Specialized pro-resolving lipid mediators: A future for conventional endodontics-A review (original) (raw)
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Pulpal Inflammation: Harmonizing The DoubleEdged Sword
2021
The Unique Defensive Response Of Dental Pulp To Any External Stimuli By Inflammation Has Long Been A Mechanism Of Interest For Us. On One Hand, It Marks The Beginning Of Any Dental Pathology Whereas On The Other It Also Marks The Initiation Of Dental Repair And Regeneration. Thus We Have Been Attempting To Better Comprehend The Inflammatory Biomarkers Associated And Also The Most Practical And Reliable Site To Assay The Same. This Review Article Assembles Few Of The Studies Undertaken For Harmonizing This Double Edged Sword And Hence Provide Better Endodontic Therapeutics.
Effects of inflammation in dental pulp cell differentiation and reparative response
Frontiers in dental medicine, 2022
The responsiveness of the dentin-pulp complex is possible due to the stimulation of dental pulp cells, which begin to synthesize and secrete dentin matrix. The inflammatory process generated by harmful stimuli should be understood as a natural event of the immune response, resulting in the recruitment of hematopoietic cells, which cross the endothelial barrier and reach the site a ected by the injury in order to eliminate the damage and provide an appropriate environment for the restoration of homeostasis. The repair process occurs in the presence of adequate blood supply, absence of infection, and with the participation of pro-inflammatory cytokines, growth factors, extracellular matrix components, and other biologically active molecules. Prostaglandins and leukotrienes are bioactive molecules derived from the metabolism of arachidonic acid, as a result of a variable range of cellular stimuli. The aim of this review is to describe the process of formation and biomineralization of the dentin-pulp complex and how pro-inflammatory events can modify this response, with emphasis on the lipid mediators prostaglandins and leukotrienes derived from arachidonic acid metabolism.
Deciphering Reparative Processes in the Inflamed Dental Pulp
Frontiers in Dental Medicine, 2021
Research over several decades has increased our understanding of the nature of reparative and regenerative processes in the dental pulp, at both the cellular and molecular level. However, advances in scientific knowledge have not translated into novel clinical treatment strategies for caries-induced pulpitis. This narrative review explores the evidence regarding the ability of inflamed pulp tissue to heal and how this knowledge may be used therapeutically. A literature search and evidence analysis covering basic, translational and clinical pulp biology research was performed. The review focuses on (1) the regenerative and defense capabilities of the pulp during caries-induced inflammation; (2) the potential of novel biomaterials to harness the reparative and regenerative functions of the inflamed pulp; and (3) future perspectives and opportunities for conservative management of the inflamed pulp. Current conservative management strategies for pulpitis are limited by a combination of...
Infectious Disorders - Drug Targets, 2013
Periodontal diseases are comprised of a group of inflammatory conditions that result in the destruction of the supporting structures of the dentition. Emphasis has traditionally been placed on the deleterious actions of lipid mediators, such as prostanoids and leukotrienes, in propagating the inflammatory response and enhancing tissue destruction. Recently, the emerging understanding of the molecular basis of inflammation has elucidated that return of tissue homeostasis, triggered as part of a normal inflammatory response i.e. resolution of inflammation is an active, agonist-mediated, well-orchestrated phenomenon. The naturally-occurring pro-resolution lipid mediators, lipoxins, resolvins, protectins, maresins etc. have been identified as a novel genus of potent and stereoselective players that counter-regulate excessive acute inflammation and stimulate molecular and cellular events that define resolution. In this Review, we provide an update and overview of newly identified mediators that play pivotal roles in resolution and focus on the emerging appreciation of the endogenous pathways and mediators that control timely resolution which can be exploited as novel drug targets to extend the pharamaceutical armamentarium to combat chronic inflammation, thus controlling periodontal inflammation and the associated systemic inflammatory effects on the body, in general.
Inflammation and Regeneration in the Dentin-Pulp Complex: A Double-edged Sword
Journal of Endodontics, 2014
The balance between the immune/inflammatory and regenerative responses in the diseased pulp is central to the clinical outcome, and this response is unique within the body because of its tissue site. Cariogenic bacteria invade the dentin and pulp tissues, triggering molecular and cellular events dependent on the disease stage. At the early onset, odontoblasts respond to bacterial components in an attempt to protect the tooth's hard and soft tissues and limit disease progression. However, as disease advances, the odontoblasts die, and cells central to the pulp core, including resident immune cells, pulpal fibroblasts, endothelial cells, and stem cells, respond to the bacterial challenge via their expression of a range of pattern recognition receptors that identify pathogen-associated molecular patterns. Subsequently, recruitment and activation occurs of a range of immune cell types, including neutrophils, macrophages, and T and B cells, which are attracted to the diseased site by cytokine/chemokine chemotactic gradients initially generated by resident pulpal cells. Although these cells aim to disinfect the tooth, their extravasation, migration, and antibacterial activity (eg, release of reactive oxygen species [ROS]) along with the bacterial toxins cause pulp damage and impede tissue regeneration processes. Recently, a novel bacterial killing mechanism termed neutrophil extracellular traps (NETs) has also been described that uses ROS signaling and results in cellular DNA extrusion. The NETs are decorated with antimicrobial peptides (AMPs), and their interaction with bacteria results in microbial entrapment and death. Recent data show that NETs can be stimulated by bacteria associated with endodontic infections, and they may be present in inflamed pulp tissue. Interestingly, some bacteria associated with pulpal infections express deoxyribonuclease enzymes, which may enable their evasion of NETs. Furthermore, although NETs aim to localize and kill invading bacteria using AMPs and histones, limiting the spread of the infection, data also indicate that NETs can exacerbate inflammation and their components are cytotoxic. This review considers the potential role of NETs within pulpal infections and how these structures may influence the pulp's vitality and regenerative responses.
Emerging Concepts in the Resolution of Periodontal Inflammation: A Role for Resolvin E1
Frontiers in immunology, 2017
Inflammatory response is a protective biological process intended to eliminate the harmful effect of the insulting influx. Resolution of inflammation constitutes an active sequence of overlapping events mediated by specialized proresolving mediators, such as lipoxins, resolvins, protectins, and maresins, which originate from the enzymatic conversion of polyunsaturated fatty acids (PUFAs). An unresolved acute inflammatory response results in chronic inflammation, which is a leading cause of several common pathological conditions. Periodontitis is a biofilm-induced chronic inflammatory disease, which results in loss of periodontal connective tissue and alveolar bone support around the teeth, leading to tooth exfoliation. An inadequate proresolving host response may constitute a mechanism explaining the pathogenesis of periodontal disease. An emerging body of clinical and experimental evidence has focused on the underlying molecular mechanisms of resolvins and particularly Resolvin E1 ...
Intracanal Delivery of Resolvin E1 Controls Inflammation in Necrotic Immature Rat Teeth
Journal of Endodontics, 2014
Introduction: Pulp necrosis in immature teeth and the resulting periodontal apical inflammation negatively affect root formation. Resolvin E1 (RvE1) is a lipidderived endogenous pro-resolution molecule that controls inflammation. The aim of this investigation was to evaluate the impact of RvE1 applied as an intracanal medication on root formation in nonvital immature teeth. Methods: To arrest root development, pulpectomy was performed in the lower first molars of 4week-old Wistar rats. After 3 weeks, irrigation with 2.5% sodium hypochlorite and 0.9% sterile saline was performed, and either a triple antibiotic paste (TAP) or RvE1 in saline was applied into the root canals. In the control group, access openings drilled into molars were left exposed to the oral environment. Root development and periapical repair were evaluated radiographically and histologically at 3 and 6 weeks after treatment. Results: RvE1 reduced periapical lesion size compared with the control at 3 weeks, which was similar to TAP. Inflammatory response in the RvE1treated group was markedly reduced compared with both TAP and control specimens. At 6 weeks, root development was observed in both groups, but RvE1 treatment produced less cellularity with more regular calcified tissue deposition. Conclusions: RvE1 and TAP had a positive impact on reducing inflammation and promoting root formation. RvE1 was more effective in reducing inflammation at earlier stages. RvE1 has potential to be used as root canal dressing to control inflammation in endodontically compromised teeth before complete root formation. Stability of RvE1 within the root canal and its delivery are issues to be addressed before its clinical use. (J Endod 2014;40:678-682)
2017
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Role of Cytokines, Endotoxins (LPS), and Lipoteichoic Acid (LTA) in Endodontic Infection
The most common etiological factor for pulpal or periapical disease is microorganisms. Apical periodontitis is considered as an inflammatory reaction in the peri-apical tissues to the presence of micro-flora and their components within the root canal system. The composition of micro-flora of root canal has been studied extensively over the years and the presence of gram-positive, gram-negative bacteria and their components are considered to be the main reason for endodontic treatment failure. Bacterial components such as Lipo Poly Saccharide (LPS) and Lipoteichoic Acid (LTA) can enter the peri-apical tissue and initiate the inflammatory process by increasing the level of cytokines. Therefore, this review was done to understand the role of Lipopolysaccharide (LPS), Lipoteichoic acid (LTA) and cytokines in endodontic infection and study their relationship between each other. Data from various resources were gathered and analyzed. The activation pathway and biological effects of cytokines were also studied and it was observed that cytokines especially TNF-α (Tumour Necrosis Factor), IL-1β (Interleukin), IL-6 and IL-8 are up-regulated as a consequence of the immune response generated against the LPS and LTA. Chemokines CXCL2 (Chemokine (C-X-C motif) ligand) and CXCL10 were also shown to have increased level due to the presence of LTA. Cytokines are required to combat the foreign material during an infection, but when the level of cytokines is too high, it can cause injuries to the host itself through peri-apical bone destruction. More studies should be carried out in order to better understand the significance of each cytokine during an endodontic infection and to improve the treatment given for the patients depending on their infection status.