Significant Alveolar Bone Loss Research Articles

Transferrin receptor 2 mitigates periodontitis-driven alveolar bone loss.

Periodontitis is associated with significant alveolar bone loss. Patients with iron overload suffer more frequently from periodontitis, however, the underlying mechanisms remain largely elusive. Here, we investigated the role of transferrin receptor 2 (Tfr2), one of the main regulators of iron homeostasis, in the pathogenesis of periodontitis and the dental phenotype under basal conditions in mice. As Tfr2 suppresses osteoclastogenesis, we hypothesized that deficiency of Tfr2 may exacerbate periodontitis-induced bone loss. Mice lacking Tfr2 (Tfr2-/- ) and wild-type (Tfr2+/+ ) littermates were challenged with experimental periodontitis. Mandibles and maxillae were collected for microcomputed tomography and histology analyses. Osteoclast cultures from Tfr2+/+ and Tfr2-/- mice were established and analyzed for differentiation efficiency, by performing messenger RNA expression and protein signaling pathways. After 8 days, Tfr2-deficient mice revealed a more severe course of periodontitis paralleled by higher immune cell infiltration and a higher histological inflammation index than Tfr2+/+ mice. Moreover, Tfr2-deficient mice lost more alveolar bone compared to Tfr2+/+ littermates, an effect that was only partially iron-dependent. Histological analysis revealed a higher number of osteoclasts in the alveolar bone of Tfr2-deficient mice. In line, Tfr2-deficient osteoclastic differentiation ex vivo was faster and more efficient as reflected by a higher number of osteoclasts, a higher expression of osteoclast markers, and an increased resorptive activity. Mechanistically, Tfr2-deficient osteoclasts showed a higher p38-MAPK signaling and inhibition of p38-MAPK signaling in Tfr2-deficient cells reverted osteoclast formation to Tfr2+/+ levels. Taken together, our data indicate that Tfr2 modulates the inflammatory response in periodontitis thereby mitigating effects on alveolar bone loss.

Using Distracting Capsule and Resin Bridge for Segmental Distraction Osteogenesis for an Implant-supported Ceramic Crown in the Esthetic Zone of the Anterior Maxilla: 10-year Clinical Report

Implant therapy for the esthetic zone of the anterior maxilla is a challenge when the support is deficient with the loss of alveolar bone. This article presents a 10-year clinical report of implant therapy for 23-year-old woman with a significant loss of alveolar bone following a loss of the maxillary right central incisor. The central incisor was restored with a screw-retained single implant ceramic crown where the implant site was augmented through sectional distraction osteogenesis involving a distracting capsule and a resin bridge to restore the missing span and serve as an anchorage for distraction. At the 10-year follow-up appointment, the implant-supported crown was stable with no signs or symptoms of biological and/or mechanical complications.

Incisors' bone height and inclination changes after orthodontic treatment with a self-ligating passive system.

This study aimed to evaluate changes in the alveolar buccal bone height of maxillary and mandibular incisors after orthodontic treatment with a self-ligating passive system and to assess the correlation between bone height and incisor inclination. Pre (T1) and post-treatment (T2) cone-beam computed tomography images of patients treated with the Damon 3MX appliance system were measured to quantify the alveolar buccal bone height of the maxillary incisors. The incisor's inclination was measured in digital models. Paired t-test was used to evaluate the changes between T1 and T2, and Pearson's coefficient was used to test the correlation. All teeth presented statistically significant alveolar buccal bone loss at T2. A statistically significant buccal inclination was observed only for the lower left lateral incisors. There was no correlation between bone height changes and incisor inclination. Orthodontic treatment with a self-ligating passive system showed changes in alveolar height, but these changes were not correlated with incisor inclination. Key words:Passive self-ligating brackets, orthodontics, corrective, treatment outcome, alveolar bone loss.

Andrews Bridge Fixed Removable System: A Clinical Case Report

The aesthetic zone presents a dilemma for prosthetic rehabilitation. Prosthetic restoration of significant alveolar bone loss in the aesthetic zone is often challenging. The Andrews Bridge fixed removable system can be used in such cases as it combines the benefits of a Fixed Partial Denture (FPD) with the aesthetics of a Removable Partial Denture (RPD) to restore lost teeth and gingiva while addressing the aesthetic challenge of significant alveolar bone loss. It reduces the denture bulk and provides good retention and patient comfort. There is no need for palatal or lingual flange covering, as in a regular RPD.

Topical application of Porphyromonas gingivalis into thegingival pocket in mice leads to chronic‑activeinfection, periodontitis and systemic inflammation.

Porphyromonas gingivalis (Pg), one of the 'red-complex' perio-pathogens known to play a critical role in the development of periodontitis, has been used in various animal models to mimic human bacteria-induced periodontitis. In order to achieve a more realistic animal model of human Pg infection, the present study investigated whether repeated small-volume topical applications of Pg directly into the gingival pocket can induce local infection, including periodontitis and systemic vascular inflammation in wild-type mice. Freshly cultured Pg was topically applied directly into the gingival pocket of the second molars for 5 weeks (3 times/week). After the final application, the mice were left in cages for 4 or 8 weeks and sacrificed. The status of Pg colony formation in the pocket, gingival inflammation, alveolar bone loss, the expression levels of pro-inflammatory cytokines in the serum and aorta, the presence of anti-Pg lipopolysaccharide (LPS) and gingipain (Kpg and RgpB) antibodies in the serum, as well as the accumulation of Pg LPS and gingipain aggregates in the gingiva and arterial wall were evaluated. The topical application of Pg into the gingival pocket induced the following local and systemic pathohistological changes in mice when examined at 4 or 8 weeks after the final topical Pg application: Pg colonization in the majority of gingival pockets; increased gingival pocket depths; gingival inflammation indicated by the increased expression of TNF-α, IL-6 and IL-1β; significant loss of alveolar bone at the sites of topical Pg application; and increased levels of pro-inflammatory cytokines, such as TNF-α, IL-1β, IL-17, IL-13, KC and IFN-γ in the serum in comparison to those from mice receiving PBS. In addition, the Pg application/colonization model induced anti-Pg LPS and gingipain antibodies in serum, as well as the accumulation of Pg LPS and gingipain aggregates in the gingivae and arterial walls. To the best of our knowledge, this mouse model represents the first example of creating a more sustained local infection in the gingival tissues of wild-type mice and may prove to be useful for the investigation of the more natural and complete pathogenesis of the bacteria in the development of local oral and systemic diseases, such as atherosclerosis. It may also be useful for the determination of a treatment/prevention/efficacy model associated with Pg-induced colonization periodontitis in mice.

Microglial response to experimental periodontitis in a murine model of Alzheimer’s disease

Periodontal disease (PD) has been suggested to be a risk factor for Alzheimer’s disease (AD). We tested the impact of ligature-induced PD on 5xFAD mice and WT littermates. At baseline, 5xFAD mice presented significant alveolar bone loss compared to WT mice. After the induction of PD, both WT and 5xFAD mice experienced alveolar bone loss. PD increased the level of Iba1-immunostained microglia in WT mice. In 5xFAD mice, PD increased the level of insoluble Aβ42. The increased level in Iba1 immunostaining that parallels the accumulation of Aβ in 5xFAD mice was not affected by PD except for a decrease in the dentate gyrus. Analysis of double-label fluorescent images showed a decline in Iba1 in the proximity of Aβ plaques in 5xFAD mice with PD compared to those without PD suggesting a PD-induced decrease in plaque-associated microglia (PAM). PD reduced IL-6, MCP-1, GM-CSF, and IFN-γ in brains of WT mice and reduced IL-10 in 5xFAD mice. The data demonstrated that PD increases neuroinflammation in WT mice and disrupts the neuroinflammatory response in 5xFAD mice and suggest that microglia is central to the association between PD and AD.

Osteopenic effects of high-fat diet-induced obesity on mechanically induced alveolar bone remodeling.

The aim of the study was to investigate the effect of obesity on the tissue and molecular reactions of alveolar bone in response to orthodontic force and its underlying mechanisms. Sixty-four rats were randomly divided into normal diet (ND) and high-fat diet (HFD) groups for eight weeks of dietary treatment. OTM was induced using nickel-titanium springs between the upper left first molar and incisor. After 1, 3, 7, and 14days of OTM, the maxillary alveolar bone and gingival tissues were harvested and analyzed. Compared with the ND rats, the HFD rats had greater OTM distance, serum levels of tartrate-resistant acid phosphatase (TRAP), and tumor necrosis factor α (TNF-α), as well as significant alveolar bone loss and bone architecture deterioration on both the compression and tension sides (p<.05 for all). This response was linked to the increased osteoclast numbers and functional activity and decreased osteoblast activity in the periodontal ligament, gingival tissue, and alveolar bone. HFD-induced obesity promoted mechanically induced alveolar bone remodeling and detrimental changes in alveolar bone microstructure by increasing osteoclastogenesis and regulating inflammatory cytokine expression. The increased alveolar bone remodeling in the obese rats lead to an accelerated OTM.

Effect of VEGFC on lymph flow and inflammation-induced alveolar bone loss.

The lymphatic system plays a crucial role in the maintenance of tissue fluid homeostasis and the immunological response to inflammation. The effects of lymphatic drainage dysfunction on periodontitis have not been well studied. Here we show that lymphatic vessel endothelial receptor 1 (LYVE1)+ /podoplanin (PDPN)+ lymphatic vessels (LVs) are increased in the periodontal tissues, with accumulation close to the alveolar bone surface, in two murine periodontitis models: rheumatoid arthritis (RA)-associated periodontitis and ligature-induced periodontitis. Further, PDPN+ /alpha-smooth muscle actin (αSMA)- lymphatic capillaries are increased, whereas PDPN+ /αSMA+ collecting LVs are decreased significantly in the inflamed periodontal tissues. Both mouse models of periodontitis have delayed lymph flow in periodontal tissues, increased TRAP-positive osteoclasts, and significant alveolar bone loss. Importantly, the local administration of adeno-associated virus for vascular endothelial growth factor C, the major growth factor that promotes lymphangiogenesis, increases the area and number of PDPN+ /αSMA+ collecting LVs, promotes local lymphatic drainage, and reduces alveolar bone loss in both models of periodontitis. Lastly, LYVE1+ /αSMA- lymphatic capillaries are increased, whereas LYVE1+ /αSMA+ collecting LVs are decreased significantly in gingival tissues of patients with chronic periodontitis compared with those of clinically healthy controls. Thus, our findings reveal an important role of local lymphatic drainage in periodontal inflammation-mediated alveolar bone loss. © 2020 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.

Polymicrobial periodontal disease triggers a wide radius of effect and unique virome

Periodontal disease is a microbially-mediated inflammatory disease of tooth-supporting tissues that leads to bone and tissue loss around teeth. Although bacterially-mediated mechanisms of alveolar bone destruction have been widely studied, the effects of a polymicrobial infection on the periodontal ligament and microbiome/virome have not been well explored. Therefore, the current investigation introduced a new mouse model of periodontal disease to examine the effects of a polymicrobial infection on periodontal ligament (PDL) properties, changes in bone loss, the host immune response, and the microbiome/virome using shotgun sequencing. Periodontal pathogens, namely Porphyromonas gingivalis, Treponema denticola, Tannerella forsythia, and Fusobacterium nucleatum were used as the polymicrobial oral inoculum in BALB/cByJ mice. The polymicrobial infection triggered significant alveolar bone loss, a heightened antibody response, an elevated cytokine immune response, a significant shift in viral diversity and virome composition, and a widening of the PDL space; the latter two findings have not been previously reported in periodontal disease models. Changes in the PDL space were present at sites far away from the site of insult, indicating that the polymicrobial radius of effect extends beyond the bone loss areas and site of initial infection and wider than previously appreciated. Associations were found between bone loss, specific viral and bacterial species, immune genes, and PDL space changes. These findings may have significant implications for the pathogenesis of periodontal disease and biomechanical properties of the periodontium. This new polymicrobial mouse model of periodontal disease in a common mouse strain is useful for evaluating the features of periodontal disease.

Management of pyogenic granuloma in pediatric patients using electrocautery–Case reports

The oral pyogenic granuloma, a tumor-like growth is a non-specific infection and considered being nonneoplastic in nature with various clinical and histopathological forms. It occurs mainly in the second decade of life in young individuals and rarely causes significant alveolar bone loss. The present article describes the management of pyogenic granuloma by electrosurgery in a 10-year-old male child and an 11-year-old female child. Keywords: Pyogenic granuloma, Gingival hyperplasia, Hyperactive lesion.

Pam2CSK4 (TLR2 agonist) induces periodontal destruction in mice.

Lipoproteins are important bacterial immunostimulating molecules capable of inducing receptor activator of nuclear factor-κB (RANKL) and osteoclast formation in vitro and in vivo . Although these molecules are present in periodontopathogenic bacteria, their role in periodontitis is not known. In this study, we used Pam2CSK4 (PAM2), a synthetic molecule that mimics bacterial lipoprotein, to investigate the effects of lipoproteins on periodontitis in mice. C57BL/6 male mice were randomly divided into three experimental groups: 1) Negative control group: animals received vehicle injection; 2) Positive control group: animals received injection of Escherichia coli lipopolysaccharide (LPS); 3) PAM2 group: animals received PAM2 injection. All the injections were performed bilaterally every other day into the palatal mucosa between first and second molars. After twenty-four days, the animals were euthanized to assess alveolar bone volume (micro-CT), cellular and extracellular composition in the gingiva (stereometric analysis), and osteoclast numbers (TRAP staining). Treatment with either PAM2 or LPS induced gingival inflammation, as demonstrated by increased infiltration of inflammatory cells and enhanced angiogenesis, associated with a smaller number of fibroblasts and decreased extracellular matrix. Importantly, treatment not only with LPS but also with PAM2 resulted in a larger number of TRAP+ multinucleated osteoclasts and significant loss of alveolar bone. Collectively, our data demonstrate that PAM2 can induce gingival inflammation and bone loss in mice, broadening the avenues of investigation into the role of lipoproteins in the pathogenesis of periodontal disease.

Loss of Discoidin Domain Receptor 1 Predisposes Mice to Periodontal Breakdown

The discoidin domain receptors, DDR1 and DDR2, are nonintegrin collagen receptors and tyrosine kinases. DDRs regulate cell functions, and their extracellular domains affect collagen fibrillogenesis and mineralization. Based on the collagenous nature of dentoalveolar tissues, we hypothesized that DDR1 plays an important role in dentoalveolar development and function. Radiography, micro–computed tomography (micro-CT), histology, histomorphometry, in situ hybridization (ISH), immunohistochemistry (IHC), and transmission electron microscopy (TEM) were used to analyze Ddr1 knockout (Ddr1−/−) mice and wild-type (WT) controls at 1, 2, and 9 mo, and ISH and quantitative polymerase chain reaction (qPCR) were employed to assess Ddr1/DDR1 messenger RNA expression in mouse and human tissues. Radiographic images showed normal molars but abnormal mandibular condyles, as well as alveolar bone loss in Ddr1−/− mice versus WT controls at 9 mo. Histological, histomorphometric, micro-CT, and TEM analyses indicated no differences in enamel or dentin Ddr1−/− versus WT molars. Total volumes (TVs) and bone volumes (BVs) of subchondral and ramus bone of Ddr1−/− versus WT condyles were increased and bone volume fraction (BV/TV) was reduced at 1 and 9 mo. There were no differences in alveolar bone volume at 1 mo, but at 9 mo, severe periodontal defects and significant alveolar bone loss (14%; P < 0.0001) were evident in Ddr1−/− versus WT mandibles. Histology, ISH, and IHC revealed disrupted junctional epithelium, connective tissue destruction, bacterial invasion, increased neutrophil infiltration, upregulation of cytokines including macrophage colony-stimulating factor, and 3-fold increased osteoclast numbers (P < 0.05) in Ddr1−/− versus WT periodontia at 9 mo. In normal mouse tissues, ISH and qPCR revealed Ddr1 expression in basal cell layers of the oral epithelia and in immune cells. We confirmed a similar expression pattern in human oral epithelium by ISH and qPCR. We propose that DDR1 plays an important role in periodontal homeostasis and that absence of DDR1 predisposes mice to periodontal breakdown.

Periodontitis and vascular inflammatory biomarkers: an experimental in vivo study in rats

The objective of this preclinical in vivo study was to determine changes in vascular inflammatory biomarkers in systemic circulation after injection of lipopolysaccharide (LPS) from Porphyromonas gingivalis (Pg) in rats. Experimental periodontitis was induced by injections of Pg-LPS. Gingival soft and hard tissues changes were analysed by means of magnetic resonance imaging and micro computed tomography. Serum levels of interleukin (IL)-6, IL-10, pentraxin (PTX) 3, and soluble fragment of tumor necrosis factor-like weak inducer of apoptosis (sTWEAK) were determined at baseline and 24 h, 7, 14, and 21 days after periodontal induction. Significant periodontal inflammation and alveolar bone loss were evident at the end of periodontal induction. Experimental periodontitis posed an acute systemic inflammatory response with increased serum levels of IL-6 and PTX3 at 24 h post-induction, followed by a significant overexpression of sTWEAK at 7 days. This inflammatory state was maintained until the end of the experiment (21 days). As expected, IL-10 serum levels were significantly lower during the follow-up compared to baseline concentrations. In the present animal model, experimental periodontitis is associated with increased systemic inflammation. Further studies are needed to confirm whether PTX3 and sTWEAK could be useful biomarkers to investigate potential mechanisms underlying the relationship between periodontitis and atherosclerotic vascular diseases.

Odontogenic Keratocyst: A Case Report Emphasizing on Root Canal Treatment after Surgical Intervention.

This article presents a case of odontogenic keratocyst (OKC) located in the mandible, involving teeth 36 to 45, with significant loss of alveolar bone and aseptic pulp necrosis, emphasizing on root canal treatment after surgical intervention. Orthopantomogram and computed tomography examinations revealed an extensive, well-defined, and multilocular radiolucent lesion. Histopathological examination after incisional biopsy confirmed OKC, which was removed completely with enucleation and curettage, followed by the endodontic treatments of teeth 36 to 45 using reciprocating nickel-titanium files (Reciproc) in a single session. Afterwards, teeth 33 to 36 underwent apical surgery to create an appropriate bone development. Panoramic radiographic images showed bone formation and no sign of recurrence after one-year follow-up. In conclusion, this surgical approach, combined with the endodontic treatments of the teeth involved in the lesion, was effective for the management of OKC, promoting injury regression and preservation of the natural teeth.

Characterization of ligature-induced experimental periodontitis.

We sought to better characterize the progression of periodontal tissue breakdown in rats induced by a ligature model of experimental periodontal disease (PD). A total of 60 male Sprague-Dawley rats were evenly divided into an untreated control group and a PD group induced by ligature bilaterally around first and second maxillary molars. Animals were sacrificed at 1, 3, 5, 7, 14, and 21 days after the induction of PD. Alveolar bone loss was evaluated by histomorphometry and microcomputed tomography (μCT). The immune-inflammatory process in the periodontal tissue was assessed using descriptive histologic analysis and quantitative polymerase chain reaction (qPCR). This ligature model resulted in significant alveolar bone loss and increased inflammatory process of the periodontal tissues during the initial periods of evaluation (0-14 days). A significant increase in the gene expression of pro-inflammatory cytokines, interleukin-1β (IL-1β), interleukin-6 (IL-6), and tumor necrosis factor-α (TNF-α), and proteins involved in osteoclastogenesis, receptor activator of nuclear factor-k B ligand (RANKL) and osteoprotegerin (OPG) was observed in the first week of analysis. In the later periods of evaluation (14-21 days), no significant alterations were noted with regard to inflammatory processes, bone resorption, and expression of cytokine genes. The ligature-induced PD model resulted in progressive alveolar bone resorption with two different phases: Acute (0-14 days), characterized by inflammation and rapid bone resorption, and chronic (14-21 days) with no significant progression of bone loss. Furthermore, the gene expressions of IL-6, IL-1β, TNF-α, RANKL, and OPG were highly increased during the progress of PD in the early periods. RESEARCH HIGHLIGHTS: Ligature-induced bone resorption in rats occurred in the initial periods after disease induction The bone resorption was characterized by two distinct phases: Acute (0-14 days), with pronounced inflammation and alveolar bone loss Chronic phase (14-21 days): No further disease progression Several pro-inflammatory cytokines were increased during the progress of periodontitis.

Interplay between P. gingivalis, F. nucleatum and A. actinomycetemcomitans in murine alveolar bone loss, arthritis onset and progression

Increasing evidence supports the association of periodontitis with rheumatoid arthritis. Even though a prominent role has been postulated for Porphyromonas gingivalis, many bacterial species contribute to the pathogenesis of periodontal disease. We therefore investigated the impact of Porphyromonas gingivalis as well as other major pathobionts on the development of both, periodontitis and arthritis in the mouse. Pathobionts used - either alone or in combination - were Porphyromonas gingivalis, Fusobacterium nucleatum and Aggregatibacter actinomycetemcomintans. Periodontitis was induced via oral gavage in SKG, DBA/1 and F1 (DBA/1 × B10.Q) mice and collagen-induced arthritis was provoked via immunization and boost with bovine collagen type II. Alveolar bone loss was quantified via micro computed tomography, arthritis was evaluated macroscopically and histologically and serum antibodies were assessed. Among the strains tested, only F1 mice were susceptible to P. gingivalis induced periodontitis and showed significant alveolar bone loss. Bone loss was paralleled by antibody titers against P. gingivalis. Of note, mice inoculated with the mix of all three pathobionts showed less alveolar bone loss than mice inoculated with P. gingivalis alone. However, oral inoculation with either F. nucleatum or A. actinomycetemcomintans alone accelerated subsequent arthritis onset and progression. This is the first report of a triple oral inoculation of pathobionts combined with collagen-induced arthritis in the mouse. In this interplay and this particular genetic setting, F. nucleatum and A. actinomycetemcomitans exerted a protective impact on P. gingivalis induced alveolar bone loss. By themselves they did not induce periodontitis yet accelerated arthritis onset and progression.

The Impact of Orthodontic Bands on the Marginal Periodontium of Maxillary First Molars: A Retrospective Cross-Sectional Radiographic Analysis.

Aim:Available information on the effect of orthodontic treatment on crestal alveolar bone levels measured in radiographs is contradictory. The aim of this study was to compare the alveolar bone level and periodontal ligament space of banded upper first molars to untreated controls.Materials and Methods:This retrospective cross-sectional radiographic study investigated alveolar bone levels of upper first molars of an orthodontic test group and an untreated control group of comparable age (15-16.25 years), using existing bitewing radiographs.Eighty-six individuals were included in each group. Three parameters were measured mesially and distally on both sides of the patient as follows: I) Alveolar Bone Level (ABL): measured as the distance between the cemento-enamel junction and the alveolar crest, II) the Periodontal Ligament Space (PLS): measured as the most coronal distance between the alveolar crest and the tooth surface, and III) angle between the lines (alveolar crests mesial and distal) and (cemento-enamel junction mesial and distal).Results:The mean duration of the orthodontic treatment in the test group was 2.5 years. The periodontal ligament space was statistically significantly wider on mesial areas of right molars (mean 0.2 mm, p<0.01), but there was no statistically significant difference found in the three other areas (distal part of the right molar, mesial and distal parts of the left molar). There was a statistically significant mean alveolar bone loss in the right and left mesial areas, respectively accounting for 0.3 mm (p<0.001) and 0.2 mm (p<0.01). No statistically significant alveolar bone loss was measured on the distal surfaces of the upper molars. The angle was wider on both sides for the test group (right p<0.001 and left p<0.05).Conclusions:A significant alveolar bone loss on the mesial tooth surface of upper first molars after orthodontic treatment was found with concurrent different levelling angles in the test group. On all other sites, no statistically significant changes were found. There was some minimal statistical significant alveolar bone loss after finishing treatment in patients who had orthodontic bands placed on their maxillary 1st molars, but no clinical significance was found.

Rapamycin treatment attenuates age-associated periodontitis in mice.

Interventions that target biological mechanisms of aging have great potential to enhance quality of life by delaying morbidity and mortality. The FDA-approved drug rapamycin is a compelling candidate for such an intervention. In a previous study, it was reported that 3months of rapamycin treatment is sufficient to increase life expectancy and remodel the gut microbiome in aged mice. Transient treatment with rapamycin or a rapamycin derivative has also been shown to delay immune stem cell senescence and rejuvenate immune function in aged mice and elderly people. Periodontal disease is an important age-related disease involving altered immune function, pathological changes to the oral microbiome, and systemic inflammation. Periodontal disease is defined clinically by loss of alveolar bone and by connective tissue degeneration. Here, we describe significant alveolar bone loss during aging in two different mouse strain backgrounds and report that rapamycin treatment is sufficient to reverse age-associated periodontal disease in mice. Partial restoration of youthful levels of alveolar bone is observed in 22-month-old rapamycin-treated mice as rapidly as 8weeks after initiation of treatment. To the best of our knowledge, this represents the first intervention shown to substantially prevent or reverse age-associated alveolar bone loss. These findings suggest the possibility that inhibition of mTOR with rapamycin or other pharmacological agents may be useful to treat a clinically relevant condition for which there is currently no effective treatment.

Complete dentures supported on mini implants: A literature review

Introduction. Significant loss of alveolar ridge in edentulism is clinically difficult situation that requires above-standard solutions. Overdenture supported by intraosseous implants can be distinguished among the methods of treatment. Aim of the study. To analyze the available literaturę on the possibility of using miniscrews to improve the overall stability of the prosthesis. Methods. The ProQuest database has been analyzed. 26 original articles were qualified for future research. Results and conclusions. Retention and stability can be largely improved by the use of miniscrews. A simple method of implantation can be used even in cases of significant loss of alveolar bone without augmentation procedures. The authors recommend the use of miniscrews in the elderly when extensive implant surgery cannot be performed. The studies showed improvements in stability, comfort, mastication and speech. An overdenture stabilized on the mini implants is auseful solution in clinically difficult situations.

Periodontal inflammation affects the mechanical and immune barrier functions of mice gut

To explore the effects of periodontal inflammation on the functions of gut barrier (ecological barrier, mechanical barrier, and immune barrier) in mice. Twenty male C57BL/6J mice were randomly divided into perio-dontitis (P) or control (C) groups. The P group was subjected under a 10-day ligation with Porphyromonas gingivalis to induce periodontitis, whereas the C group was ligated with sham. Maxillae were obtained to assess alveolar bone loss. The phylogenetic structure and diversity of microbial communities in the gut were analyzed by 16s rRNA pyrosequencing. Immunohisto-chemical analysis was performed to determine the expressions of occludin, claudin2, and NOD2 in the ileum. Com-pared with the C group, the P group displayed significant alveolar bone loss (P<0.001). In addition, no significant influence on the main phyla and genus Parabacteroides of the two groups was observed (P>0.05). However, the ileum of the P group showed significantly upregulated occludin, claudin2, and NOD2 (P=0.039, P=0.011, and P=0.039, respectively). Periodontal inflammation influences to some extent the mechanical and immune barrier functions of the mice gut. .