90 (90-day-old control), E345 (345-day-old control), E428 (428-day-old control), EA345 (345-day-old supplemented with AA from 90-day-old on) and EA428 (428-day-old supplemented with AA from 90-day-old on). We analyzed the thickness, density of fibroblasts and blood vessels and collagen fibers types in the PL. In group J90 there was predominantly type III collagen fibers (87.64%). In animals supplemented with AA, the area filled by type I fibers (group EA345: 65.67%, group EA428: 52.23%) was higher than type III fibers. PL in group EA428 was thicker than the one observed in group E428 (P < 0.05). During natural aging process, AA promoted the maturation of collagen fibers and enhanced angiogenesis in periodontal ligament. One can conclude that the supplementation with AA represented a beneficial factor for the development of PL in aged rats.

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Li, Qian, Yushi Ma, Yunyan Zhu, Ting Zhang, and Yanheng Zhou. "Declined Expression of Histone Deacetylase 6 Contributes to Periodontal Ligament Stem Cell Aging." Journal of Periodontology 88, no. 1 (January 2017): e12-e23. http://dx.doi.org/10.1902/jop.2016.160338.

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Shimizu, N., T. Goseki, M. Yamaguchi, T. Iwasawa, H. Takiguchi, and Y. Abiko. "In vitro Cellular Aging Stimulates Interleukin-1β Production in Stretched Human Periodontal-ligament-derived Cells." Journal of Dental Research 76, no. 7 (July 1997): 1367–75. http://dx.doi.org/10.1177/00220345970760070601.

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Although the severity of periodontal disease is known to be affected by host age, the pathological role of aging in periodontal disease, and especially that attributable to trauma from occlusion, has not been well-characterized. Interleukin (IL)-1β is a key mediator involved in periodontal diseases, a potent stimulator of bone resorption. Furthermore, it is produced by human periodontal ligament (PDL) cells in response to mechanical stress. To investigate the age-related changes in the biosynthetic capacity of IL-1β in PDL cells, we examined the effects of in vitro cellular aging with mechanical stress on IL-1β protein and gene expression by human PDL cells. Human PDL cells (young = 5th or 6th passage; old = 18-20th passage) were cultured on flexible-bottomed culture plates, and the cells were deformed at 6 cycles per min at 2 steps of tension force for 1 to 5 days. We found a two-fold increase in IL-lp production by old PDL cells subjected to mechanical tension compared with that by young PDL cells, although the constitutive levels of IL-1β were similar in both the young and old PDL cells. This increase was tension-dependent. IL-1β mRNA was also detected in both the cell types under basal conditions, and its expression was further enhanced by application of mechanical tension by use of reverse-transcription-polymerase chain-reaction (RT-PCR) and in situ hybridization methods. The increase in signal rate was higher in the old cells than in the young cells. IL-1β-converting enzyme mRNA remained unchanged. It is possible that a large amount of IL-1β produced by PDL cells from an aged host in response to mechanical force may be positively related to the accleration of alveolar bone resorption.

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Fang, Hui, Kun Yang, Ping Tang, Na Zhao, Rui Ma, Xin Luo, and Qi Liu. "Glycosylation end products mediate damage and apoptosis of periodontal ligament stem cells induced by the JNK-mitochondrial pathway." Aging 12, no. 13 (June 30, 2020): 12850–68. http://dx.doi.org/10.18632/aging.103304.

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Benatti, Bruno Braga, Karina Gonzales Silvério, Márcio Zaffalon Casati, Enilson Antônio Sallum, and Francisco Humberto Nociti Jr. "Inflammatory and bone-related genes are modulated by aging in human periodontal ligament cells." Cytokine 46, no. 2 (May 2009): 176–81. http://dx.doi.org/10.1016/j.cyto.2009.01.002.

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Zhang, Yunyan, Yuzhi Yang, Mingxue Xu, Jingwen Zheng, Yuchan Xu, Guoqing Chen, Qiang Guo, Weidong Tian, and Weihua Guo. "The Dual Effects of Reactive Oxygen Species on the Mandibular Alveolar Bone Formation in SOD1 Knockout Mice: Promotion or Inhibition." Oxidative Medicine and Cellular Longevity 2021 (February 3, 2021): 1–15. http://dx.doi.org/10.1155/2021/8847140.

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The status of reactive oxygen species (ROS) correlates closely with the normal development of the oral and maxillofacial tissues. Oxidative stress caused by ROS accumulation not only affects the development of enamel and dentin but also causes pathological changes in periodontal tissues (periodontal ligament and alveolar bone) that surround the root of the tooth. Although previous studies have shown that ROS accumulation plays a pathologic role in some oral and maxillofacial tissues, the effects of ROS on alveolar bone development remain unclear. In this study, we focused on mandibular alveolar bone development of mice deficient in superoxide dismutase1 (SOD1). Analyses were performed using microcomputerized tomography (micro-CT), TRAP staining, immunohistochemical (IHC) staining, and enzyme-linked immunosorbent assay (ELISA). We found for the first time that slightly higher ROS in mandibular alveolar bone of SOD1(-/-) mice at early ages (2-4 months) caused a distinct enlargement in bone size and increased bone volume fraction (BV/TV), trabecular thickness (Tb.Th), and expression of alkaline phosphatase (ALP), Runt-related transcription factor 2 (Runx2), and osteopontin (OPN). With ROS accumulation to oxidative stress level, increased trabecular bone separation (Tb.Sp) and decreased expression of ALP, Runx2, and OPN were found in SOD1(-/-) mice at 6 months. Additionally, dosing with N-acetylcysteine (NAC) effectively mitigated bone loss and normalized expression of ALP, Runx2, and OPN. These results indicate that redox imbalance caused by SOD1 deficiency has dual effects (promotion or inhibition) on mandibular alveolar bone development, which is closely related to the concentration of ROS and the stage of growth. We present a valuable model here for investigating the effects of ROS on mandibular alveolar bone formation and highlight important roles of ROS in regulating tissue development and pathological states, illustrating the complexity of the redox signal.

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Tan, Jingyi, Anna Dai, Lai Pan, Lan Zhang, Zhongxiu Wang, Ting Ke, Weilian Sun, Yanmin Wu, Pei-Hui Ding, and Lili Chen. "Inflamm-Aging-Related Cytokines of IL-17 and IFN-γ Accelerate Osteoclastogenesis and Periodontal Destruction." Journal of Immunology Research 2021 (August 4, 2021): 1–12. http://dx.doi.org/10.1155/2021/9919024.

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Periodontal disease (PD), as an age-related disease, prevalent in middle-aged and elderly population, is characterized as inflammatory periodontal tissue loss, including gingival inflammation and alveolar bone resorption. However, the definite mechanism of aging-related inflammation in PD pathology needs further investigation. Our study is aimed at exploring the effect of inflamm-aging-related cytokines of interleukin-17 (IL-17) and interferon-γ (IFN-γ) on osteoclastogenesis in vitro and periodontal destruction in vivo. For receptor activator of nuclear factor-κB ligand- (RANKL-) primed bone marrow macrophages (BMMs), IL-17 and IFN-γ enhanced osteoclastogenesis, with the expression of osteoclastogenic mRNA (TRAP, c-Fos, MMP-9, Ctsk, and NFATc1) and protein (c-Fos and MMP-9) upregulated. Ligament-induced rat models were established to investigate the role of IL-17 and IFN-γ on experimental periodontitis. Both IL-17 and IFN-γ could enhance the local inflammation in gingival tissues. Although there might be an antagonistic interaction between IL-17 and IFN-γ, IL-17 and IFN-γ could facilitate alveolar bone loss and osteoclast differentiation.

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Li, Xiaoyu, Bowen Zhang, Hong Wang, Xiaolu Zhao, Zijie Zhang, Gang Ding, and Fulan Wei. "Aging affects responsiveness of peripheral blood mononuclear cells to immunosuppression of periodontal ligament stem cells." Journal of International Medical Research 48, no. 7 (July 2020): 030006052093085. http://dx.doi.org/10.1177/0300060520930853.

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Objectives The effect of age on the response of peripheral blood mononuclear cells (PBMCs) to immunosuppression induced by human periodontal ligament stem cells (hPDLSCs) is unclear. The identity of the cytokines most effective in inducing the PBMC immune response remains unknown. This study investigated the effects of age on immunophenotype, proliferation, activation, and cytokine secretion capacities of PBMCs following co-culture with hPDLSCs. Methods PBMCs were collected from younger (16–19 years) and older (45–55 years) donors, then co-cultured with confirmed hPDLSCs for various lengths of time. T lymphocyte proliferation and cell surface marker expression were analyzed by flow cytometry. Cytokine expression levels were measured by quantitative polymerase chain reaction assays and enzyme-linked immunosorbent assays. Results CD28 expression by T lymphocytes decreased with age, indicating reduced proliferation; CD95 expression increased with age, indicating enhanced apoptosis. Moreover, hPDLSCs inhibited T lymphocyte proliferation in both age groups; this inhibition was stronger in cells from older donors than in cells from younger donors. Age reduced the secretion of interleukin-2 and interferon-γ, whereas it increased the secretion of tumor necrosis factor-β by PBMCs cultured with hPDLSCs. Conclusions Aging may have a robust effect on the response of PBMCs towards hPDLSC-induced immunosuppression.

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Miura, Shigeru, Masaru Yamaguchi, Noriyoshi Shimizu, and Yoshimitsu Abiko. "Mechanical stress enhances expression and production of plasminogen activator in aging human periodontal ligament cells." Mechanisms of Ageing and Development 112, no. 3 (January 2000): 217–31. http://dx.doi.org/10.1016/s0047-6374(99)00095-0.

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Aung, Kyaw Thu, Kentaro Akiyama, Masayoshi Kunitomo, Aung Ye Mun, Ikue Tosa, Ha Thi Thu Nguyen, Jiewen Zhang, et al. "Aging-Affected MSC Functions and Severity of Periodontal Tissue Destruction in a Ligature-Induced Mouse Periodontitis Model." International Journal of Molecular Sciences 21, no. 21 (October 30, 2020): 8103. http://dx.doi.org/10.3390/ijms21218103.

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Mesenchymal stem cells (MSCs) are known to play important roles in the repair of lost or damaged tissues and immunotolerance. On the other hand, aging is known to impair MSC function. However, little is currently known about how aged MSCs affect the host response to the local inflammatory condition and tissue deterioration in periodontitis, which is a progressive destructive disease of the periodontal tissue potentially leading to multiple tooth loss. In this study, we examined the relationship between aging-induced impairment of MSC function and the severity of periodontal tissue destruction associated with the decrease in host immunomodulatory response using a ligature-induced periodontitis model in young and aged mice. The results of micro computerized tomography (micro-CT) and histological analysis revealed a more severe bone loss associated with increased osteoclast activity in aged (50-week-old) mice compared to young (5-week-old) mice. Immunostaining analysis revealed that, in aged mice, the accumulation of inflammatory T and B cells was higher, whereas the percentage of platelet-derived growth factor receptor α (PDGFRα)+ MSCs, which are known to modulate the apoptosis of T cells, was significantly lower than in young mice. In vitro analysis of MSC function showed that the expression of surface antigen markers for MSCs (Sca-1, CD90, CD146), colony formation, migration, and osteogenic differentiation of aged MSCs were significantly declined compared to those of young MSCs. Moreover, a significantly higher proportion of aged MSCs were positive for the senescence-associated β galactosidase activity. Importantly, aged MSCs presented a decreased expression of FAS-L, which was associated with a lower immunomodulatory property of aged MSCs to induce T cell apoptosis in co-cultures compared with young MSCs. In summary, this is the first study showing that aging-induced impairment of MSC function, including immunomodulatory response, is potentially correlated with progressive periodontal tissue deterioration.

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Liu, Yi, Chunpeng Liu, Ankui Zhang, Shichang Yin, Ting Wang, Yan Wang, Meiming Wang, et al. "Down-regulation of long non-coding RNA MEG3 suppresses osteogenic differentiation of periodontal ligament stem cells (PDLSCs) through miR-27a-3p/IGF1 axis in periodontitis." Aging 11, no. 15 (August 9, 2019): 5334–50. http://dx.doi.org/10.18632/aging.102105.

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Zhang, Jing, Ying An, Li-Na Gao, Yong-Jie Zhang, Yan Jin, and Fa-Ming Chen. "The effect of aging on the pluripotential capacity and regenerative potential of human periodontal ligament stem cells." Biomaterials 33, no. 29 (October 2012): 6974–86. http://dx.doi.org/10.1016/j.biomaterials.2012.06.032.

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Ohi, T., Y. Uehara, M. Takatsu, M. Watanabe, and T. Ono. "Hypermethylation of CpGs in the Promoter of the COL1A1 Gene in the Aged Periodontal Ligament." Journal of Dental Research 85, no. 3 (March 2006): 245–50. http://dx.doi.org/10.1177/154405910608500308.

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Although the human periodontal ligament shows age-associated histological alterations, the molecular mechanisms are not yet understood. We previously found that COL1A1 gene expression declines with age. In this study, we asked whether DNA methylation in the regulatory region of the gene alters in the aging process, as a possible cause of the decline. The method used was a bisulfite modification of cytosine and nucleotide sequencing of DNA. While the 1st intron region was kept demethylated at young and old ages, the levels of methylation at most CpG sites in the proximal and distal regions of the promoter showed elevation at older ages. Analysis of the data indicates the possible importance of DNA hypermethylation in the promoter region for the age-associated decrease of COL1A1 gene expression.

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Ohzeki, Kimimaro, Masaru Yamaguchi, Noriyoshi Shimizu, and Yoshimitsu Abiko. "Effect of cellular aging on the induction of cyclooxygenase-2 by mechanical stress in human periodontal ligament cells." Mechanisms of Ageing and Development 108, no. 2 (May 1999): 151–63. http://dx.doi.org/10.1016/s0047-6374(99)00006-8.

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Mayahara, Kotoe, Yasuko Kobayashi, Kiyomi Takimoto, Naoto Suzuki, Narihiro Mitsui, and Noriyoshi Shimizu. "Aging stimulates cyclooxygenase-2 expression and prostaglandin E2production in human periodontal ligament cells after the application of compressive force." Journal of Periodontal Research 42, no. 1 (February 2007): 8–14. http://dx.doi.org/10.1111/j.1600-0765.2006.00885.x.

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Lossdörfer, S., D. Kraus, and A. Jäger. "Aging affects the phenotypic characteristics of human periodontal ligament cells and the cellular response to hormonal stimulation in vitro." Journal of Periodontal Research 45, no. 6 (July 29, 2010): 764–71. http://dx.doi.org/10.1111/j.1600-0765.2010.01297.x.

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Koliyath, Sulakshana, Nandakumar Vijayaragavan, and Manoj Manoharan. "Expression patterns of miR-34b, miR-34c, and miR-141 during aging and mechanical force application in periodontal ligament cells." Journal of Indian Orthodontic Society 50, no. 3 (September 2016): 171–76. http://dx.doi.org/10.4103/0301-5742.186379.

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Koliyath, Sulakshana, Nandakumar Vijayaragavan, and Manoj Manoharan. "Expression patterns of miR-34b, miR-34c, and miR-141 during aging and mechanical force application in periodontal ligament cells." Journal of Indian Orthodontic Society 50, no. 3 (September 2016): 171–76. http://dx.doi.org/10.1177/0974909820160307.

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Goseki, Takemi, Noriyoshi Shimizu, Tadamasa Iwasawa, Hisashi Takiguchi, and Yoshimitsu Abiko. "Effects of in vitro cellular aging on alkaline phosphatase, cathepsin activities and collagen secretion of human periodontal ligament derived cells." Mechanisms of Ageing and Development 91, no. 3 (November 1996): 171–83. http://dx.doi.org/10.1016/s0047-6374(96)01785-x.

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Trubiani, O., R. Di Primio, T. Traini, J. Pizzicannella, A. Scarano, A. Piattelli, and S. Caputi. "Morphological and Cytofluorimetric Analysis of Adult Mesenchymal Stem Cells Expanded Ex Vivo from Periodontal Ligament." International Journal of Immunopathology and Pharmacology 18, no. 2 (April 2005): 213–21. http://dx.doi.org/10.1177/039463200501800204.

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Many adult tissues contain a population of stem cells that have the ability of regeneration after trauma, disease or aging. Recently, there has been great interest in mesenchymal stem cells and their roles in maintaining physiological structure tissues and their studies have been considered very important and intriguing after having shown that this cell population can be expanded ex vivo to regenerate tissues not only of the mesenchymal lineage, such as intervertebral disc cartilage, bone, tooth-associated tissue, cardiomyocytes, but also to differentiate into cells derived from other embryonic layers, including neurons. Currently, different efforts have been focused on the identification of odontogenic progenitors from oral tissues. In this study we isolated and characterized a population of homogeneous human mesenchymal stem cells proliferating in culture with an attached well-spread morphology derived from periodontal ligament, tissue of ectomesenchymal origin, with the ability to form a specialized joint between alveolar bone and tooth. The adherent cells were harvested and expanded ex vivo under specific conditions and analysed by FACScan flow cytometer and morphological analysis was carried out by light, scanning and transmission electron microscopy. Our results displayed highly evident cells with a fibroblast like morphology and a secretory apparatus, probably indicating, that the enhanced function of the secretory apparatus of the mesenchymal stem cells may be associated with the secretion of molecules that are required to survive and proliferate. Moreover, the presence in periodontal ligament of CD90, CD29, CD44, CD166, CD 105, CD13 positive cells, antigens that are also identified as stromal precursors of the bone marrow, indicate that the periodontal ligament may turn out to be a new efficient source of the cells with intrinsic capacity to self-renewal, high ability to proliferate and differentiate, that can be utilized for a new approach to regenerative medicine and tissue engineering.

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Pant, Bhawana Neupane, Rajesh Kumar Goit, Biswas Satyal, and Abhishek Poudel. "Prevalence of Periodontitis among the People with Diabetes Mellitus." Journal of Nepalgunj Medical College 18, no. 2 (August 9, 2021): 72–74. http://dx.doi.org/10.3126/jngmc.v18i2.38915.

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Introduction: Diabetes mellitus is a metabolic disorder characterized by a chronic high level of blood sugar with disturbances in carbohydrate, fat, and protein metabolism resulting from defects in insulin secretion, action or both. Periodontitis is a chronic infectious disease which leads to the destruction of the periodontal ligament fibers and alveolar bone until tooth loss. Among the several factors that may manifest periodontitis like aging, genetic factors, poor oral hygiene, obesity and virulence of the attacking micro-organisms, type 2 diabetes mellitus has received the greatest attention. Aims: The aim of the study was to determine the association type 2 diabetes mellitus with periodontal condition among population in mid-western region of Nepal. Methods: We screened 200 subjects of age group from 30 to 50 years and divided into two groups: Group I – diabetic person and Group II were non diabetic. Oral examination was done to get the Community Periodontal Index of Treatment Need score and correlation between Diabetes mellitus and periodontal disease was determined. Results: Our result showed strong correlation between diabetes mellitus and periodontitis. When the evaluation was done for prevalence of periodontal disease according to diabetes mellitus, the prevalence of periodontal disease was significantly higher in diabetic person compared to non-diabetic individuals (88% vs 74.4%, P=0.03). [Odds Ratio = 11.826 and 95% confidence interval: 5.415-21.828]. Conclusion: Provided Diabetes mellitus related morbidity and mortality is burgeoning in our society and it is imperative to identify right indicators of periodontal disease for specific population.

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Caracostea Objelean, Adriana, Anca Labunet, Laura Silaghi-Dumitrescu, Marioara Moldovan, Sorina Sava, and Mindra Eugenia Badea. "In Vitro Chewing Simulation Model Influence on the Adhesive-Tooth Structure Interface." Key Engineering Materials 695 (May 2016): 77–82. http://dx.doi.org/10.4028/www.scientific.net/kem.695.77.

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Loss of hard dental tissues of the posterior teeth during caries removal represents an important issue for conservative dentistry. The use of direct dental biomaterials in this case have to satisfy the requirements of the restored area. The studies have shown higher values of chewing forces at the molar teeth level (20-120N) compared to other teeth [1,2]. Thus, for a long-term clinical success the dental biomaterials have to assure a good marginal sealing and a high resistance to thermal and mechanical stresses developed in the lateral zones of the oral cavity [3]. The aim of this study was carried out to assess the effect of an in vitro chewing simulation model on the adhesively-bonded resin composite restorations. Standardized extended proximal cavities were prepared and restored in forty five sound human third molars. Three in vitro aging methods: a chewing simulation model (mechanical cycling and periodontal ligament simulation) (MC+PDL), thermocycling (TC) and distilled water storage (WS), were used to test the marginal sealing behavior of two adhesive techniques (an adhesive-free flowable resin composite and a self-etch all-in-one adhesive system). A weight-controlled dual-axis chewing device (CS-4.2, SD Mechatronik, Germany) was used for mechanical testing (MC) of the samples. Significantly higher marginal leakage values were observed for the chewing simulation model (MC) compared to TC and WS groups (p<0.05). No statistical correlations were found with regard to aging methods for the tracer’s infiltration of the two adhesive techniques. The dual-axis chewing simulator (CS-4.2) due to its facile mechanical adjustment system may be used for different other in vitro aging models or simulated clinical settings.

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Fukusato, Shin, Masashi Nagao, Kei Fujihara, Taiju Yoneda, Kiyotaka Arai, Manuel Koch, Kazuo Kaneko, Muneaki Ishijima, and Yayoi Izu. "Collagen XII Deficiency Increases the Risk of Anterior Cruciate Ligament Injury in Mice." Journal of Clinical Medicine 10, no. 18 (September 7, 2021): 4051. http://dx.doi.org/10.3390/jcm10184051.

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Anterior cruciate ligament (ACL) rupture is a common knee injury for athletes. Although surgical reconstruction is recommended for the treatment of ACL ruptures, 100% functional recovery is unlikely. Therefore, the discovery of risk factors for ACL ruptures may prevent injury. Several studies have reported an association between polymorphisms of the collagen XII gene COL12A1 and ACL rupture. Collagen XII is highly expressed in tendons and ligaments and regulates tissue structure and mechanical property. Therefore, we hypothesized that collagen XII deficiency may cause ACL injury. To elucidate the influence of collagen XII deficiency on ACL, we analyzed a mouse model deficient for Col12a1. Four- to 19-week-old male Col12a1-/- and wild-type control mice were used for gait analysis; histological and immunofluorescent analysis of collagen XII, and real-time RT-PCR evaluation of Col12a1 mRNA expression. The Col12a1-/- mice showed an abnormal gait with an approximately 2.7-fold increase in step angle, suggesting altered step alignment. Col12a1-/- mice displayed 20–60% ACL discontinuities, but 0% discontinuity in the posterior cruciate ligament. No discontinuities in knee ligaments were found in wild-type mice. Collagen XII mRNA expression in the ACL tended to decrease with aging. Our study demonstrates for the first time that collagen XII deficiency increases the risk of ACL injury.

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Steinkamp, H. M., J. D. Hathaway-Schrader, M. B. Chavez, J. D. Aartun, L. Zhang, T. Jensen, A. Shojaee Bakhtiari, et al. "Tristetraprolin Is Required for Alveolar Bone Homeostasis." Journal of Dental Research 97, no. 8 (March 7, 2018): 946–53. http://dx.doi.org/10.1177/0022034518756889.

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Tristetraprolin (TTP) is an RNA-binding protein that targets numerous immunomodulatory mRNA transcripts for degradation. Many TTP targets are key players in the pathogenesis of periodontal bone loss, including tumor necrosis factor–α. To better understand the extent that host immune factors play during periodontal bone loss, we assessed alveolar bone levels, inflammation and osteoclast activity in periodontal tissues, and immune response in draining cervical lymph nodes in TTP-deficient and wild-type (WT) mice in an aging study. WT and TTP-deficient (knockout [KO]) mice were used for all studies under specific pathogen-free conditions. Data were collected on mice aged 3, 6, and 9 mo. Microcomputed tomography (µCT) was performed on maxillae where 3-dimensional images were generated and bone loss was assessed. Decalcified sections of specimens were scored for inflammation and stained with tartrate-resistant acid phosphate (TRAP) to visualize osteoclasts. Immunophenotyping was performed on single-cell suspensions isolated from primary and peripheral lymphoid tissues using flow cytometry. Results presented indicate that TTP KO mice had significantly more alveolar bone loss over time compared with WT controls. Bone loss was associated with significant increases in inflammatory cell infiltration and an increased percentage of alveolar bone surfaces apposed with TRAP+ cells. Furthermore, it was found that the draining cervical lymph nodes were significantly enlarged in TTP-deficient animals and contained a distinct pathological immune profile compared with WT controls. Finally, the oral microbiome in the TTP KO mice was significantly different with age from WT cohoused mice. The severe bone loss, inflammation, and increased osteoclast activity observed in these mice support the concept that TTP plays a critical role in the maintenance of alveolar bone homeostasis in the presence of oral commensal flora. This study suggests that TTP is required to inhibit excessive inflammatory host responses that contribute to periodontal bone loss, even in the absence of specific periodontal pathogens.

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Jung, Hangsul, Mariko Horiuchi, and Kunimichi Soma. "Changes in the Distribution of Nerve Fibers Immunoreactive to Calcitonin Gene-Related Peptide According to Growth and Aging in Rat Molar Periodontal Ligament." Angle Orthodontist 80, no. 2 (March 2010): 309–15. http://dx.doi.org/10.2319/040109-185.1.

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Koffi, Kouassi Armel, Sophie Doublier, Jean-Marc Ricort, Sylvie Babajko, Ali Nassif, and Juliane Isaac. "The Role of GH/IGF Axis in Dento-Alveolar Complex from Development to Aging and Therapeutics: A Narrative Review." Cells 10, no. 5 (May 12, 2021): 1181. http://dx.doi.org/10.3390/cells10051181.

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The GH/IGF axis is a major regulator of bone formation and resorption and is essential to the achievement of normal skeleton growth and homeostasis. Beyond its key role in bone physiology, the GH/IGF axis has also major pleiotropic endocrine and autocrine/paracrine effects on mineralized tissues throughout life. This article aims to review the literature on GH, IGFs, IGF binding proteins, and their respective receptors in dental tissues, both epithelium (enamel) and mesenchyme (dentin, pulp, and tooth-supporting periodontium). The present review re-examines and refines the expression of the elements of the GH/IGF axis in oral tissues and their in vivo and in vitro mechanisms of action in different mineralizing cell types of the dento-alveolar complex including ameloblasts, odontoblasts, pulp cells, cementoblasts, periodontal ligament cells, and jaw osteoblasts focusing on cell-specific activities. Together, these data emphasize the determinant role of the GH/IGF axis in physiological and pathological development, morphometry, and aging of the teeth, the periodontium, and oral bones in humans, rodents, and other vertebrates. These advancements in oral biology have elicited an enormous interest among investigators to translate the fundamental discoveries on the GH/IGF axis into innovative strategies for targeted oral tissue therapies with local treatments, associated or not with materials, for orthodontics and the repair and regeneration of the dento-alveolar complex and oral bones.

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Yang, Yang, Bo Zhang, Yufan Yang, Bibo Peng, and Rui Ye. "PLGA Containing Human Adipose-Derived Stem Cell-Derived Extracellular Vesicles Accelerates the Repair of Alveolar Bone Defects via Transfer of CGRP." Oxidative Medicine and Cellular Longevity 2022 (June 11, 2022): 1–14. http://dx.doi.org/10.1155/2022/4815284.

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Calcitonin gene-related peptide (CGRP) is an important neuropeptide expressed in the nerve fibers during bone repair. Here, we aimed to pinpoint the role of CGRP in the osteogenic differentiation property of human periodontal ligament stem cells (hPDLSCs) and the resultant repair of alveolar bone defect. The key factor related to the osteogenic differentiation of hPDLSCs was retrieved from the GEO database. After extraction from hADSCs (hADSC-EVs) and identification, EVs were subjected to coculture with hPDLSCs, in which the expression patterns of CGRP and osteogenic differentiation marker proteins (ALP, RUNX2, and OCN), as well as ALP activity, were detected. A novel cell-free tissue-engineered bone (TEB) comprised of PLGA/pDA and hADSC-EVs was implanted into the rats with alveolar bone defects to evaluate the repair of alveolar bone defects. CGRP was enriched in hADSC-EVs. hADSCs delivered CGRP to hPDLSCs through EVs, thereby promoting the osteogenic differentiation potential of hPDLSCs. The PLGA/pDA-EV scaffold released EVs slowly, and its implantation into the rat alveolar bone defect area significantly induced bone defect repair, which was reversed by further knockdown of CGRP. In conclusion, our newly discovered cell-free system consisted of hADSC-EVs, and PLGA/pDA scaffold shows promising function in repairing alveolar bone defects.

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Dong, Xiaofei, Chang Yang, Yao Luo, Wei Dong, Xiaoxiao Xu, Yanru Wu, and Jiawei Wang. "USP7 Attenuates Endoplasmic Reticulum Stress and NF-κB Signaling to Modulate Chondrocyte Proliferation, Apoptosis, and Inflammatory Response under Inflammation." Oxidative Medicine and Cellular Longevity 2022 (April 6, 2022): 1–24. http://dx.doi.org/10.1155/2022/1835900.

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The purpose of this research was to observe the functions and mechanisms of ubiquitin-specific peptidase 7 (USP7) on chondrocytes under tumor necrosis factor alpha- (TNF-α-) induced inflammation. Knee osteoarthritis (OA) models of mice were constructed by anterior cruciate ligament transection. The knee joint of mice was observed by histological staining, and the expression of USP7 was measured by immunohistochemistry staining. After knocking down or inhibiting USP7, chondrocyte proliferation was measured by histological staining and the CCK-8 assay; apoptosis was measured by western blot, flow cytometry, Caspase-3 activity, and TUNEL staining; and inflammatory response was measured by qRT-PCR and ELISA. The 4-phenylbutyric acid (4-PBA), siRNA of CHOP (si-CHOP), and QNZ were used to verify the signaling pathways. It was found that USP7 was reduced in the knee joint cartilage of OA mice. The knockdown of USP7 or its inhibitor decreased chondrocyte proliferation and accelerated apoptosis and inflammatory response under inflammation. The USP7 inhibitor exacerbated cartilage destruction in mice with OA. The knockdown of USP7 or its inhibitor activated the BiP-eIF2α-ATF4-CHOP signaling of endoplasmic reticulum stress (ERS) and NF-κB/p65 signaling. 4-PBA, si-CHOP, and QNZ partly reversed chondrocyte proliferation, apoptosis, and inflammatory response caused by USP7 knockdown. In conclusion, through inhibiting the BiP-eIF2α-ATF4-CHOP signaling of ERS and NF-κB/p65 signaling, USP7 promotes chondrocyte proliferation and suppresses the apoptosis and inflammatory response under TNF-α-induced inflammation.

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Uraguchi, Kensuke, Yukihide Maeda, Junko Takahara, Ryotaro Omichi, Shohei Fujimoto, Shin Kariya, Kazunori Nishizaki, and Mizuo Ando. "Upregulation of a nuclear factor-kappa B-interacting immune gene network in mice cochleae with age-related hearing loss." PLOS ONE 16, no. 10 (October 22, 2021): e0258977. http://dx.doi.org/10.1371/journal.pone.0258977.

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Epidemiological data suggest that inflammation and innate immunity play significant roles in the pathogenesis of age-related hearing loss (ARHL) in humans. In this mouse study, real-time RT-PCR array targeting 84 immune-related genes revealed that the expressions of 40 genes (47.6%) were differentially regulated with greater than a twofold change in 12-month-old cochleae with ARHL relative to young control mice, 33 (39.3%) of which were upregulated. These differentially regulated genes (DEGs) were involved in functional pathways for cytokine–cytokine receptor interaction, chemokine signaling, TNF signaling, and Toll-like receptor signaling. An NF-κB subunit, Nfkb1, was upregulated in aged cochleae, and bioinformatic analyses predicted that NF-κB would interact with the genomic regulatory regions of eight upregulated DEGs, including Tnf and Ptgs2. In aging cochleae, major proinflammatory molecules, IL1B and IL18rap, were upregulated by 6 months of age and thereafter. Remarkable upregulations of seven immune-related genes (Casp1, IL18r1, IL1B, Card9, Clec4e, Ifit1, and Tlr9) occurred at an advanced stage (between 9 and 12 months of age) of ARHL. Immunohistochemistry analysis of cochlear sections from the 12-month-old mice indicated that IL-18r1 and IL-1B were localized to the spiral ligament, spiral limbus, and organ of Corti. The two NF-κB-interacting inflammatory molecules, TNFα and PTGS2, immunolocalized ubiquitously in cochlear structures, including the lateral wall (the stria vascularis and spiral ligament), in the histological sections of aged cochleae. IBA1-positive macrophages were observed in the stria vascularis and spiral ligament in aged mice. Therefore, inflammatory and immune reactions are modulated in aged cochlear tissues with ARHL.

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Caputi, Sergio, Oriana Trubiani, Bruna Sinjari, Svetlana Trofimova, Francesca Diomede, Natalia Linkova, Anastasia Diatlova, and Vladimir Khavinson. "Effect of short peptides on neuronal differentiation of stem cells." International Journal of Immunopathology and Pharmacology 33 (January 2019): 205873841982861. http://dx.doi.org/10.1177/2058738419828613.

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It has been demonstrated that short peptides play an important role in the transmission of biological information, modulation of transcription, and restoring genetically conditioned alterations occurring with age. Peptidergic regulation of homeostasis occupies an important place in physiological processes, which lead to the aging of cells, tissues, and organs, consisting in the involution of major regulatory systems—the nervous, the endocrine, and the immune. The effect of AED (Ala-Glu-Asp), KED (Lys-Glu-Asp), KE (Lys-Glu), AEDG (Ala-Glu-Asp-Gly) peptides and their compound on neuronal differentiation of human periodontal ligament stem cells (hPDLSCs) was studied by immunofluorescence and western blot analysis. Growth-Associated Protein 43 (GAP43), which implements neurotransmission mechanisms and neuroplasticity, demonstrated an increased expression in hPDLSCs cultured with a compound of all studied peptides and with KED alone. The peptide compound and KED, increase the expression of Nestin (neurofilament protein), expressed in early neuronal precursors in hPDLSCs cultures. Thus, the compound of peptides AEDG, KE, AED, and KED could promote the neuronal differentiation of hPDLSCs and be a promising tool for the study of peptides as a modulator of neurogenesis in neurodegenerative diseases studied in animal models.

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Burleson, Gary R. "Immunological Variation Due to Genetics of Inflammatory SNPs and Age and Impact on Disease Manifestation." Toxicologic Pathology 45, no. 1 (November 15, 2016): 146–49. http://dx.doi.org/10.1177/0192623316677070.

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The immune system is a critical component in defense against viral, bacterial, parasitic, and fungal diseases. Immunological mechanisms, including immunological mediators, innate immunity, cell-mediated immunity, and humoral-mediated immunity, serve to maintain homeostasis and protect the host from disease. Immunological variation can impact defense mechanisms, however. Two factors in particular that can influence immune function are the single nucleotide polymorphisms (SNPs) and aging. SNPs affecting inflammatory cytokines are an important modifier involved in a number of diseases such as asthma, periodontal disease, atherosclerosis, diabetic retinopathy, psoriasis, and osteoporosis. Age-related alterations to the immune system have also been studied and documented. The genetic makeup of different strains of mice and the age of these different strains cause large differences in susceptibility to infection, with influenza virus infection among the most widely studied. The mechanism of these differences due to either genetics or age is not known but can be investigated in strain- and age-specific infectious disease models.

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Bao, Xiao-Yi, Li-Hui Deng, Zi-Jun Huang, Abdirizak S. Daror, Zi-Hao Wang, Wang-Jun Jin, Zhuang Zhuang, Qiang Tong, Guo-Qing Zheng, and Yan Wang. "Buyang Huanwu Decoction Enhances Revascularization via Akt/GSK3β/NRF2 Pathway in Diabetic Hindlimb Ischemia." Oxidative Medicine and Cellular Longevity 2021 (December 3, 2021): 1–15. http://dx.doi.org/10.1155/2021/1470829.

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Background. Peripheral arterial disease (PAD) is a typical disease of atherosclerosis, most commonly influencing the lower extremities. In patients with PAD, revascularization remains a preferred treatment strategy. Buyang Huanwu decoction (BHD) is a popular Chinese herbal prescription which has showed effects of cardiovascular protection through conducting antioxidant, antiapoptotic, and anti-inflammatory effects. Here, we intend to study the effect of BHD on promoting revascularization via the Akt/GSK3β/NRF2 pathway in diabetic hindlimb ischemia (HLI) model of mice. Materials and Methods. All db/db mice ( n = 60 ) were randomly divided into 6 groups by table of random number. (1) Sham group ( N = 10 ): 7-0 suture thread passed through the underneath of the femoral artery and vein without occlusion. The remaining 5 groups were treated differently on the basis of the HLI (the femoral artery and vein from the inguinal ligament to the knee joint were transected and the vascular stump was ligated with 7-0 silk sutures) model: (2) HLI+NS group ( N = 15 ): 0.2 ml NS was gavaged daily for 3 days before modeling and 14 days after occlusion; (3) HLI+BHD group ( N = 15 ): 0.2 ml BHD (20 g/kg/day) was gavaged daily for 3 days before modeling and 14 days after occlusion; (4) HLI+BHD+sh-NC group ( N = 8 ): local injection of adenovirus vector carrying the nonsense shRNA (Ad-GFP) in the hindlimbs of mice before treatment; (5) HLI+BHD+sh-NRF2 group ( N = 8 ): knockdown of NRF2 in the hindlimbs of mice by local intramuscular injection of adenovirus vector carrying NRF2 shRNA (Ad-NRF2-shRNA) before treatment; and (6) HLI+BHD+LY294002 group ( N = 4 ): intravenous injection of LY294002 (1.5 mg/kg) once a day for 14 days on the basis of the HLI+BHD group. Laser Doppler examination, vascular cast, and immunofluorescence staining were applied to detect the revascularization of lower limbs in mice. Western blot analysis was used to detect the expression of vascular endothelial growth factor (VEGF), interleukin-1beta (IL-1β), interleukin-6 (IL-6), tumor necrosis factor- (TNF-) α, heme oxygenase-1 (HO-1), NAD(P)H dehydrogenase quinone-1 (NQO-1), catalase (CAT), glyceraldehyde-3-phosphate dehydrogenase (GAPDH), phosphorylated protein kinase B (p-AKT), and phosphorylated glycogen synthase kinase-3 beta (p-GSK3β). HE staining was used to assess the level of muscle tissue damage and inflammation in the lower extremities. Local multipoint injection of Ad-NRF2-shRNA was used to knock down NRF2, and qPCR was applied to detect the mRNA level of NRF2. The blood glucose, triglyceride, cholesterol, MDA, and SOD levels of mice were tested using corresponding kits. The SPSS 20.0 software and GraphPad Prism 6.05 were used to do all statistics. Values of P < 0.05 were considered as statistically significant. Results and Conclusions. BHD could enhance the revascularization of lower limbs in HLI mice, while BHD has no effect on blood glucose and lipid level in db/db mice ( P > 0.05 ). BHD could elevate the protein expression of VEGF, HO-1, NQO-1, and CAT ( P < 0.05 ) and decrease the expression of IL-1β, IL-6, and TNF-α ( P < 0.05 ) in HLI mice. Meanwhile, BHD could activate NRF2 and promote the phosphorylation of AKT/GSK3β during revascularization ( P < 0.05 ). In contrast, knockdown of NRF2 impaired the protective effects of BHD on HLI ( P < 0.05 ). LY294002 inhibited the upregulation of NRF2 activated by BHD through inhibiting the phosphorylation of the AKT/GSK3β pathway ( P < 0.05 ). The present study demonstrated that BHD could promote revascularization on db/db mice with HLI through targeting antioxidation, anti-inflammation, and angiogenesis via the AKT/GSK3β/NRF2 pathway.

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Benavides, Adriana, Elizabeth Fernandez, Z. Sharp, Randy Strong, Sue Stacy, Anthony Infante, Martin Javors, Arlan Richardson, and Ellen Kraig. "Long-term oral delivery of encapsulated rapamycin is not detrimental to immunity in old mice (178.11)." Journal of Immunology 188, no. 1_Supplement (May 1, 2012): 178.11. http://dx.doi.org/10.4049/jimmunol.188.supp.178.11.

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Abstract Recently, encapsulated rapamycin (e-rapa) was shown to extend lifespan in mice when given at an old age (Harrison Nature 2009), so it has been suggested that this mTOR inhibitor may be efficacious in slowing the aging process. However, use of rapa in the elderly might further compromise immune competence. Therefore, we sought to test the effects of e-rapa on immunity in older individuals by looking at T cell and B cell responses. Because rapa has been shown to be protective against some bacteria and viruses, effects on humoral immunity to a viable microbe were tested. Adult (4 months) and old (20 months) mice on e-rapa or control diets were challenged with the periodontal bacteria Aggregatibacter actinomycetemcomitans; e-rapa did not negatively impact the antibody titers seen in either age group. E-rapa effects on responses to a protein antigen, TAChRα, were also tested. No significant e-rapa effect was seen on antibody titers following primary or boost immunizations. Moreover, pilot data show that T cell proliferation to p146-162, the immunodominant epitope of TAChRα, was not significantly affected by the encapsulated drug. Since TAChR is the autoantigen in Myasthenia Gravis, we also immunized TAChRα transgenic mice (JI 169:6570) and showed that tolerance was maintained and the levels of TREGS were unaffected by e-rapa treatment. To-date, our data suggest that encapsulated rapamycin will not negatively impact immune regulation in old individuals.

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Huard, Johnny, Ping Guo, Matthieu Huard, Xueqin Gao, Vihang A. Narkar, Scott Tashman, Johnny Huard, and Aiping Lu. "Poster 247: Muscle ERRγ Overexpression Mitigates the Muscle Atrophy after ACL injury." Orthopaedic Journal of Sports Medicine 10, no. 7_suppl5 (July 1, 2022): 2325967121S0080. http://dx.doi.org/10.1177/2325967121s00808.

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Objectives: Anterior cruciate ligament (ACL) reconstruction is the 6th most common orthopedic procedure performed in the United States (1,2). There is substantial evidence to suggest that muscle weakness significantly contributes to adverse outcomes after ACL injury/reconstruction (3). Despite efforts to improve rehabilitation methods, there are currently no effective strategies for restoring pre-injury muscle strength in ACL-injured limbs. Our team has identified that estrogen-related receptor gamma (ERRγ) is a crucial regulator of paracrine angiogenesis in the skeletal muscle (4). Selective over-expression of ERRγ in the skeletal muscle [ERRGO mice] activates a robust paracrine angiogenic gene program involving myofibrillar induction and secretion of a battery of angiogenic factors resulting in muscle vascularization (4). To determine if muscle ERRγ-driven angiogenesis can mitigate muscle atrophy after ACL injury, we performed ACL injury on the ERRGO mice, as well as age-matched wild-type (WT) littermate control mice. In this model, we found that ERRGO mice with muscle ERRγ overexpression significantly mitigated muscle atrophy compared to WT control mice 4 weeks after ACL injury. This finding strongly suggests that muscle-specific ERRγ activation may reduce muscle atrophy after ACL injury as a consequence of increased muscle angiogenesis. This preventive effect is potentially linked to developing a therapeutic approach to reverse these muscle changes after ACL surgery. Methods:Animals: 12 weeks old male and female ERRGO and WT mice obtained from Dr. Narkar’s laboratory were used for this study. The ACL injury was conducted as previously described (5). We performed ACL injury on the right leg, and the left leg was used as non-injured control. The mice were euthanized four weeks after injury. The muscle tissues were harvested, the gastrocnemius muscle (GM) mass was weighted, flash-frozen in liquid nitrogen-cooled 2-methylbutane, and cryo-sectioned. H&E staining was performed on 10 µm cryosections from GM according to the manufacturer’s instructions. Immunohistochemical staining: The muscle sections were fixed with 4% paraformaldehyde. A Mouse on Mouse kit (Vector) was used for anti-muscle RING-finger protein-1 (MuRF1, marker for muscle atrophy) staining according to the manufacturer’s protocol. Statistical analysis: All results are presented as mean ± standard deviation (SD). Means from ACL injured and non-injured of WT and ERRGO mice were compared using Student’s t-test. Differences were considered statistically significant when the P-value was < 0.05. Results: We performed the following experiments to determine if ERRγ overexpression in the muscle can prevent muscle weakness after ACL injury. The ACLs on the right leg of ERRGO and WT mice were excised. 4 weeks after injury, the mice were sacrificed, and muscle tissues were collected for histology analysis. First, we observed that muscles in the hindlimbs of WT mice were atropied, as expected, after ACL injury compared to the muscles in the non-injured hindlimb (Fig.1A). Strikingly, after ACL injury, the hindlimb muscles in ERRGO mice were resiliant to atrophy (Fig.1A). Quantitatively, we found that the gastrocnemius muscles weights were significantly reduced in WT mice after ACL injury compared to the GM weights from the non-injured leg. However, this ACL injury-induced reduction in gastrocnemius weight was not observed in ERRGO mice after ACL injury (Fig.1 B). The myofiber cross-sectional area (CSA) was measured based on the H&E staining on the GM muscle of ERRGO and WT mice to evaluate the muscle atrophy further. We found that the CSA of muscle fibers in WT mice was significantly smaller after ACL injury than in the non-injured control muscle (Fig. 2A, 2C, P<0.05). The average size of muscle fibers was not significantly decreased in the muscle of ERRGO mice after ACL injury compared to non-injured muscle. (Fig. 2A, 2C, P>0.05). Since MuRF1 is a biomarker of myofiber atrophy (6), we evaluated the MuRF1 expression in muscle sections by immunostaining. The result showed an increase in MuRF1 expression in the WT muscle compared to ERRGO muscle after ACL injury (Fig. 2B). Together, those results demonstrated that muscle-specific ERRγ activation mitigates muscle atrophy after ACL injury. Conclusions: Skeletal muscle is adversely affected by the ACL injury, and post-reconstruction recovery is limited by muscle weakness. It has been reported that ERRγ expression in the skeletal muscle directly correlates with vascular density, and ERRγ is highly expressed in well-vascularized muscle beds (4). Based on our preliminary data, we observed that the ERRGO mice with muscle-specific ERRγ activation have the capacity to mitigate the muscle atrophy after ACL injury. As we know, exercise induces muscle angiogenesis, and regular physical activity has been considered a therapeutic modality for preventing aging-related muscle wasting. Although exercise is the primary method for alleviating muscle weakness, many patients cannot achieve the exercise intensity that is necessary to prevent or reverse muscle atrophy. Drugs targeting ERRγ will likely be safe as ERRγ belongs to the nuclear receptor superfamily, which are excellent ‘druggable’ targets with unique ligand-binding pockets that facilitate selective and specific drug design. Future studies will investigate the beneficial effects of ERRγ overexpression in ERRGO mice on muscle atrophy after ACL injury at different time points and determine if muscle-specific activation of ERRγ can mitigate age-related muscle progenitor cells dysfunction and offset the infiltration and activation of FAPs and senescent cells after ACL injury

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An, Jonathan Y., Kristopher A. Kerns, Andrew Ouellette, Laura Robinson, H. Douglas Morris, Catherine Kaczorowski, So-Il Park, et al. "Rapamycin rejuvenates oral health in aging mice." eLife 9 (April 28, 2020). http://dx.doi.org/10.7554/elife.54318.

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Periodontal disease is an age-associated disorder clinically defined by periodontal bone loss, inflammation of the specialized tissues that surround and support the tooth, and microbiome dysbiosis. Currently, there is no therapy for reversing periodontal disease, and treatment is generally restricted to preventive measures or tooth extraction. The FDA-approved drug rapamycin slows aging and extends lifespan in multiple organisms, including mice. Here, we demonstrate that short-term treatment with rapamycin rejuvenates the aged oral cavity of elderly mice, including regeneration of periodontal bone, attenuation of gingival and periodontal bone inflammation, and revertive shift of the oral microbiome toward a more youthful composition. This provides a geroscience strategy to potentially rejuvenate oral health and reverse periodontal disease in the elderly.

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Albuquerque-Souza, E., K. E. Crump, K. Rattanaprukskul, Y. Li, B. Shelling, X. Xia-Juan, M. Jiang, and S. E. Sahingur. "TLR9 Mediates Periodontal Aging by Fostering Senescence and Inflammaging." Journal of Dental Research, August 2, 2022, 002203452211101. http://dx.doi.org/10.1177/00220345221110108.

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TLR9 is a critical nucleic acid sensing receptor in mediating periodontitis and periodontitis-associated comorbidities. Emerging evidence implicates TLR9 as a key sensor during aging, although its participation in periodontal aging is unexplored. Here, we investigated whether TLR9-mediated host responses can promote key hallmarks of aging, inflammaging, and senescence, in the course of periodontitis using a multipronged approach comprising clinical and preclinical studies. In a case-control model, we found increased TLR9 gene expression in gingival tissues of older (≥55 y) subjects with periodontitis compared to older healthy subjects as well as those who are younger (<55 y old) with and without the disease. Mechanistically, this finding was supported by an in vivo model in which wild-type (WT) and TLR9–/– mice were followed for 8 to 10 wk (young) and 18 to 22 mo (aged). In this longitudinal model, aged WT mice developed severe alveolar bone resorption when compared to their younger counterpart, whereas aged TLR9–/– animals presented insignificant bone loss when compared to the younger groups. In parallel, a boosted inflammaging milieu exhibiting higher expression of inflammatory/osteoclast mediators ( Il-6, Rankl, Cxcl8) and danger signals ( S100A8, S100A9) was noted in gingival tissues of aged WT mice compared to the those of aged TLR9–/– mice. Consistently, WT aged mice displayed an increase in prosenescence balance as measured by p16 INK4a/p19 ARF ratio compared to the younger groups and aged TLR9–/– animals. Ex vivo experiments with bone marrow–derived macrophages primed by TLR9 ligand (ODN 1668) further corroborated in vivo and clinical data and showed enhanced inflammatory-senescence circuit followed by increased osteoclast differentiation. Together, these findings reveal first systematic evidence implicating TLR9 as one of the drivers of periodontitis during aging and functioning by boosting a deleterious inflammaging/senescence environment. This finding calls for further investigations to determine whether targeting TLR9 will improve periodontal health in an aging population.

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Li, Xiaoyu, Bowen Zhang, Hong Wang, Xiaolu Zhao, Zijie Zhang, Gang Ding, and Fulan Wei. "The effect of aging on the biological and immunological characteristics of periodontal ligament stem cells." Stem Cell Research & Therapy 11, no. 1 (July 29, 2020). http://dx.doi.org/10.1186/s13287-020-01846-w.

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Zayed, Mohammed, and Koichiro Iohara. "Age Related Senescence, Apoptosis, and Inflammation Profiles in Periodontal Ligament Cells from Canine Teeth." Current Molecular Medicine 22 (May 20, 2022). http://dx.doi.org/10.2174/1566524022666220520124630.

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Objective: The periapical tissues including periodontal ligament cells (PDLCs) are playing an important role in repairing the surrounding tissue of the teeth. A decrease in the regenerative potentiality of resident stem cells (PDLCs) has been suggested to be attributed to the decline of pulp regeneration. Therefore, it is necessary to examine the functional changes in periodontal tissue and cells that occur during the aging process. Methods: The changes in the cementum extract (CE) and PDLCs isolated from young and aged dog teeth were evaluated. PDLCs growth rate, senescence markers, p16 and p21, and proinflammatory cytokines, IL-6, IL-1β, and TNF-α were analyzed by RT-PCR. Bax, an apoptosis marker, Bcl-2, a marker for cell survival, and IL-6 were examined by Western blot analyses to detect their variance expression in the CE. Results: Our results demonstrated that aged PDLCs exhibit low growth rate and an increased expression of p16, however, no change has been demonstrated in the expression of p21. The chronic inflammatory molecules, IL-6 and TNF-α were significantly upregulated compared to young PDLCs. Western blot analyses showed decreased expression of Bcl-2 in the CE of the aged tooth (p < 0.001). Conclusion: Taken together, aging influences the functional changes of PDLCs and CE and increases senescence, chronic inflammation, and apoptosis markers. As a result, donor age is a key factor influencing the utilization of PDLCs for tooth regeneration.

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Láng, Orsolya, Krisztina S. Nagy, Julia Láng, Katalin Perczel-Kovách, Anna Herczegh, Zsolt Lohinai, Gábor Varga, and László Kőhidai. "Comparative study of hyperpure chlorine dioxide with two other irrigants regarding the viability of periodontal ligament stem cells." Clinical Oral Investigations, October 12, 2020. http://dx.doi.org/10.1007/s00784-020-03618-5.

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Abstract Objectives Periodontal ligament stem cells (PDLSCs) have an underlined significance as their high proliferative capacity and multipotent differentiation provide an important therapeutic potential. The integrity of these cells is frequently disturbed by the routinely used irrigative compounds applied as periodontal or endodontic disinfectants (e.g., hydrogen peroxide (H2O2) and chlorhexidine (CHX)). Our objectives were (i) to monitor the cytotoxic effect of a novel dental irrigative compound, chlorine dioxide (ClO2), compared to two traditional agents (H2O2, CHX) on PDLSCs and (ii) to test whether the aging factor of PDLSC cultures determines cellular responsiveness to the chemicals tested. Methods Impedimetry (concentration-response study), WST-1 assays (WST = water soluble tetrazolium salt), and morphology analysis were performed to measure changes in cell viability induced by the 3 disinfectants; immunocytochemistry of stem cell markers (STRO-1, CD90, and CD105) measured the induced mesenchymal characteristics. Results Cell viability experiments demonstrated that the application of ClO2 does not lead to a significant decrease in viability of PLDSCs in concentrations used to kill microbes. On the contrary, traditional irrigants, H2O2, and CHX are highly toxic on PDLSCs. Aging of PLDSC cultures (passages 3 vs. 7) has characteristic effects on their responsiveness to these agents as the increased expression of mesenchymal stem cell markers turns to decreased. Conclusions and clinical relevance While the active ingredients of mouthwash (H2O2, CHX) applied in endodontic or periodontitis management have a serious toxic effect on PDLSCs, the novel hyperpure ClO2 is less toxic providing an environment favoring dental structure regenerations during disinfectant interventions.

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Aljohani, Hanan, Linda T. Senbanjo, Mohammed Al Qranei, Joseph P. Stains, and Meenakshi A. Chellaiah. "Methylsulfonylmethane Increases the Alveolar Bone Density of Mandibles in Aging Female Mice." Frontiers in Physiology 12 (October 4, 2021). http://dx.doi.org/10.3389/fphys.2021.708905.

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Methylsulfonylmethane (MSM) is a naturally occurring anti-inflammatory compound that effectively treats multiple degenerative diseases such as osteoarthritis and acute pancreatitis. Our previous studies have demonstrated the ability of MSM to differentiate stem cells from human exfoliated deciduous (SHED) teeth into osteoblast-like cells. This study examined the systemic effect of MSM in 36-week-old aging C57BL/6 female mice in vivo by injecting MSM for 13 weeks. Serum analyses showed an increase in expression levels of bone formation markers [osteocalcin (OCN) and procollagen type 1 intact N-terminal propeptide (P1NP)] and a reduction in bone resorption markers [tartrate-resistant acid phosphatase (TRAP) and C-terminal telopeptide of type I collag (CTX-I)] in MSM-injected animals. Micro-computed tomographic images demonstrated an increase in trabecular bone density in mandibles. The trabecular bone density tended to be higher in the femur, although the increase was not significantly different between the MSM- and phosphate-buffered saline (PBS)-injected mice. In mandibles, an increase in bone density with a corresponding decrease in the marrow cavity was observed in the MSM-injected mice. Furthermore, immunohistochemical analyses of the mandibles for the osteoblast-specific marker – OCN, and the mesenchymal stem cell-specific marker – CD105 showed a significant increase and decrease in OCN and CD105 positive cells, respectively. Areas of bone loss were observed in the inter-radicular region of mandibles in control mice. However, this loss was considerably decreased due to stimulation of bone formation in response to MSM injection. In conclusion, our study has demonstrated the ability of MSM to induce osteoblast formation and function in vivo, resulting in increased bone formation in the mandible. Hence, the application of MSM and stem cells of interest may be the right combination in alveolar bone regeneration under periodontal or other related diseases that demonstrate bone loss.

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Wu, Hongle, Wei Qiu, Xiaofang Zhu, Xiangfen Li, Zhongcong Xie, Isabel Carreras, Alpaslan Dedeoglu, et al. "The Periodontal Pathogen Fusobacterium nucleatum Exacerbates Alzheimer’s Pathogenesis via Specific Pathways." Frontiers in Aging Neuroscience 14 (June 23, 2022). http://dx.doi.org/10.3389/fnagi.2022.912709.

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Alzheimer’s Disease (AD) is the most common form of dementia in older adults and has a devastating impact on the patient’s quality of life, which creates a significant socio-economic burden for the affected individuals and their families. In recent years, studies have identified a relationship between periodontitis and AD. Periodontitis is an infectious/inflammatory disease that destroys the supporting periodontal structure leading to tooth loss. Dysbiosis of the oral microbiome plays a significant role in the onset and development of periodontitis exhibiting a shift to overgrowth of pathobionts in the normal microflora with increasing local inflammation. Fusobacterium nucleatum is a common pathogen that significantly overgrows in periodontitis and has also been linked to various systemic diseases. Earlier studies have reported that antibodies to F. nucleatum can be detected in the serum of patients with AD or cognitive impairment, but a causal relationship and a plausible mechanism linking the two diseases have not been identified. In this study, we conducted both in vivo and in vitro experiments and found that F. nucleatum activates microglial cells causing morphological changes, accelerated proliferation and enhanced expression of TNF-α and IL-1β in microglial cells. In our in vivo experiments, we found that F. nucleatum-induced periodontitis resulted in the exacerbation of Alzheimer’s symptoms in 5XFAD mice including increased cognitive impairment, beta-amyloid accumulation and Tau protein phosphorylation in the mouse cerebrum. This study may suggest a possible link between a periodontal pathogen and AD and F. nucleatum could be a risk factor in the pathogenesis of AD. We are currently further identifying the pathways through which F. nucleatum modulates molecular elements in enhancing AD symptoms and signs. Data are available via ProteomeXchange with identifier PXD033147.

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Clark, D., B. Halpern, T. Miclau, M. Nakamura, Y. Kapila, and R. Marcucio. "The Contribution of Macrophages in Old Mice to Periodontal Disease." Journal of Dental Research, April 27, 2021, 002203452110094. http://dx.doi.org/10.1177/00220345211009463.

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The prevalence of periodontal disease increases with age. Systemic inflammatory dysregulation also increases with age and has been reported to contribute to the myriad of diseases and conditions that become more prevalent with advanced age. As periodontal disease involves a dysregulated host inflammatory response, the age-related inflammatory dysregulation may contribute to the pathogenesis of periodontal disease in aging populations. However, our understanding of what drives the age-related inflammatory dysregulation is limited. Here, we investigate the macrophage and its contribution to periodontal disease in old and young mice using a ligature-induced periodontal disease model. We demonstrate that control old mice present with an aged periodontal phenotype, characterized by increased alveolar bone loss and increased local inflammatory cytokine expression compared to young mice. Macrophages were demonstrated to be present in the periodontium of old and young mice in equal numbers in controls, during disease induction, and during disease recovery. However, it appears age may have a detrimental effect on macrophage activity during disease recovery. Depletion of macrophages during disease recovery in old mice resulted in decreased inflammatory cytokines within the gingiva and decreased bone loss as measured by micro–computed tomography. In young mice, macrophage depletion during disease recovery had no beneficial or detrimental effect. Macrophage depletion during disease induction resulted in decreased disease severity similarly in young and old mice. Findings from this work support the diverse roles of macrophages in disease induction as well as the active roles of disease recovery, including the resolution of inflammation. Here, we conclude that age-related changes to the macrophage appear to be detrimental to the recovery from disease and may explain, in part, the age-related increase in prevalence of periodontal disease. Future studies examining the specific intrinsic age-related changes to the macrophage will help identify therapeutic targets.

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Mohanakumar, Aravind, Geethu L. Vijay, Nandakumar Vijayaraghavan, Rahul S. Rajendran, Madhav B. Chandran, Midhun U. Thulasidharan, Deepak R. Damodaran, Chandrima Sreekumar, and Vinod Krishnan. "Morphological alterations, activity, mRNA fold changes, and aging changes before and after orthodontic force application in young and adult human-derived periodontal ligament cells." European Journal of Orthodontics, May 27, 2021. http://dx.doi.org/10.1093/ejo/cjab025.

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Abstract Background The response of periodontal ligament cells (PDLC) from adult subjects in comparison to those obtained from younger ones to mechanical forces has been a matter of interest recently because of induced senescent changes. This study evaluated and compared cell surface changes and activity, integrin beta 1, and β-actin mRNA fold changes as well as klotho protein secretion capabilities of PDLC from young and adult donors before and after subjecting to orthodontic forces. Methods A total of 40 subjects with bimaxillary dentoalveolar protrusion requiring extraction of first premolars for orthodontic treatment were selected and divided into two groups. Force ranging from 80 to 90 g was applied to maxillary first premolars and extraction was carried out at two different time periods—pre-treatment (control group) and 28 days after force application (experimental group). Periodontal ligament was obtained, and cell surface changes and activity were observed with atomic force microscopy (AFM) and fluorescent tagging. mRNA fold change of integrin beta-1 and β-actin mRNA, as well as beta-galactosidase assay, was performed, and levels of klotho protein were evaluated. Results AFM nanoindentation and fluorescent tagging indicated increased surface morphological changes in younger cells compared to adult ones. We observed a decrease in integrin beta 1 but an increase in β-actin mRNA levels in PDLC obtained from younger subjects compared to adults, while an increase was observed in SA-β-GAL from adult cells. The level of klotho protein was lower in adult cells in comparison to younger ones. Limitations Large sample studies are required to find out a variation in aging characteristics between young and adult PDLC. Conclusions The study observed significant differences between PDLC obtained from younger and adult subjects in response to orthodontic force application.

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Zhou, Mi, and Dana T. Graves. "Impact of the host response and osteoblast lineage cells on periodontal disease." Frontiers in Immunology 13 (October 11, 2022). http://dx.doi.org/10.3389/fimmu.2022.998244.

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Periodontitis involves the loss of connective tissue attachment and alveolar bone. Single cell RNA-seq experiments have provided new insight into how resident cells and infiltrating immune cells function in response to bacterial challenge in periodontal tissues. Periodontal disease is induced by a combined innate and adaptive immune response to bacterial dysbiosis that is initiated by resident cells including epithelial cells and fibroblasts, which recruit immune cells. Chemokines and cytokines stimulate recruitment of osteoclast precursors and osteoclastogenesis in response to TNF, IL-1β, IL-6, IL-17, RANKL and other factors. Inflammation also suppresses coupled bone formation to limit repair of osteolytic lesions. Bone lining cells, osteocytes and periodontal ligament cells play a key role in both processes. The periodontal ligament contains cells that exhibit similarities to tendon cells, osteoblast-lineage cells and mesenchymal stem cells. Bone lining cells consisting of mesenchymal stem cells, osteoprogenitors and osteoblasts are influenced by osteocytes and stimulate formation of osteoclast precursors through MCSF and RANKL, which directly induce osteoclastogenesis. Following bone resorption, factors are released from resorbed bone matrix and by osteoclasts and osteal macrophages that recruit osteoblast precursors to the resorbed bone surface. Osteoblast differentiation and coupled bone formation are regulated by multiple signaling pathways including Wnt, Notch, FGF, IGF-1, BMP, and Hedgehog pathways. Diabetes, cigarette smoking and aging enhance the pathologic processes to increase bone resorption and inhibit coupled bone formation to accelerate bone loss. Other bone pathologies such as rheumatoid arthritis, post-menopausal osteoporosis and bone unloading/disuse also affect osteoblast lineage cells and participate in formation of osteolytic lesions by promoting bone resorption and inhibiting coupled bone formation. Thus, periodontitis involves the activation of an inflammatory response that involves a large number of cells to stimulate bone resorption and limit osseous repair processes.

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Bian, Minxia, Yan Yu, Yuzhi Li, Zhou Zhou, Xiao Wu, Xiaying Ye, and Jinhua Yu. "Upregulating the Expression of LncRNA ANRIL Promotes Osteogenesis via the miR-7-5p/IGF-1R Axis in the Inflamed Periodontal Ligament Stem Cells." Frontiers in Cell and Developmental Biology 9 (February 22, 2021). http://dx.doi.org/10.3389/fcell.2021.604400.

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BackgroundLong non-coding RNA (lncRNA) antisense non-coding RNA in the INK4 locus (ANRIL) is a base length of about 3.8 kb lncRNA, which plays an important role in several biological functions including cell proliferation, migration, and senescence. This study ascertained the role of lncRNA ANRIL in the senescence and osteogenic differentiation of inflamed periodontal ligament stem cells (iPDLSCs).MethodsHealthy periodontal ligament stem cells (hPDLSCs) and iPDLSCs were isolated from healthy/inflamed periodontal ligament tissues, respectively. The proliferation abilities were determined by CCK-8, EdU assay, and flow cytometry (FCM). The methods of Western blot assay (WB), quantitative real-time polymerase chain reaction (qRT-PCR), alizarin red staining, alkaline phosphatase (ALP) staining, ALP activity detection, and immunofluorescence staining were described to determine the biological influences of lncRNA ANRIL on iPDLSCs. Senescence-associated (SA)-β-galactosidase (gal) staining, Western blot analysis, and qRT-PCR were performed to determine cell senescence. Dual-luciferase reporter assays were conducted to confirm the binding of lncRNA ANRIL and miR-7-5-p, as well as miR-7-5p and insulin-like growth factor receptor (IGF-1R).ResultsHPDLSCs and iPDLSCs were isolated and cultured successfully. LncRNA ANRIL and IGF-1R were declined, while miR-7-5p was upregulated in iPDLSCs compared with hPDLSCs. Overexpression of ANRIL enhanced the osteogenic protein expressions of OSX, RUNX2, ALP, and knocked down the aging protein expressions of p16, p21, p53. LncRNA ANRIL could promote the committed differentiation of iPDLSCs by sponging miR-7-5p. Upregulating miR-7-5p inhibited the osteogenic differentiation of iPDLSCs. Further analysis identified IGF-1R as a direct target of miR-7-5p. The direct binding of lncRNA ANRIL and miR-7-5p, miR-7-5p and the 3′-UTR of IGF-1R were verified by dual-luciferase reporter assay. Besides, rescue experiments showed that knockdown of miR-7-5p reversed the inhibitory effect of lncRNA ANRIL deficiency on osteogenesis of iPDLSCs.ConclusionThis study disclosed that lncRNA ANRIL promotes osteogenic differentiation of iPDLSCs by regulating the miR-7-5p/IGF-1R axis.

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Oliveira, LRS, C. Moura, KGBA Cavalcanti, PBF Soares, AFM Cardenas, and CJ Soares. "Effects of Adjacent Tooth Type and Occlusal Fatigue on Proximal Contact Force of Posterior Bulk Fill and Incremental Resin Composite Restoration." Operative Dentistry, January 28, 2022. http://dx.doi.org/10.2341/20-019-l.

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SUMMARY Objectives: To measure the proximal contact force in newtons (N) between incremental and bulk fill class II resin composite restorations and implant molar teeth or adjacent premolar teeth with simulated periodontal ligament. Methods: The model used was created with a typodont first molar tooth with two bilateral occlusal-proximal class II cavities, an adjacent tooth simulating an implanted molar tooth (Titamax CM, Neodent, Curtiba, PR, Brazil) and a premolar with simulated periodontal ligament. Two resin composite restorative techniques were used: Inc-Z350XT, (Filtek Z350, 3M Oral Care, St. Paul, MN, USA) inserted incrementally and Bulk-OPUS, (Opus Bulk Fill APS, FGM, Joinville, SC, Brazil) high viscosity bulk fill resin composite (n=10). As a control, a typodont having intact teeth without restorations was used. After the restorative procedure, each specimen was radiographed using a digital system (Dürr Dental, Bietigheim-Bissingen, Germany). The proximal contact force (N) was measured using dental floss with a microtensile machine (Microtensile ODEME, Luzerna, SC, Brazil). The specimens were then subjected to mechanical fatigue cycling to simulate 5 years of aging. All the parameters were measured after aging. The X-rays were blindly qualitatively analyzed by two operators to identify the loss of proximal contact. One-way ANOVA was used for comparing the initial contact force between restored and intact teeth. Two-way ANOVA followed by Tukey testing was performed for contact area data and for the contact force/contact area ratio. The proximal contact force data were analyzed using one-way repeated measurement ANOVA followed by Tukey testing (α=0.05). The X-ray proximal contact analyses were described by the frequency. Results: The initial proximal contact force was similar for intact and restored teeth. The contact force and contact area with the molar were significantly higher than with the premolar; however the contact force/contact area ratio was similar for all tested groups. The bulk fill technique showed a contact force similar to the incremental filling technique. Fatigue resulted in a significant reduction in the proximal contact force (p<0.001), irrespective of the region analyzed or restorative material used. The digital X-rays detected no alteration in the proximal contact after occlusal fatigue. Conclusions: Larger contact area resulted in higher proximal contact force. Proximal contact force decreased with 5 years of simulated occlusal fatigue. The bulk fill technique showed a proximal contact force similar to that of the incremental filling technique.

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Journal articles on the topic 'Mice – Aging; Periodontal ligament – Aging'

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