Destruction Of Periodontal Ligament Research Articles

Nano-Based Drug Delivery Systems for Periodontal Tissue Regeneration.

Periodontitis is a dysbiotic biofilm-induced and host-mediated inflammatory disease of tooth supporting tissues that leads to progressive destruction of periodontal ligament and alveolar bone, thereby resulting in gingival recession, deep periodontal pockets, tooth mobility and exfoliation, and aesthetically and functionally compromised dentition. Due to the improved biopharmaceutical and pharmacokinetic properties and targeted and controlled drug release, nano-based drug delivery systems have emerged as a promising strategy for the treatment of periodontal defects, allowing for increased efficacy and safety in controlling local inflammation, establishing a regenerative microenvironment, and regaining bone and attachments. This review provides an overview of nano-based drug delivery systems and illustrates their practical applications, future prospects, and limitations in the field of periodontal tissue regeneration.

Treatment of aggressive periodontitis with photodynamic therapy and ozonated water irrigation as an adjunct to scaling and root planing: A case report

Aggressive periodontitis (AgP) is a type of periodontitis which causes rapid destruction of periodontal ligament and alveolar bone and occurs in otherwise systemically healthy individuals generally of a younger age group, but patients may be older. Ozonated water strongly inhibits the formation of oral biofilm and reduces the number of subgingival microbes. The photodynamic therapy (PDT) leads to formation of highly reactive nacent oxygen which causes bacterial cell death. This case report compares the treatment outcome of AgP with antimicrobial photodynamic therapy and ozonized water. The right side of a AgP diagnosed patient was treated by scaling and root planing (SRP) followed by subgingival irrigation with ozone water, while the left side was treated with SRP followed by PDT. After four sessions of irrigation, higher pocket reduction, more clinical attachment gain, and lower bacterial load were found in the segment treated with PDT.

Necrotising periodontal diseases

Necrotising periodontal diseases (NPDs) are a group of infectious diseases that include necrotising gingivitis (NG), necrotising periodontitis (NP) and necrotising stomatitis (NS). These three clinical presentations may represent different stages of a continuum of the same disease process, with shared aetiological factors, and broadly similar initial clinical features and treatments. The term ‘ulcerative’ is no longer used in classification as ulceration is considered secondary to the gingival necrosis present. NP may result in destruction of periodontal ligament and supporting bone, while in NS, destruction progresses to deeper tissues such as the lip, cheeks and tongue. These presentations are more frequently seen in patients with HIV/AIDS or other systemic/immune compromise and, in developing countries, among those with severe malnourishment, respectively. In an Irish context, NG will represent the most common clinical form seen in general dental practice and may present as an acute condition requiring urgent management. Consequently, the current review will focus on NG. Table 1 provides an overview of the key aspects of NG.

Laporan Kasus: Perawatan Splinting Wire pada Pasien Periodontitis disertai Diabetes Melitus

Periodontitis causes destruction of tooth attachment to bone and may predispose to systemic disease. Diabetes mellitus is a risk factor for periodontal disease, these two diseases are correlated; periodontal disease can be favored by bacterial infection caused by an alteration of the immune system because of diabetes mellitus as well as chronic inflammation caused by periodontal disease leads to poor glycemic control in these patients. Case report: A 56 years old female complaining of mobility at anterior teeth. Intra oral examination was found oral hygiene tends to be poor, 11th grade 2 luxation, 6,5 mm clinical loss attachment, 3,5 mm gingival recession, and 3 mm probing depth. She had been diagnosed diabetes mellitus and 2 years ago and has medical treatment for this diseases. The therapy provided is in the form of education, scaling, and splinting wire. Discussion: Diabetes mellitus is associated with periodontal ligament destruction which subsequently can lead to tooth loss. Gingival crevicular fluids and saliva have higher concentrations of inflammatory mediators including different types of cytokines among diabetic patients with periodontitis as compared to non-diabetic individuals with periodontal disease. Conclusion: Chronic periodontitis in patients with diabetes melitus must be monitored periodically both blood glucose levels and plaque control in the oral cavity.

The α-mangostin effect on the quantity of TGF-β1 titer relate to the mandibular bone volume of Rattus novergicus in the periodontitis model

Context: Periodontitis causes pocket formation, gingival recession, and destruction of periodontal ligaments and alveolar bone. Periodontitis disturbs the attachment of periodontal ligaments to the maxillary and mandibular bones. The α-mangostin has shown role-playing in the bone remodeling process. Aims: To evaluate the potential of α-mangostin induce the TGFβ1 titer associated with the increased mandibular bone volume on the alveolar bone remodeling of periodontitis of Rattus novergicus. Methods: The α-mangostin used to the single administration dosage on the rat periodontitis model on the 7 and 14 days. TGF-β1 titer tested by enzyme-linked immunosorbent assay, while the X-Ray Micro-CT/Micro Computed Tomography examined the volume’s development of the mandibular bone. Results: At the 7 days, 0.5 and 1% of α-mangostin had a better effect to increase the bone volume, and TGF-β1 titer has linearity of bone development at concentrations of 0.5 to 2%. At 14 days, 1 and 2% of α-mangostin exhibited a better effect on inducing an increase in mandibular bone volume and TGF-β1 titer. The linearity of both occurs at concentrations of 0.5 to 1%. The Micro-CT of the mandibular bone showed callus or new bone formation at the edge of each treatment group’s lesion as an indicator of bone remodeling. Conclusions: α-Mangostin induced an increase in the TGF-β1 titer, which was in line with the rise in the volume of the mandibular bone of Rattus novergicus.

Regeneration of intrabony defects using equine-derived biomaterials: a retrospective study

Objectives Periodontitis is an inflammatory disease caused by the formation of a bacterial biofilm that, espe­cially in predisposed subjects, may lead to periodontal ligament destruction and alveolar bone re­sorption. The aim of this work was to study the effectiveness of the treat­ment of intrabony defects due to periodontitis using bone granules and equine-derived pericardium membranes. … Continued

Bone Morphogenetic Protein 7 Expression in Alveolar Bone Addition With Autologous Blood, Lyophilized Bone and Atelocollagen.

The biomaterials used in guided bone regeneration have undergone significant diversification in recent years. This study aimed to evaluate alveolar bone addition and bone morphogenetic protein 7 (BMP7) expression using an improved autologous and xenogeneic biomaterial. Chronic marginal periodontitis was induced in sheep; the intervention group received bone addition as periodontal therapy, using a composite system with lyophilized bovine bone enriched with atelocollagen type 1, platelet-rich plasma and advanced platelet-rich fibrin (A-PRF). Six weeks after the intervention, the dentoalveolar structures were evaluated using hematoxylin-eosin and immunohistochemical staining, to evaluate bone addition and BMP7 expression. The untreated sheep showed inflammation, periodontal ligament destruction, remnants of calculus and bacterial plaque as well as foreign bodies in the desmodontal space, without sings of repair. In the treated sheep, fibroblasts/fibrosis, cartilage and/or new bone, cellular cementum and desmodontium, along with remnants of biomaterial with various degrees of cellularity were observed. In the untreated group, the presence of BMP7 was found in osteoblasts and osteocytes while in the treated group, it was mainly found in the biomaterial remnants, while immunohistochemical staining was less intense in the newly formed osteo-periodontal tissues. Quantitative analysis using the Mann-Whitney U-test showed highly statistically significant differences between the two groups, demonstrating the efficiency of this composite system. The current composite system meets all the necessary conditions for promising guided alveolar bone regeneration.

The Junctional Epithelium Is Maintained by a Stem Cell Population

The most fundamental function of an epithelial tissue is to act as a barrier, regulating interactions between the external environment and the body. This barrier function typically requires a contiguous cell layer but since teeth penetrate the oral epithelium, a modified barrier has evolved, called the junctional epithelium (JE). In health, the JE attaches to the tooth, sealing the inside of the body against oral micro-organisms. Breakdown of the JE barrier results in periodontal ligament (PDL) disintegration, alveolar bone resorption, and ultimately tooth loss. Using lineage tracing and DNA pulse-chase analyses, we identified an anatomical location in the JE that supported both fast- and slow-cycling Wnt-responsive stem cells that contributed to self-renewal of the tissue. Stem cells produced daughter cells with an extraordinarily high rate of turnover that maintained JE integrity for 1.4 y in mice. Blocking cell proliferation via a chemotherapeutic agent 5-fluorouracil (5-Fu) eliminated fast-cycling stem cells, which caused JE degeneration, PDL destruction, and bone resorption. Upon removal of 5-Fu, slow-cycling stem cells regenerated both the structure and barrier function of the JE. Taken together, our studies identified a stem cell population in the JE and have potential clinical implications for prevention and treatment of periodontitis.

Targeting NLRP3 Inflammasome Reduces Age-Related Experimental Alveolar Bone Loss

The cause of chronic inflammatory periodontitis, which leads to the destruction of periodontal ligament and alveolar bone, is multifactorial. An increasing number of studies have shown the clinical significance of NLRP3-mediated low-grade inflammation in degenerative disorders, but its causal linkage to age-related periodontitis has not yet been elucidated. In this study, we investigated the involvement of the NLRP3 inflammasome and the therapeutic potential of NLRP3 inhibition in age-related alveolar bone loss by using in vivo and in vitro models. The poor quality of alveolar bones in aged mice was correlated with caspase-1 activation by macrophages and elevated levels of IL-1β, which are mainly regulated by the NLRP3 inflammasome, in periodontal ligament and serum, respectively. Aged mice lacking Nlrp3 showed better bone mass than age-matched wild-type mice via a way that affects bone resorption rather than bone formation. In line with this finding, treatment with MCC950, a potent inhibitor of the NLRP3 inflammasome, significantly suppressed alveolar bone loss with reduced caspase-1 activation in aged mice but not in young mice. In addition, our in vitro studies showed that the addition of IL-1β encourages RANKL-induced osteoclastogenesis from bone marrow–derived macrophages and that treatment with MCC950 significantly suppresses osteoclastic differentiation directly, irrelevant to the inhibition of IL-1β production. Our results suggest that the NLRP3 inflammasome is a critical mediator in age-related alveolar bone loss and that targeting the NLRP3 inflammasome could be a novel option for controlling periodontal degenerative changes with age.

Methodology in Wistar rats periodontitis induction: A modified ligation technique with injection of bacteria

Introduction: Periodontitis is an inflammation affecting the supporting tissue of the teeth. It is characterized by periodontal ligament destruction and progressive alveolar bone loss. Periodontitis is often induced in laboratory animal models, such as Wistar rats used for experimental models. This study was conducted to develop a reproducible technique for induction of periodontitis in the mandible of Wistar rats using a modified ligation technique with an additional injection of Aggregatibacter actinomycetemcomitans. Context: Periodontitis is an inflammation affecting the supporting tissue of the teeth. It is characterized by periodontal ligament destruction and progressive alveolar bone loss. Aims: The aim of this study was to develop a reproducible technique for induction of periodontitis in the mandible of Wistar rats using a modified ligation technique with an additional injection of A. actinomycetemcomitans. Settings and Design: The study was conducted at LPPT Unit IV Universitas Gadjah Mada, Yogyakarta. Subjects and Methods: Ten 2-month-old male adult Wistar rats were used as experimental subjects with an average weight of 150–200 g. Nonresorbable silk ligature wire (4/0) was used as ligatures and placed with an “8”-shaped knot technique. The ligatures were placed in between both central incisors of the mandible for 7 days with additional injections of A. actinomycetemcomitans on the 1st day. The procedure was performed under ketamine anesthesia. After 7 days, ligatures were removed and the animal subjects were euthanized with cervical dislocation method and samples of mandibles were preserved in formalin solution and processed histologically and radiographically. Results: Modified induction technique of periodontitis with ligatures and additional injection of A. actinomycetemcomitans showed significant clinical inflammation, periodontal ligament widening, attachment loss, and alveolar bone loss. Conclusions: We demonstrated clinical, radiographic, and histological evaluation from this modified induction technique and concluded that it has several advantages: shorter period of induction time with more significant clinical changes and advanced bone loss, simplifying the technique for induction of periodontitis.

Quantitative Evaluation of Porphyromonas gingivalis in Indian Subjects With Chronic Periodontitis by Real-Time Polymerase Chain Reaction

Background and Aims:Porphyromonas gingivalis ( P. gingivalis) is considered as an important pathogen responsible for periodontal disease which is characterized by inflammation of gingiva and destruction of periodontal ligament and alveolar bone leading to loss of tooth. Along with clinical investigations, suitable microbiological analysis needs to be performed which could provide more insight into the disease severity. We aim to quantify P. gingivalis by real-time PCR (RT-PCR) and analyze its association with demographic data including clinical parameters.Materials and Methods:The study consisted of chronic periodontitis patients (CP group) and healthy subjects (H group) with 120 samples in each group. RT-PCR was carried out by the SYBR Green assay to target 16S ribosomal ribonucleic acid species-specific region of P. gingivalis. Standard strain of P. gingivalis ATCC 33277 was used as a control.Results:In the CP group, 79.16% samples were found positive for P. gingivalis, whereas 29.17% samples were positive in the H group. A significant difference was found when the prevalence was compared within males and females ( P < .001 for both). In the older age groups, we found a higher rate of detection of P. gingivalis. As analyzed by Spearman’s correlation test, the number of cells of P. gingivalis was significantly associated with probing depth ( P = .02) and clinical attachment level ( P = .01) in the CP group. The mean cell number of P. gingivalis was found to be increasing with increasing levels of probing depth and clinical attachment level ( P < .001 and P = .01, respectively).Conclusion:The present study reaffirms that the P. gingivalis microbe is significantly associated with the chronic periodontitis and that its level varies with the severity of the disease. Colonization of the bacterium is significantly associated with severe forms of the disease.

Induction of chondrogenic or mesenchymal stem cells from human periodontal ligament cells through inhibition of Twist2 or Klf12.

Periodontitis leads to destruction of periodontal ligament, cementum and alveolar bone. Regeneration of periodontal tissue is dependent on mesenchymal stem cells (MSC) present in the periodontal ligament, and transcription factors determine the direction of MSC differentiation. The present study was conducted to investigate the transcription factors that are crucial for maintaining the characteristics of the periodontal ligament. The mRNA levels of several transcription factors were measured in cultured human periodontal ligament (HPDL) cells, human gingival fibroblasts and osteoblast-like Saos2 cells. HPDL cells were transfected for 72 h with siTwist2, siKlf12, or siMix (siTwist2, siPax9, and siKlf12). The cells were then harvested and subjected to real-time PCR and Western blotting. siTwist2 suppressed the levels of Twist2, Sox2 and Col1a1 mRNAs, and increased those of Sox5 and aggrecan mRNAs. siKlf12 decreased the mRNA levels of Klf12, Runx3, Zfp521, and Stab2, and increased those of Sox2, Klf4, and the MSC markers CD90 and CD105. These results suggest that transfection with siMix and siTwist2 induced chondrogenesis, and that siKlf12 induced the differentiation of MSC in HPDL cells. Thus, inhibition of Twist2 or Klf12 induced the differentiation of chondrogenic or mesenchymal stem cells in this setting, suggesting that the characteristics of HPDL cells may be altered by inhibition of specific transcription factors.

Development and Characterization of Novel Medicated Nanofiber for the Treatment of Periodontitis.

Periodontitis is a common microbial infection that involves pocket formation due to the destruction of periodontal ligament. The present work is oriented to provide a holistic approach for the treatment of periodontitis comprising localized delivery of nanometric hydroxyapatite as a reinforcing filler and silver-metronidazole as periodontal pocket disinfectant adjunct to current periodontal therapy because of its broad-spectrum antimicrobial activity and low systemic toxicity. In the present work, electrospinning technique was used to prepare medicated nanofiber enriched with antibacterial-hydroxyapatite layers for dental application. The optimized formulation was characterized by SEM, FTIR, DSC, XRD, etc. Safety assessment and therapeutic potential of optimized formulation was evaluated in both in vitro and in vivo animal models. The newly synthesized complex (silver-metronidazole) exhibited higher antibacterial activity against the selected strain over the referenced silver and metronidazole. Results of in vitro studies suggested good compatibility of the metal complex with the polymer matrix. The drug release behavior from optimized formulation shows constant in vitro release behavior. Both in vitro and in vivo studies show broad-spectrum antimicrobial activity of the metal complex and demonstrate the potential of biomimetic nano-hydroxyapatite for filling periodontal defects. All these observations indicated that the above formulation could play a useful role in the treatment of periodontitis. Graphical Abstract ᅟ.

Inhibition of angiotensin II receptor I prevents inflammation and bone loss in periodontitis

Periodontal disease is characterized by alveolar bone destruction and degenerative lesions of the periodontal ligament (PDL); it is initiated by bacterial infection of the oral cavity, but the clinical effects are secondary to an aberrant host immune response. Primary hypertension (PH), which causes significant morbidity and mortality worldwide, has also been shown to be an inflammatory disease characterized by aberrant immune cell infiltration and activation. Clinical retrospective studies have shown a link between PH and periodontitis with PH exacerbating periodontitis and vice versa, but the pathophysiologic mechanisms responsible for this remain unknown. In this study, we investigate the underlying mechanisms behind PH exacerbation of periodontitis by using a bacteria-induced periodontitis model in normotensive and hypertensive (Nos3-/- ) mice treated with or without an Angiotensin II (Ang II) specific receptor 1 (AT1) antagonist, losartan. The histologic analyses including immunohistochemistry, immunofluorescence were carried out. The qRT-PCR and ELISAs were applied for the target gene and protein detection. We find that PH worsens bone resorption and PDL destruction in periodontitis and that treatment with losartan, rescues this. We also show that PH increases dendritic cell (DC) and osteoclast (OC) infiltration in periodontitis, which is also dependent on Ang II. Finally, we show that PH augments the pro-inflammatory state in periodontitis infiltrating DCs in an Ang II-dependent manner and use in vitro studies to show that Ang II directly augments DC Toll-like receptor 4 (TLR4) signaling. Our studies show a central role for Ang II as a pro-inflammatory Toll-like receptor mediator in the pathogenesis of PH-exacerbated periodontitis, indicating that Ang II may be a reasonable target in patients with PH and periodontitis comorbidity.

The effect of dental facilities on the processes of tooth loss between urban and rural populations in Edo State, Nigeria

Objectives: The objective of this study was to ascertain the effect of the presence of dental facilities on the various processes of tooth loss in the study population and if there were differences between urban and rural subjects.Methods: A total of 2,161 subjects were examined, comprising 769 from one urban area and 1392 from three rural areas of the State. Examinations were conducted with the use of a wooden spatula and the Community Periodontal Index of Treatment Need probe.Results: The predominant process of permanent tooth loss in the entire study population was by extraction, followed by trauma and exfoliation. However, there was a statistical significant difference between the urban and rural subjects of the state. While the predominant process of tooth loss in urban subjects was by extraction but it varied from extraction through trauma to exfoliation amongst rural subjects.Discussion: The predominant tooth loss in the urban subjects could be attributed to the presence and access to dental facilities located in the urban area of this study. Here extraction was the most common procedure carried out due to its low cost, relative to restoration or endodontics. This was the result of the poor state of the economy and the high prevalence of caries. The process of tooth loss by exfoliation, which was predominant in the rural subjects, is the result of periodontal ligament destruction and alveolar bone resorption. This could be attributed to a higher prevalence of periodontal disease and the non-existence of dental facilities and personnel where extraction could have been done without the long await for self-exofoliation.Conclusion: This study has shown that the presence or absence of dental facilities and personnel are contributory factors to the different patterns of tooth loss in urban and rural populace.Keywords: dental facilities, tooth loss, urban and rural population

Impact of nicotine on the interplay between human periodontal ligament cells and CD4+ T cells.

Periodontitis is a common infectious disease associated with destruction of periodontal ligaments and alveolar bones. CD4(+) T cell-mediated immune response is involved in the progression of periodontitis. Tobacco consumption increases the risk of periodontal disease. However, the impact of nicotine on the interaction between human periodontal ligament (PDL) cells and CD4(+) T cells remains unrevealed. Our study aims to investigate the effect of nicotine on PDL cells and the cocultured CD4(+) T cells. The PDL cell cultures were established by explants from healthy individuals, exposed to nicotine or α-bungarotoxin (α-BTX), and incubated solely or in combination with CD4(+) T cells. Afterwards, cell viability, secreted cytokines, and matrix metalloproteinases (MMPs) were evaluated. In monoculture of PDL cells, nicotine dramatically repressed cell viability and increased apoptosis. Meanwhile, α-BTX largely reversed the nicotine-induced apoptosis and increased viability of PDL cells. Compared with the monoculture, MMP-1, MMP-3, interleukin (IL)-1β, IL-6, IL-17, and IL-21 in supernatant of cocultures were markedly elevated after treatment with nicotine. Moreover, α-BTX significantly attenuated nicotine-triggered production of these components either in mono- or co-cultures. In addition, PDL cell-derived CXCL12 following nicotine treatment recruited CD4(+) T cells. Above all, nicotine deteriorated periodontitis partially by promoting PDL cell-CD4(+) T cell-mediated inflammatory response and matrix degradation.

The General Awareness among People about the Prevalence of Periodontitis

Periodontal ligament is a specialised connective tissue supporting the tooth within its socket and the ligament lies between the cementum and the alveolar bone. The ligament fibres in the periapical region of the tooth is much prone to pathological lesions and inflammations. One such inflammatory disorder concerning the periodontal ligament destruction in the oral cavity is Periodontitis. 1, 2 The term periodontitis is derived from the Greek word ‘pyorrhea ’which means discharge of matter and can be defined as disease of the periodontium characterized by inflammation of the gums, resorption of the alveolar bone, and degeneration of the periodontal membrane 3, 4, 5. Periodontitis can be caused by the microorganisms that adheres to the tooth surface along with an over aggressive immune response against these microbes. The disease has also been linked with several other risk factors including increased risk of stroke, myocardial infarction, atherosclerosis and erectile dysfunction. Smoking and diabetes is considered to be one of the prime cause for periodontitis and it may have adverse impacts6. General oral hygiene habits such as brushing properly, flossing, using antiseptic mouth wash can be widely used to prevent periodontitis.

Uncovering the molecular networks in periodontitis.

Periodontitis is a complex immune-inflammatory disease that results from a preestablished infection in gingiva, mainly due to Gram-negative bacteria that colonize deeper in gingival sulcus and latter periodontal pocket. Host inflammatory and immune responses have both protective and destructive roles. Although cytokines, prostaglandins, and proteases struggle against microbial burden, these molecules promote connective tissue loss and alveolar bone resorption, leading to several histopathological changes, namely destruction of periodontal ligament, deepening of periodontal pocket, and bone loss, which can converge to attain tooth loss. Despite the efforts of genomics, transcriptomics, proteomics/peptidomics, and metabolomics, there is no available biomarker for periodontitis diagnosis, prognosis, and treatment evaluation, which could assist on the established clinical evaluation. Nevertheless, some genes, transcripts, proteins and metabolites have already shown a different expression in healthy subjects and in patients. Though, so far, 'omics approaches only disclosed the host inflammatory response as a consequence of microbial invasion in periodontitis and the diagnosis in periodontitis still relies on clinical parameters, thus a molecular tool for assessing periodontitis lacks in current dental medicine paradigm. Saliva and gingival crevicular fluid have been attracting researchers due to their diagnostic potential, ease, and noninvasive nature of collection. Each one of these fluids has some advantages and disadvantages that are discussed in this review.

Multifactorial relationship of obesity and periodontal disease.

Obesity is a chronic disease of mutifactorial origin, where there is increase in body fat. Periodontitis is an inflammatory disease of tooth supporting tissues resulting in destruction of periodontal ligament and alveolar bone. Periodontitis and obesity are both chronic health problems and the literature supports this association. A hyperinflammatory state observed in obesity is proposed as a mechanism to explain this association. This low grade inflammation in obese subjects triggers the worsening of non transmissible chronic diseases like periodontitis. So the aim of this article is to get the overview of association between adipose tissue derived cytokines and periodontal disease.

Periodontal Vaccine—A Boon In Periodontics

Periodontal disease though is multifactorial it is thought to be caused by group of gram negative anaerobic bacteria resulting in destruction of periodontal ligament and alveolar bone. The current treatment of periodontitis is non specific and is centered on removal of supragingival and subgingival plaque by mechanical debridement and surgical procedures. Due to its high prevalence rate this disease has created an innovative interest to find a solution in the form of vaccine. The search for periodontal vaccine revolves around the antigenic factors of the periodontal pathogens. The objective of periodontal vaccine is to identify the antigens involved in the destructive process of periodontitis against which antibodies would be evoked to exert protection. It also aims to induce mucosal antibody response with little or moderate doses of vaccine. Till date no preventive modality exists for periodontal disease and treatment rendered is palliative. Thus availability of periodontal vaccine would not only prevent and modulate periodontal disease but also enhance the quality of life for whom periodontal treatment cannot be easily obtained.