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Caries is the most common cause of pulp-periapical disease. When the pulp tissue involved in caries becomes irreversibly inflamed and progresses to necrosis, the treatment option is root canal therapy because the infected or non-infected necrotic pulp tissue in the root canal system is not accessible to the host’s innate and adaptive immune defense mechanisms and antimicrobial agents. Therefore, the infected or non-infected necrotic pulp tissue must be removed from the canal space by pulpectomy. As our knowledge in pulp biology advances, the concept of treatment of pulpal and periapical disease also changes. Endodontists have been looking for biologically based treatment procedures, which could promote regeneration or repair of the dentin-pulp complex destroyed by infection or trauma for several decades. After a long, extensive search in in vitro laboratory and in vivo preclinical animal experiments, the dental stem cells capable of regenerating the dentin-pulp complex were discovered. Consequently, the biological concept of ‘regenerative endodontics’ emerged and has highlighted the paradigm shift in the treatment of immature permanent teeth with necrotic pulps in clinical endodontics. Regenerative endodontics is defined as biologically based procedures designed to physiologically replace damaged tooth structures, including dentin and root structures, as well as the pulp-dentin complex. According to the American Association of Endodontists’ Clinical Considerations for a Regenerative Procedure, the primary goal of the regenerative procedure is the elimination of clinical symptoms and the resolution of apical periodontitis. Thickening of canal walls and continued root maturation is the secondary goal. Therefore, the primary goal of regenerative endodontics and traditional non-surgical root canal therapy is the same. The difference between non-surgical root canal therapy and regenerative endodontic therapy is that the disinfected root canals in the former therapy are filled with biocompatible foreign materials and the root canals in the latter therapy are filled with the host’s own vital tissue. The purpose of this article is to review the potential of using regenerative endodontic therapy for human immature and mature permanent teeth with necrotic pulps and/or apical periodontitis, teeth with persistent apical periodontitis after root canal therapy, traumatized teeth with external inflammatory root resorption, and avulsed teeth in terms of elimination of clinical symptoms and resolution of apical periodontitis.

The goal of endodontic treatment is to obtain effective cleaning and removal of the smear layer, bacteria and their by products within the root canal system. Endodontic techniques use mechanical instruments as well as ultrasonic and chemical irrigation in an attempt to shape, clean and completely decontaminate the endodontic system, but still fall short of elimination of the same. A recent advancement in the delivery of laser energy into the root canal system has been investigated, specifically the creation of a system of laser-activated irrigation (LAI) .In this work, a novel tapered and stripped tip of a laser-activated irrigation technique called photon induced Photo-acoustic streaming (PIPS) was used. PIPS is a unique laser application utilizing the Er 2,940 nm wavelength. The Er:YAG is used because of its high affinity, chromophore, for water, and its hydroxyl group with low energy levels of 20 mJ creates a significant and profound photo acoustic shock wave that allows for 3-dimensional (3-D) movement of the irrigants without the need to place the tip close to the apical terminus. PIPS has significantly demonstrated the ability to remove smear layer, debride canals, lateral tubules, delicate apical morphology, and eliminating bacteria.Unlike other laser systems, this application with these specific settings and the unique PIPS tip design yields a nonthermal subablative effect. The purpose of this article is to introduce the experimental background of this laser technique in removing bacterial load in areas where traditional methods may fail to succeed and to introduce the clinical protocol.

INTRODUCTION:

Infective endocarditis (IE) is still associated with high mortality, and antibiotic prophylaxis strategies are under intense debate. We evaluated the incidence of bacteremia after root canal preparation in teeth with necrotic pulps and apical periodontitis.

METHODS:

Blood samples were taken before and 5 and 30 minutes after endodontic treatment in teeth with apical periodontitis from individuals at high (n = 21) or no risk (n = 11) for IE. The former received prophylactic antibiotic therapy. Bacteriologic samples were taken from root canals before chemomechanical preparation to confirm pulp infection. Samples were subjected to aerobic and anaerobic culture and quantitative real-time polymerase chain reaction (qPCR), the latter to determine the total bacterial and streptococcal levels.

RESULTS:

Culture revealed no bacteremia in all individuals. Analysis by qPCR showed that bacterial DNA occurred in all root canal samples. qPCR showed a similar incidence of bacteremia between patients who received or did not receive prophylactic antibiotic therapy (P > .05). In blood samples taken 5 minutes after endodontic procedures, bacteria were detected in 2 of 11 (18%) individuals not taking antibiotics and in 4 of 21 (19%) patients under prophylaxis. After 30 minutes, the incidence of bacteremia decreased to 2 of 21 (10%) in patients taking antibiotics and was undetectable in patients at no risk of IE. The incidence of bacteremia by streptococci was identical as that for total bacteria.

CONCLUSIONS:

No detectable bacteremia was evident by culture after treatment of infected root canals. Molecular analysis revealed bacterial DNA and streptococci in blood from some patients without a significant difference between individuals receiving or not receiving antibiotic prophylaxis.

INTRODUCTION:

This multicenter, prospective, nonsignificant risk clinical study evaluated healing rates for molars 12 months after endodontic therapy using the GentleWave System (Sonendo, Inc, Laguna Hills, CA).

METHODS:

Eighty-nine patients needing endodontic therapy who met the inclusion criteria consented for this clinical study. All enrolled patients were treated with a standardized protocol consisting of conservative access, shaping of canals to #20/.07, GentleWave treatment, and warm vertical obturation. Six endodontists performed the clinical procedures and follow-up evaluations. Preoperative, intraoperative, and postoperative data were collected from the consented patients. Each patient was evaluated for clinical signs and symptoms. Two trained, blinded, and independent evaluators scored the subject’s radiographs for signs of apical periodontitis using a periapical index. The teeth classified as healing or healed were considered as a success and accounted for the cumulative success rate of healing. Statistical analysis was performed by using the Fisher exact test, Pearson correlation, and multivariate logistic regression analyses of the preoperative prognostic factors at P = .05.

RESULTS:

Seventy-five teeth in 75 patients were evaluated at 12 months with a follow-up rate of 84.3%. The cumulative success of endodontic therapy was 97.3%. The success rates of necrotic and irreversible pulpitis were 92.9% and 98.4%, respectively; 3.8% of the patients experienced moderate postoperative pain within 2 days and no incidence of pain at 14 days, 6 months, and 12 months of initial therapy. Ten prognostic factors were identified using bivariate analyses. Using logistic analyses, the prognostic significant variable that was directly correlated to healing was the preoperative presence of lesions (P = .026).

CONCLUSIONS:

In this 12-month prospective multicenter clinical study, the GentleWave System showed a high level of success after a 12-month follow-up.

The Trial to Assess Chelation Therapy (TACT) was a randomized double-blind placebo-controlled trial enrolling patients age ≥50 years with prior myocardial infarction. TACT used a 2 × 2 factorial design to study ethylene diamine tetraacetic acid (EDTA) chelation and high-dose vitamin supplementation. Chelation provided a modest but significant reduction in cardiovascular endpoints. The benefit was stronger and significant among participants with diabetes but absent in those without diabetes. Mechanisms by which chelation might reduce cardiovascular risk in persons with diabetes include the effects of EDTA chelation on transition and toxic metals. Transition metals, particularly copper and iron, play important roles in oxidative stress pathways. Toxic metals, in particular cadmium and lead, are toxic for the cardiovascular system. This review discusses the epidemiologic evidence and animal and human studies supporting the role of these metals in the development of diabetes and ischemic heart disease and potential ways by which EDTA chelation could confer cardiovascular benefit.

Endodontic disease is a biofilm-mediated infection, and primary aim in the management of endodontic disease is the elimination of bacterial biofilm from the root canal system. The most common endodontic infection is caused by the surface-associated growth of microorganisms. It is important to apply the biofilm concept to endodontic microbiology to understand the pathogenic potential of the root canal microbiota as well as to form the basis for new approaches for disinfection. It is foremost to understand how the biofilm formed by root canal bacteria resists endodontic treatment measures. Bacterial etiology has been confirmed for common oral diseases such as caries and periodontal and endodontic infections. Bacteria causing these diseases are organized in biofilm structures, which are complex microbial communities composed of a great variety of bacteria with different ecological requirements and pathogenic potential. The biofilm community not only gives bacteria effective protection against the host’s defense system but also makes them more resistant to a variety of disinfecting agents used as oral hygiene products or in the treatment of infections. Successful treatment of these diseases depends on biofilm removal as well as effective killing of biofilm bacteria. So, the fundamental to maintain oral health and prevent dental caries, gingivitis, and periodontitis is to control the oral biofilms. From these aspects, the formation of biofilms carries particular clinical significance because not only host defense mechanisms but also therapeutic efforts including chemical and mechanical antimicrobial treatment measures have the most difficult task of dealing with organisms that are gathered in a biofilm. The aim of this article was to review the mechanisms of biofilms’ formation, their roles in pulpal and periapical pathosis, the different types of biofilms, the factors influencing biofilm formation, the mechanisms of their antimicrobial resistance, techniques to identify biofilms.

This review, gathered from diverse sources, shows how our microbiome influences health and ultimately how well we age. Evidence linking oral bacteria to Alzheimer’s disease (AD) is discussed in the context of aging, drawing together data from epidemiological, experimental, genetic, and environmental studies. Immunosenescence results in increased bacterial load as cell-mediated and humoral immune responses wane. The innate immune system gradually takes over; contributing to the rise in circulating proinflammatory cytokines such as TNFα. Maintaining the integrity of the blood-brain barrier (BBB) against a backdrop of increasing bacterial load is important. Aging may favor the proliferation of anaerobes in the mouth eliciting a robust TNFα response from the oral epithelium. Prolonged exposure to high levels of circulating TNFα compromises the integrity of the BBB. Sensitive techniques now detect the “asymptomatic” presence of bacteria in areas previously thought to be sterile, providing new insights into the wider distribution of components of the microbiome. These “immune-tolerated” bacteria may slowly multiply elsewhere until they elicit a chronic inflammatory response; some are now considered causal in instances of atherosclerosis and back pain. Inflammatory processes have long been associated with AD. We propose for a subset of AD patients, aging favors the overgrowth of oral anaerobes established earlier in life provoking a pro-inflammatory innate response that weakens the BBB allowing bacteria to spread and quietly influence the pathogenesis of AD. Finally, we suggest that human polymorphisms considered alongside components of the microbiome may provide new avenues of research for the prevention and treatment of disease.