Periodontitis is a common inflammatory disease of infectious origins that often evolves into a chronic condition. Aside from its importance as a stomatologic ailment, chronic periodontitis has gained relevance since it has been shown that it can develop into a systemic condition characterized by unresolved hyper-inflammation, disruption of the innate and adaptive immune system, dysbiosis of the oral, gut and other location's microbiota and other system-wide alterations that may cause, coexist or aggravate other health issues associated to elevated morbi-mortality. The relationships between the infectious, immune, inflammatory, and systemic features of periodontitis and its many related diseases are far from being fully understood and are indeed still debated. However, to date, a large body of evidence on the different biological, clinical, and policy-enabling sources of information, is available. The aim of the present work is to summarize many of these sources of information and contextualize them under a systemic inflammation framework that may set the basis to an integral vision, useful for basic, clinical, and therapeutic goals.

/pdf/periodontal-inflammation-and-systemic-diseases-an-overview-123omdkbud.pdf

Periodontal Inflammation and Systemic Diseases: An Overview

The aim of this paper is to provide a review on the role of inflammation in orthodontically induced inflammatory root resorption (OIIRR) and accelerating orthodontic tooth movement (AOTM) in orthodontic treatment. Orthodontic tooth movement (OTM) is stimulated by remodeling of the periodontal ligament (PDL) and alveolar bone. These remodeling activities and tooth displacement are involved in the occurrence of an inflammatory process in the periodontium, in response to orthodontic forces. Inflammatory mediators such as prostaglandins (PGs), interleukins (Ils; IL-1, -6, -17), the tumor necrosis factor (TNF)-α superfamily, and receptor activator of nuclear factor (RANK)/RANK ligand (RANKL)/osteoprotegerin (OPG) are increased in the PDL during OTM. OIIRR is one of the accidental symptoms, and inflammatory mediators have been detected in resorbed roots, PDL, and alveolar bone exposed to heavy orthodontic force. Therefore, these inflammatory mediators are involved with the occurrence of OIIRR during orthodontic tooth movement. On the contrary, regional accelerating phenomenon (RAP) occurs after fractures and surgery such as osteotomies or bone grafting, and bone healing is accelerated by increasing osteoclasts and osteoblasts. Recently, tooth movement after surgical procedures such as corticotomy, corticision, piezocision, and micro-osteoperforation might be accelerated by RAP, which increases the bone metabolism. Therefore, inflammation may be involved in accelerated OTM (AOTM). The knowledge of inflammation during orthodontic treatment could be used in preventing OIIRR and AOTM.

Is Inflammation a Friend or Foe for Orthodontic Treatment?: Inflammation in Orthodontically Induced Inflammatory Root Resorption and Accelerating Tooth Movement

Late-onset periodontitis is associated with a series of inflammatory reactions induced by periodontal pathogens, such as Porphyromonas gingivalis, a keystone pathogen involved in periodontitis. Neutrophils are the most abundant leukocytes in the periodontal pocket/gingival crevice and inflamed periodontal tissues. They form a "wall" between the dental plaque and the junctional epithelium, preventing microbial invasion. The balance between neutrophils and the microbial community is essential to periodontal homeostasis. Excessive activation of neutrophils in response to periodontal pathogens can induce tissue damage and lead to periodontitis persistence. Therefore, illuminating the interactions between neutrophils and periodontal pathogens is critical for progress in the field of periodontitis. The present review aimed to summarize the interactions between neutrophils and periodontal pathogens in late-onset periodontitis, including neutrophil recruitment, neutrophil mechanisms to clear the pathogens, and pathogen strategies to evade neutrophil-mediated elimination of bacteria. The recruitment is a multi-step process, including tethering and rolling, adhesion, crawling, and transmigration. Neutrophils clear the pathogens mainly by phagocytosis, respiratory burst responses, degranulation, and neutrophil extracellular trap (NET) formation. The mechanisms that pathogens activate to evade neutrophil-mediated killing include impairing neutrophil recruitment, preventing phagocytosis, uncoupling killing from inflammation, and resistance to ROS, degranulation products, and NETs.

/pdf/interactions-between-neutrophils-and-periodontal-pathogens-1acbd042cr.pdf

Interactions Between Neutrophils and Periodontal Pathogens in Late-Onset Periodontitis.

Periodontal diseases include periodontitis and gingival overgrowth. Periodontitis is a bacterial infectious disease, and its pathological cascade is regulated by many inflammatory cytokines secreted by immune or tissue cells, such as interleukin-6. In contrast, gingival overgrowth develops as a side effect of specific drugs, such as immunosuppressants, anticonvulsants, and calcium channel blockers. Human gingival fibroblasts (HGFs) are the most abundant cells in gingival connective tissue, and human periodontal ligament fibroblasts (HPLFs) are located between the teeth and alveolar bone. HGFs and HPLFs are both crucial for the remodeling and homeostasis of periodontal tissue, and their roles in the pathogenesis of periodontal diseases have been examined for 25 years. Various responses by HGFs or HPLFs contribute to the progression of periodontal diseases. This review summarizes the biological effects of HGFs and HPLFs on the pathogenesis of periodontal diseases.

/pdf/biological-roles-of-fibroblasts-in-periodontal-diseases-2qsx66oy.pdf

Biological Roles of Fibroblasts in Periodontal Diseases

The oral–gut microbiome axis in health and disease

Periodontitis is a common inflammatory periodontal disease affecting a wide range of population all over the world The causing bacteria releases chemicals which activate the innate immune system to release proinﬂammatory cytokines contributing to more progression This activates the acquired immune system leading to more progression of periodontitis As the immune response goes on, released cytokines and chemokines can damage the periodontal ligaments, gingiva, and alveolar bone There are many types of cytokines and chemokines in periodontitis Cytokines are peptide mediators who are responsible for cell signaling and communication Chemokines are a large subfamily of cytokines having the ability to coordinate leukocyte recruitment and activation This paper is a narrative review of the literatureThis review ensures that inflammatory mediators in the case of periodontitis can cause a noticeable damage in the whole apparatus of the periodontium It causes soft tissue inflammation and bone damage affected by the mediators of both innate and acquired immune systemThe inflammatory process is accompanied by large network of cytokines and chemokines There is high expression of proinflammatory cytokines such as interleukin (IL)-1α, IL-1β, IL-6, IL-12, tumor necrosis factor (TNF)-α, and regulatory cytokines such as IL-4, IL-1(RA) receptor antagonist, IL-10, and induced protein (IP)-10 There is also increased production of cytokines IL-10, IL-12, interferon-γ, IP-10, IL-1RA, and IL-4 Cytokines IL-17, IL-6, IL-1β, TNF-α, macrophage colony-stimulating factor, and prostaglandin E2 trigger the osteoclast activity causing bone resorption

/pdf/cytokines-and-chemokines-in-periodontitis-4k2zga0094.pdf

Cytokines and Chemokines in Periodontitis.

Abstract Objective  Topical application of ambonese banana ( Musa paradisiaca var. sapientum (L.) kuntze) stem sap gel (GEGPA) on the socket wound area showed an increase in the expression of platelet-derived growth factor-BB, while decrease in the expression of matrix metalloproteinase-2 and 9. The aim of this study is to achieve standard formulation of GEGPA through stability, viscosity, distribution area, and drugs release for oral gel wound healing. Materials and Methods  This is an in vitro and in vivo study with the randomized posttest only control group design. The gel was formulated according to the composition of each group by adding hydroxypropyl methylcellulose (HPMC), Lexgard, propylene glycol, and cold water to obtain 100 g of gel. Observations were made through the following tests: stability, viscosity, distribution area, drug release, and histopathological analysis of tooth extraction wound healing. Statistical analysis  Data were analyzed using a one-way analysis of variance ( α = 0.05) with GraphPad Prism-8 statistical software. Results  The study showed that the GEGPA formulation was stable against changes in consistency, color, smell, homogeneity, and pH value. There is a significant difference between groups with respect to viscosity ( p  = 0.0001), adhesion ( p  = 0.004), dispersion ( p  = 0.000), and fibroblast cell numbers on days 3 and 5 ( p  = 0.007 and p  = 0.001). There is no interaction between the active ingredients and the gel base of all formulations. Formulation 3 had better properties in terms of viscosity, broad distribution, and drug release compared with other groups. Application of GEGPA to tooth extraction wounds showed a significant proliferation of fibroblast cells on days 3 and 5. Conclusions  The formulation of M. paradisiaca var. sapientum (L.) kuntze extract with HPMC and propylene glycol obtained a gel preparation, GEGPA, that was organoleptically stable and met the topical gel standard for wounds in the oral cavity.

/pdf/topical-medicine-potency-of-musa-paradisiaca-var-sapientum-l-1euhnwm2.pdf

Topical Medicine Potency of Musa paradisiaca var. sapientum (L.) kuntze as Oral Gel for Wound Healing: An In Vitro , In Vivo Study

The advancements in the cell culture studies have led to the development of regenerative medicine concept. The aim of this study is to compare the effectiveness of some washing solutions, including phosphate buffered saline (PBS), sodium chloride (NaCl), and ringer's lactate (RL) on the rate of detachment and confluency in fibroblast and osteoblast cell culture. Baby Hamster Kidney 21 clone 13 (BHK21/C13) fibroblast cells and 7F2 osteoblast were cultured on T25 flasks for 3-4 days. Three treatment groups were classified on the basis of different washing solutions used in the moment before trypsinization: PBS, 0.9% NaCl, and RL. Each group was measured for the detachment rate and cell confluence. The measurement was done in 2 passage numbers. The use of PBS, NaCl, and RL washing solution showed that detachment time was less than 5 minutes for the fibroblasts and 3 minutes for the osteoblasts. There was a significant difference in the rate of fibroblast cell detachment (p=0.006) and osteoblast (p=0.016). The capability of fibroblasts and osteoblasts to achieve a confluence of 106 cells/well on the first and second measurements was almost the same between the washing solution groups. The use of physiological 0.9% NaCl solution as a washing solution in fibroblast and osteoblast cell culture has almost the same effectiveness as PBS to help accelerate cell detachment in less than 5 minutes without influencing the capability of cells to proliferate.

Cell detachment rates and confluence of fibroblast and osteoblast cell culture using different washing solutions.

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Cytokines and Chemokines in Periodontitis.

Topical Medicine Potency of Musa paradisiaca var. sapientum (L.) kuntze as Oral Gel for Wound Healing: An In Vitro , In Vivo Study

Cell detachment rates and confluence of fibroblast and osteoblast cell culture using different washing solutions.