Alzheimer disease and the periodontal patient: New insights, connections, and therapies.

Loss of cognitive function in the aging population, particular those with Alzheimer disease, presents unique challenges to health practitioners. For the dental practitioner these include management of periodontal diseases, caries, and other dental conditions in this special population. It is well established in the cognitively impaired patient that a lack of adherence to dental hygiene routines and professional care leads to increases in the prevalence and severity of these dental conditions, leading to increased loss of teeth. More recent evidence has indicated a possible role of the microbiota of dental plaque associated with periodontal diseases in the development and progression of Alzheimer disease, thereby supporting a two-way interaction of these two diseases. New therapies are needed to address the potential upstream events that may precede overt signs of Alzheimer disease. One of these approaches would be to target these various bacterial, viral, and other microbial pathogens associated with periodontal disease that can translocate into the bloodstream and then to distal sites, such as the brain. Such microbial translocation would lead to local inflammation and buildup of the hallmark signs of Alzheimer disease, including amyloid beta deposits, tau fragmentation and tangles, breakdown of host protective molecules, such as the apolipoproteins, and neuron toxicity. In this review, evidence for the biological basis of the role of the periodontal disease microflora on the initiation and progression of Alzheimer disease will be presented with a focus on the potential role of the keystone pathogen Porphyromonas gingivalis with its family of gingipain enzymes. The various mechanisms for which P. gingivalis gingipains may contribute to the initiation and progression of Alzheimer disease are presented. Small-molecule inhibitors of these gingipains and their effects on reducing biological markers of Alzheimer disease may have beneficial effects for the initiation and progression of loss of cognitive function in Alzheimer disease. In addition to these targeted therapies for specific periodontal pathogens, considerations for the dental practitioner in applying more general approaches to reducing the periodontal plaque microflora in the management of the cognitively impaired patient are discussed for this special population.

Bacterial reduction effect of four different dental lasers on titanium surfaces in vitro.

Compare the effectiveness of selected dental lasers for decontamination of machined titanium surfaces in vitro. Seventy-two sterile machined surface titanium discs were individually inoculated with strains of Streptococcus mutans (Sm), Streptococcus oralis (So), Aggregatibacter actinomycetemcomitans (Aa), or all three bacteria together (MIX) at 34.0° C, 20.8% O2 and 5% CO2 for 12 h. After incubation, the discs were divided into six groups: 1) no treatment, 2) 0.12% chlorhexidine gluconate (CHX), and 3) 10,600 CO2, 4) 810 nm diode, 5) 2780 nm Er,Cr:YSGG, 6) 1064 nm Nd:YAG laser groups. After treatment, any remaining viable bacteria were liberated from the discs via sonication, transferred onto brain heart infusion (BHI) agar plates for culturing, and colony-forming units (CFUs) were recorded. Statistical analysis was performed. There were statistically significantly differences (SSD) (p < 0.01) in bacterial reduction of discs individually inoculated with Aa between the Er,Cr:YSGG and Nd:YAG lasers. There was also a SSD (p < 0.01) lower effect with the MIX with the Er,Cr:YSGG compared with all other modalities. Bacterial reduction with the CO2 was better (p < 0.001) than treatment with CHX or the Er,Cr:YSGG laser on killing of So. Although all modalities of treatment showed a mean of 98% or greater viable bacterial reduction, the most consistent bacterial reduction of all titanium discs was with the Nd:YAG laser (100%).

Periodontal health and gingival diseases and conditions on an intact and a reduced periodontium: Consensus report of workgroup 1 of the 2017 World Workshop on the Classification of Periodontal and Peri-Implant Diseases and Conditions.

Periodontal health is defined by absence of clinically detectable inflammation. There is a biological level of immune surveillance that is consistent with clinical gingival health and homeostasis. Clinical gingival health may be found in a periodontium that is intact, i.e. without clinical attachment loss or bone loss, and on a reduced periodontium in either a non-periodontitis patient (e.g. in patients with some form of gingival recession or following crown lengthening surgery) or in a patient with a history of periodontitis who is currently periodontally stable. Clinical gingival health can be restored following treatment of gingivitis and periodontitis. However, the treated and stable periodontitis patient with current gingival health remains at increased risk of recurrent periodontitis, and accordingly, must be closely monitored. Two broad categories of gingival diseases include non-dental plaque biofilm-induced gingival diseases and dental plaque-induced gingivitis. Non-dental plaque biofilm-induced gingival diseases include a variety of conditions that are not caused by plaque and usually do not resolve following plaque removal. Such lesions may be manifestations of a systemic condition or may be localized to the oral cavity. Dental plaque-induced gingivitis has a variety of clinical signs and symptoms, and both local predisposing factors and systemic modifying factors can affect its extent, severity, and progression. Dental plaque-induced gingivitis may arise on an intact periodontium or on a reduced periodontium in either a non-periodontitis patient or in a currently stable "periodontitis patient" i.e. successfully treated, in whom clinical inflammation has been eliminated (or substantially reduced). A periodontitis patient with gingival inflammation remains a periodontitis patient (Figure 1), and comprehensive risk assessment and management are imperative to ensure early prevention and/or treatment of recurrent/progressive periodontitis. Precision dental medicine defines a patient-centered approach to care, and therefore, creates differences in the way in which a "case" of gingival health or gingivitis is defined for clinical practice as opposed to epidemiologically in population prevalence surveys. Thus, case definitions of gingival health and gingivitis are presented for both purposes. While gingival health and gingivitis have many clinical features, case definitions are primarily predicated on presence or absence of bleeding on probing. Here we classify gingival health and gingival diseases/conditions, along with a summary table of diagnostic features for defining health and gingivitis in various clinical situations.

Post-treatment supportive care for the natural dentition and dental implants.

Long-term successful treatment of chronic periodontitis requires placement of patients on post-treatment recall programs known as either periodontal maintenance therapy or supportive periodontal therapy. Selection of the recall intervals must be based on the specific needs of individual patients. A single recall interval (e.g. 6 months) is not suitable for all patients. The main purpose of these programs is to prevent the recurrence of periodontitis. The components of every periodontal maintenance therapy program include: review of medical/dental histories; complete oral examination with an emphasis on the detection of gingival inflammation; establishing whether the maintenance program is working by monitoring clinical attachment levels; evaluation of oral hygiene; and full-mouth supragingival and subgingival debridement (i.e. biofilm removal). Long-term post-insertion care for dental implants also requires a similar patient-specific recall program of supportive implant therapy. The main purposes of a supportive implant therapy program are to maintain a healthy peri-implant mucosa and thereby prevent the development of peri-implantitis. In cases in which plaque-induced peri-implant mucositis has occurred, a well-designed supportive implant therapy program can help return the mucosa to a healthy state. At the current time there is no consensus on the optimal interventions for the treatment of peri-implant mucositis. However, all effective supportive implant therapy programs emphasize meticulous oral hygiene practices, careful peri-implant examination, thoughtful analysis of risk factors and periodic removal of microbial deposits from the implants.

An In Vitro Pilot Study on the Effects of Silver Diamine Fluoride on Periodontal Pathogens and Three-Dimensional Scaffolds of Human Fibroblasts and Epithelial Cells.

Objective: The aims of this study were to investigate the antibacterial and cytotoxic effects of silver diamine fluoride (SDF) on periodontal pathogens and human skin constructs, respectively. Background: SDF has been proven to have bactericidal effects on cariogenic bacteria. No studies to date evaluated the bactericidal effects of SDF on periodontal pathogens nor its effect on epithelium and fibroblasts. Methods: Streptococcus mutans, Porphyromonas gingivalis, and Aggregatibacter actinomycetemcomitans were cultured in monospecies biofilms, exposed to increasing concentrations of SDF and inoculated on agar plates to assess viability. Human gingival fibroblasts in 2D cultures were exposed to 1 µL of 0.394% of SDF and viewed using real-time imaging. Finally, SDF was applied to human, 3D tissue scaffolds of fibroblasts and keratinocytes, and termed human skin equivalents (HSE). A clinical dose of 38% SDF was applied, and HSE were cultured for 12 hours, 1, 3, 5, and 10 days. The tissue was observed clinically and histologically with hematoxylin and eosin staining and TUNEL. Results: S. mutans and A. actinomycetemcomitans growth was completely inhibited using all dilutions of SDF, whereas P. gingivalis was still viable with 0.197% and 0.098% of SDF. Single-layer fibroblasts experienced immediate necrosis upon contact with SDF. Application of SDF to HSE showed maturation of a whitish lesion within 24 hours, followed by pigmented, crusted tissue after 3 days. Histological evaluation of treated tissues showed apoptotic cells in the epithelium and upper half of the connective tissue. Conclusion: Our data suggest that SDF has bactericidal properties against two periodontal pathogens: P. gingivalis and A. actinomycetemcomitans. SDF caused immediate necrosis of monolayer fibroblasts, but does not extend to the full extent of layered fibroblasts in HSE.

Mandibular Anterior Lingual Recession: Keratinized Tissue Grafting and Minimally Invasive Harvesting.

INTRODUCTION: The mandibular anterior lingual (MAL) keratinized tissue (KT) band is often insufficient in dimension: <2 mm height of which <1 mm is attached gingiva (AG). Its gingival phenotype is commonly characterized as thin (<1 mm) gingival thickness (GT) and having inadequate (<1 mm) AG width. When surgical treatment is indicated, prevention of significant apical displacement of the gingival margin and improvement of long-term gingival stability are enhanced by KT increase and phenotype modification in order to establish thick GT and adequate AG. The aim of this case report is to describe a bilaminar surgical approach, the modified coronally advanced flap (mCAF) and connective tissue graft with retained KT band (mCAF + CTGkt). It is an outcomes-driven surgical approach for KT increase and phenotype modification in order to predictably establish thick GT and adequate AG. The mCAF + CTGkt procedure is minimally invasive, predictable, well-tolerated and addresses both the unique features of MAL anatomy and normal oral functioning movement during the postoperative healing phase. CASE PRESENTATION: A 48-year-old female presented with chief complaint of MAL progressive gingival recession (GR). Attachment loss of 3-4 mm and lack of both KT and AG were documented. Primary treatment outcomes objectives were GR cessation, establish KT, increase GT and AG. A secondary outcome was decreasing GR. CONCLUSION: The mCAF + CTGkt procedure resulted in KT increase, phenotype modification to establish thick GT and adequate AG, and decreased GR. It addressed unique features of MAL anatomy. Postoperative healing outcomes were not negatively impacted by normal oral functioning.

Therapeutic Prognosis System for Root Coverage Procedures.

Although several techniques and materials have been adopted to treat gingival recession, the therapeutic prognosis of various treatment modalities is not well established. This article proposes a multidimensional therapeutic prognosis system for the treatment of gingival recession based on the currently available literature. Gingival defect characteristics, patient behavioral habits, and surgical- and anatomical-related factors that may affect the outcome of root coverage procedures are reviewed. A therapeutic prognosis system is provided to enable clinicians to analyze these factors prior to the root coverage procedures. Three clinical cases are also discussed to demonstrate the assessment and validation of this therapeutic prognosis system.

Does Peri-Implant Mucosa Have a Prognostic Value?

The need for keratinized tissue around implants remains a controversial topic. However, reconstruction of keratinized mucosa may be needed to facilitate restorative procedures, improve aesthetics, and control plaque during oral hygiene. Free gingival grafts, connective tissue grafts, allogenic/xenograft materials, and apically positioned flaps have been used to augment soft tissue around implants. Four different timing protocols have been explored with regard to soft-tissue augmentation: before and during implant placement, during the second-stage surgery, or after restoration. The timing and technique of soft-tissue augmentation remain controversial and lack support from literature. Long-term clinical studies to establish clear guidelines are warranted.

Periodontal health and gingival diseases and conditions on an intact and a reduced periodontium: Consensus report of workgroup 1 of the 2017 World Workshop on the Classification of Periodontal and Peri-Implant Diseases and Conditions.

Periodontal health is defined by absence of clinically detectable inflammation. There is a biological level of immune surveillance that is consistent with clinical gingival health and homeostasis. Clinical gingival health may be found in a periodontium that is intact, i.e. without clinical attachment loss or bone loss, and on a reduced periodontium in either a non-periodontitis patient (e.g. in patients with some form of gingival recession or following crown lengthening surgery) or in a patient with a history of periodontitis who is currently periodontally stable. Clinical gingival health can be restored following treatment of gingivitis and periodontitis. However, the treated and stable periodontitis patient with current gingival health remains at increased risk of recurrent periodontitis, and accordingly, must be closely monitored. Two broad categories of gingival diseases include non-dental plaque biofilm-induced gingival diseases and dental plaque-induced gingivitis. Non-dental plaque biofilm-induced gingival diseases include a variety of conditions that are not caused by plaque and usually do not resolve following plaque removal. Such lesions may be manifestations of a systemic condition or may be localized to the oral cavity. Dental plaque-induced gingivitis has a variety of clinical signs and symptoms, and both local predisposing factors and systemic modifying factors can affect its extent, severity, and progression. Dental plaque-induced gingivitis may arise on an intact periodontium or on a reduced periodontium in either a non-periodontitis patient or in a currently stable "periodontitis patient" i.e. successfully treated, in whom clinical inflammation has been eliminated (or substantially reduced). A periodontitis patient with gingival inflammation remains a periodontitis patient (Figure 1), and comprehensive risk assessment and management are imperative to ensure early prevention and/or treatment of recurrent/progressive periodontitis. Precision dental medicine defines a patient-centered approach to care, and therefore, creates differences in the way in which a "case" of gingival health or gingivitis is defined for clinical practice as opposed to epidemiologically in population prevalence surveys. Thus, case definitions of gingival health and gingivitis are presented for both purposes. While gingival health and gingivitis have many clinical features, case definitions are primarily predicated on presence or absence of bleeding on probing. Here we classify gingival health and gingival diseases/conditions, along with a summary table of diagnostic features for defining health and gingivitis in various clinical situations.

Subepithelial connective tissue graft in a localized, plaque-induced ulcerative gingival recession: a case report.

The transposition of connective tissue to increase the zone of keratinized tissue or cover exposed root surfaces has become an integral part of the surgical dental practice. An effort to expand the surgical protocol to gingival recession of ulcerative etiology is presented. Parameters such as pathogenesis, clinical characteristic, and histopathology are analytically discussed. Furthermore, different aspects of the mucogingival therapy phase of the grafting procedure are presented.

A prospective, multicenter study of bovine pericardium membrane with cancellous particulate allograft for localized alveolar ridge augmentation.

Resorption of the alveolar ridge may lead to ridge deformities that make dental implant placement difficult or impossible. Augmentation of the alveolar ridge may restore appropriate ridge form to allow implant placement. Forty-four patients with edentulous spaces completed this multicenter prospective trial to clinically and radiographically evaluate the efficacy of a bovine pericardium membrane and a particulate mineralized cancellous bone allograft in promoting lateral ridge augmentation. Overall, 38 of 44 patients (86.4%) were able to receive dental implants in the appropriate restoratively driven position 6 months after ridge augmentation. The mean gain in clinical ridge width after augmentation was 2.61 mm, while radiographically the mean gain in ridge width was 1.65 mm at a level 3 mm apical to the bony crest and 1.93 mm at a level 6 mm apical to the crest. On average, approximately 50% of the graft material added horizontally during surgery was displaced or resorbed during healing. Histomorphometric evaluation of cores taken from the augmented ridge at 6 months revealed that approximately 58% of the tissue volume was vital bone, with 12% residual allograft particles and 30% nonmineralized tissue.