Prevalence of undiagnosed diabetes and prediabetes related to periodontitis and its risk factors in elderly individuals.

OBJECTIVE: The prevalence of undiagnosed diabetes was estimated to increase with age and can reach 3.5%. The purpose of the study was to evaluate the prevalence of undiagnosed diabetes and prediabetes in the elderly patients who attended a dental clinic and to find common risk factors. METHODS: Male patients, older than 50 years, attended their first dental visit to the School of Dentistry for a period of two years, and it was proposed to evaluate undiagnosed type 2 diabetes mellitus. Periodontal, biochemical, microbiological examinations, nutritional profile, and physical activity were performed. RESULTS: A total of 106 patients were examined, 6 (5.6%) had diabetes, and 37 (34.9%) had prediabetes without prior diagnosis. The severity of periodontitis was greater in patients with diabetes. Most of the patients were overweight and had increased systolic blood pressure. Patients with prediabetes and periodontitis had a low adherence to the Mediterranean diet. Tannerella forsythia was present in more patients with periodontitis, and the prevalence of Aggregatibacter actinomycetemcomitans is practically absent in groups with periodontitis, except for the group with diabetes. CONCLUSIONS: In the population studied, the prevalence of patients without a diagnosis of diabetes and prediabetes was very high and underestimated. The increased severity of periodontitis in patients with diabetes and in conjunction with the high level of cortisol seen in patients with periodontitis, especially those with diabetes, emphasize the dysregulation of the immunoinflammatory system. CLINICAL SIGNIFICANCE: It is essential to add all this data to our dental practice to cover patient health with a broader landscape.

Periodontitis and Other Risk Factors Related to Myocardial Infarction and Its Follow-Up.

The main issue in the prevention of myocardial infarction (MI) is to reduce risk factors. Periodontal disease is related to cardiovascular disease and both share risk factors. The purpose of this study is to investigate whether periodontitis can be considered a risk factor for MI and common risk factors in a case-control study and in a prospective follow-up study in patients with MI. The test group (MIG) was made up of 144 males who had MI in the previous 48 h. The control group (CG) was composed of 138 males without MI. Both groups were subdivided according to the presence or absence of stage III and IV of periodontitis. General data; Mediterranean diet and physical activity screening; periodontal data; and biochemical, microbiological and cardiological parameters were recorded. ANOVA, Mann-Whitney U and Kruskal-Wallis statistical tests and binary logistic regression analysis were applied. No differences in anthropometric variables were observed between the four groups. The average weekly exercise hours have a higher value in CG without periodontitis. The number of leukocytes was higher in MIG, the number of monocytes was higher in CG and the number of teeth was lower in MIG with periodontitis. Adherence to the Mediterranean diet was higher in CG. Porphyromonas gingivalis and Tannerella forsythia were higher in CG with periodontitis and in MIG with and without periodontitis. At follow-up, the left ventricular ejection fraction (LVEF) data were better in the non-periodontitis group: 15 patients had Mayor Cardiovascular Adverse Events (MACE), 13 of them had periodontitis and 2 did not show periodontitis. Periodontitis, exercise, diet and smoking are risk factors related to MI. MACE presented in the 'MI follow-up' shows periodontitis, weight, exercise hours and dyslipidemia as risk factors. LVEF follow-up values are preserved in patients without periodontitis. Our data suggest that periodontitis can be considered a risk factor for MI and MACE in the studied population.

Incidence of Peri-Implantitis and Relationship with Different Conditions: A Retrospective Study.

Articles on the prevalence of peri-implant diseases showed that 90% of peri-implant tissues had some form of inflammatory response and a prevalence of peri-implantitis from 28% to 51% according to various publications. Objective: To provide an overview of how risk factors can be related with peri-implantitis. Methods: A retrospective longitudinal study including 555 implants placed in 132 patients was evaluated based on the presence of peri-implantitis following the criteria of Renvert et al. 2018. Results: In total, 21 patients (15.9%) suffered peri-implantitis (PPG) and 111 patients (84.1%) did not suffer peri-implantitis (NPG). The results reveal that smokers have a high incidence of peri-implantitis (72.7%) compared to non-smokers (27.3%) (p < 0.0005). Another variable with significant results (p < 0.01) was periodontitis: 50% PPG and 23.9% NPG suffered advanced periodontitis. Systemic diseases such as arterial hypertension, diabetes mellitus, osteoporosis, and cardiovascular diseases do not show a statistically significant influence on the incidence of peri-implantitis. Patients who did not attend their maintenance therapy appointment had an incidence of peri-implantitis of 61.4%, compared to 27.3% in those who attend (p < 0.0001). From the results obtained, we can conclude that relevant factors affect peri-implantitis, such as tobacco habits, moderate and severe periodontitis, and attendance in maintenance therapy.

An Olive-Derived Extract 20% Rich in Hydroxytyrosol Prevents ß-Amyloid Aggregation and Oxidative Stress, Two Features of Alzheimer Disease, via SKN-1/NRF2 and HSP-16.2 in Caenorhabditis elegans.

Olive milling produces olive oil and different by-products, all of them very rich in different bioactive compounds like the phenolic alcohol hydroxytyrosol. The aim of the present study was to investigate the effects of an olive fruit extract 20% rich in hydroxytyrosol on the molecular mechanisms associated with Alzheimer disease features like Aß- and tau- induced toxicity, as well as on oxidative stress in Caenorhabditis elegans. Moreover, characterization of the extracts, regarding the profile and content of phenolics, as well as total antioxidant ability, was investigated. The study of lethality, growth, pharyngeal pumping, and longevity in vivo demonstrated the lack of toxicity of the extract. One hundred µg/mL of extract treatment revealed prevention of oxidative stress and a delay in Aß-induced paralysis related with a lower presence of Aß aggregates. Indeed, the extract showed the ability to avoid a certain degree of proteotoxicity associated with aggregation of the tau protein. According to RNAi tests, SKN-1/NRF2 transcription factor and the overexpression of HSP-16.2 were mechanistically associated in the observed effects.

An oleuropein rich-olive (Olea europaea L.) leaf extract reduces ß-amyloid and tau proteotoxicity through regulation of oxidative- and heat shock-stress responses in Caenorhabditis elegans.

Olive tree-derived products have been associated with numerous benefits for health. The aim of the present study was to characterize an olive leaf extract enriched in oleuropein (OLE) concerning phenolic content and profile as well as antioxidant capacity. Short-term and long-term toxicity, including oxidative stress, was in vivo evaluated in the experimental model Caenorhabditis elegans. Moreover, the potential therapeutic effect of the extract against Aß induced- and tau protein induced-toxicity was also evaluated in C. elegans. OLE treatment did not exert toxicity. On the contrary, the extract was able to ameliorate oxidative stress and proteotoxicity related to Aß and tau aggregation. The potential molecular mechanisms present behind the observed results explored by RNAi technology revealed that DAF-16/FOXO and SKN-1/NRF2, elements of the insulin insulin-like signalling pathway, as well as HSP-16.2 overexpression were involved.

Diabetes Mellitus and Periodontitis Share Intracellular Disorders as the Main Meeting Point.

Diabetes and periodontitis are two of the most prevalent diseases worldwide that negatively impact the quality of life of the individual suffering from them. They are part of the chronic inflammatory disease group or, as recently mentioned, non-communicable diseases, with inflammation being the meeting point among them. Inflammation hitherto includes vascular and tissue changes, but new technologies provide data at the intracellular level that could explain how the cells respond to the aggression more clearly. This review aims to emphasize the molecular pathophysiological mechanisms in patients with type 2 diabetes mellitus and periodontitis, which are marked by different impaired central regulators including mitochondrial dysfunction, impaired immune system and autophagy pathways, oxidative stress, and the crosstalk between adenosine monophosphate-activated protein kinase (AMPK) and the renin-angiotensin system (RAS). All of them are the shared background behind both diseases that could explain its relationship. These should be taken in consideration if we would like to improve the treatment outcomes. Currently, the main treatment strategies in diabetes try to reduce glycemia index as the most important aspect, and in periodontitis try to reduce the presence of oral bacteria. We propose to add to the therapeutic guidelines the handling of all the intracellular disorders to try to obtain better treatment success.

Inhibition of the NLRP3 inflammasome prevents ovarian aging.

Inflammation is a hallmark of aging and is negatively affecting female fertility. In this study, we evaluate the role of the NLRP3 inflammasome in ovarian aging and female fertility. Age-dependent increased expression of NLRP3 in the ovary was observed in WT mice during reproductive aging. High expression of NLRP3, caspase-1, and IL-1ß was also observed in granulosa cells from patients with ovarian insufficiency. Ablation of NLRP3 improved the survival and pregnancy rates and increased anti-Müllerian hormone levels and autophagy rates in ovaries. Deficiency of NLRP3 also reduced serum FSH and estradiol levels. Consistent with these results, pharmacological inhibition of NLRP3 using a direct NLRP3 inhibitor, MCC950, improved fertility in female mice to levels comparable to those of Nlrp3-/- mice. These results suggest that the NLRP3 inflammasome is implicated in the age-dependent loss of female fertility and position this inflammasome as a potential new therapeutic target for the treatment of infertility.

Sinus Floor Elevation via an Osteotome Technique without Biomaterials.

According to classic Hirschfeld studies, the first teeth to be lost are the first and second maxillary molars. After the teeth are extracted and the alveolar process is developed, the maxillary sinus is reabsorbed and pneumatized with a decrease in bone availability in the posterior sector of the maxilla. This process often creates the need to perform regeneration techniques for the placement of implants in this area due to the low availability of bone. The most frequently used and documented technique for the elevation of the sinus maxillary floor is elevation by the side window, as proposed by Tatum. In 1994, Summers proposed a technique that allowed the elevation of the sinus floor from a crestal access using an instrument called an osteotome, as well as the placement of the implant in the same surgical act. The aimed of the study was to evaluate the survival of 32 implants placed in posterior maxilla with bone availability less than 5 mm performing a sinus lift augmentation technique with osteotome without biomaterials. The results of this study show a survival rate of 100% for 32 implants placed in situations with an initial bone availability of 2 to 5 mm without the use of graft material. The infra-drilling technique used offers an increase in the primary stability of implants that allows adequate osteointegration Implants placed were charged at 12 weeks. In all cases, spontaneous bone formation was observed, even in cases where a positive Valsalva maneuver was observed. This proposed technique reduces treatment time and the need for more invasive maxillary sinus augmentation techniques.

Potential Role of the Mitochondria for the Dermatological Treatment of Papillon-Lefèvre.

The Papillon-Lefèvre syndrome (PLS) is a rare autosomal recessive disorder caused by mutations in the Cathepsin C (CTSC) gene, characterized by periodontitis and palmoplantar hyperkeratosis. The main inflammatory deficiencies include oxidative stress and autophagic dysfunction. Mitochondria are the main source of reactive oxygen species; their impaired function is related to skin diseases and periodontitis. The mitochondrial function has been evaluated in PLS and mitochondria have been targeted as a possible treatment for PLS. We show for the first time an important mitochondrial dysfunction associated with increased oxidative damage of mtDNA, reduced CoQ10 and mitochondrial mass and aberrant morphologies of the mitochondria in PLS patients. Mitochondrial dysfunction, determined by oxygen consumption rate (OCR) in PLS fibroblasts, was treated with CoQ10 supplementation, which determined an improvement in OCR and a remission of skin damage in a patient receiving a topical administration of a cream enriched with CoQ10 0.1%. We provide the first evidence of the role of mitochondrial dysfunction and CoQ10 deficiency in the pathophysiology of PLS and a future therapeutic option for PLS.

Influence of Removing or Leaving the Prosthesis after Regenerative Surgery in Peri-Implant Defects: Retrospective Study: 32 Clinical Cases with 2 to 8 Years of Follow-Up.

PURPOSE: The aim of this retrospective study was to compare the influence of removing or not removing a prosthesis after regenerative surgery on peri-implant defects. METHODS: Two different groups were compared (Group 1: removing the prosthesis; Group 2: maintaining the prosthesis), analyzing radiographic bone filling (n = 32 implants) after regenerative treatment in periapical radiographs. The peri-implant defects were measured before and after regenerative treatment using Bio-Oss® (Geistlich Pharma, Wohhusen, Switzerland) and a reabsorbable collagen membrane (Jason®, Botis, Berlin, Germany), the healing period was two years after peri-implant regenerative surgery. Statistical analysis was performed, and a Chi square test was carried out. To determine the groups that made the difference, corrected standardized Haberman residuals were used, and previously a normality test had been applied; therefore, an ANOVA or Mann-Whitney U test was used for the crossover with the non-normal variables in Group 1 and Group 2. RESULTS: The results obtained suggest that a regenerative procedure with xenograft, resorbable membrane, and detoxifying the implant surface with hydrogen peroxide form a reliable technique to achieve medium-term results, obtaining an average bone gain at a radiographic level of 2.84 mm (±1.78 mm) in patients whose prosthesis was not removed after peri-implant bone regenerative therapy and 2.18 mm (±1.41 mm) in patients whose prosthesis was removed during the healing period. CONCLUSIONS: There are no statistically significant differences in the response to treatment when removing or keeping the prosthesis after regenerative surgery in peri-implant defects.

Is AMP-Activated Protein Kinase Associated to the Metabolic Changes in Primary Ovarian Insufficiency?

Primary ovarian insufficiency (POI) is a critical fertility defect characterized by anticipated impairment of the follicular reserve, which pathophysiological mechanisms have not yet been identified. We have investigated the possible relationship between AMP-activated protein kinase (AMPK) and the pathophysiology of POI. We studied 35 POI patients with altered levels of follicle-stimulating hormone (FSH) and estradiol and increased percentage of overweight compared with 20 healthy women. Blood mononuclear cells from POI patients showed reduced levels of phosphorylated AMPK, adenosine triphosphate, and high serum levels of leptin and tumor necrosis factor-alpha. All these alterations were also observed in granulosa cells, a more closer environment of the ovary. Significant negative correlations between AMPK and body mass index, FSH and leptin levels, and a positive correlation between AMPK and estradiol levels were observed. Oral metformin supplementation restored biochemical parameters. Interestingly, AMPK levels from patients were negatively correlated with age, suggesting an accelerated aging in POI mediated by the impairment of AMPK. These results lead to the hypothesis that an impairment of AMPK could be implicated in the metabolic pathophysiology of POI indicating at AMPK induction as a possible new therapeutic target.

A Diet Rich in Saturated Fat and Cholesterol Aggravates the Effect of Bacterial Lipopolysaccharide on Alveolar Bone Loss in a Rabbit Model of Periodontal Disease.

Increasing evidence connects periodontitis with a variety of systemic diseases, including metabolic syndrome, atherosclerosis, and non-alcoholic fatty liver disease (NAFLD). The proposal of this study was to evaluate the role of diets rich in saturated fat and cholesterol in some aspects of periodontal diseases in a lipopolysaccharide (LPS)-induced model of periodontal disease in rabbits and to assess the influence of a periodontal intervention on hyperlipidemia, atherosclerosis, and NAFLD progression to non-alcoholic steatohepatitis. Male rabbits were maintained on a commercial standard diet or a diet rich in saturated fat (3% lard w/w) and cholesterol (1.3% w/w) (HFD) for 40 days. Half of the rabbits on each diet were treated 2 days per week with intragingival injections of LPS from Porphyromonas gingivalis. Morphometric analyses revealed that LPS induced higher alveolar bone loss (ABL) around the first premolar in animals receiving standard diets, which was exacerbated by the HFD diet. A higher score of acinar inflammation in the liver and higher blood levels of triglycerides and phospholipids were found in HFD-fed rabbits receiving LPS. These results suggest that certain dietary habits can exacerbate some aspects of periodontitis and that bad periodontal health can contribute to dyslipidemia and promote NAFLD progression, but only under certain conditions.

Molecular inflammation and oxidative stress are shared mechanisms involved in both myocardial infarction and periodontitis.

BACKGROUND AND OBJECTIVE: Our aims were to improve the understanding of the pathogenic relationship between cardiovascular diseases and periodontitis and to generate new perspectives in the prevention and treatment of acute myocardial infarction (AMI) and periodontitis. The present study evaluates possible differences in inflammation, oxidative stress, and autophagy markers among subject suffering AMI, periodontitis, or both, to explore possible common pathogenic mechanisms. MATERIAL AND METHODS: A total of 260 subjects were enrolled in the study: 106 subjects that survived to a first AMI (AMI group) and 154 subjects had no cardiac events in their clinical record (control group). A questionnaire was used to assess age, height, weight, blood pressure, and heart rate. The clinical probing depth, clinical attachment loss, number of remaining teeth, and average number of sites with bleeding on probing were assessed. Lipid peroxidation and protein levels of phosphorylated AMP-activated protein kinase (p-AMPK) and microtubule-associated proteins 1A/1B-light chain 3-II (LC3-II) were determined in isolated peripheral blood mononuclear cells by thiobarbituric acid reactive substances (TBARS) assay and Western blot, respectively. Plasma levels of interleukin-1ß were determined using a commercial ELISA kit. All the obtained variables were compared between subjects suffering an AMI with or without periodontitis and control subject periodontal healthy or with periodontitis. RESULTS: A higher proportion of subjects suffering AMI + periodontitis than only AMI (without periodontitis) was found. Higher levels of TBARS were found in subjects with periodontitis than in subjects without periodontitis in both AMI and control subjects. Positive correlations between IL-1ß levels and TBARS and between IL-1ß levels and LC3-II were found only in control subjects. CONCLUSION: Results from the present study are consistent with the suggestion of periodontitis as a potential risk factor for AMI. Periodontitis association with circulating lipid peroxides in both AMI and control subjects were found. The absence of differences in IL-1ß levels between AMI subjects (only AMI vs AMI + periodontitis) suggests that oxidative stress could be the main pathogenic link between AMI and periodontitis.

Blockade of the NLRP3 inflammasome improves metabolic health and lifespan in obese mice.

Aging is the major risk factor for many metabolic chronic diseases. Several metabolic pathways suffer a progressive impairment during aging including body composition and insulin resistance which are associated to autophagy dysfunction and increased inflammation. Many of these alterations are aggravated by non-healthy lifestyle such as obesity and hypercaloric diet which have been shown to accelerate aging. Here, we show that the deleterious effect of hypercaloric diets is reverted by the NLRP3 inflammasome inhibition. NLRP3 deficiency extends mean lifespan of adult mice fed a high-fat diet. This lifespan extension is accompanied by metabolic health benefits including reduced liver steatosis and cardiac damage, improved glucose and lipid metabolism, and improved protein expression profiles of SIRT-1, mTOR, autophagic flux, and apoptosis. These findings suggest that the suppression of NLRP3 prevented many age-associated changes in metabolism impaired by the effect of hypercaloric diets.

NLRP3 Inflammasome Inhibition by MCC950 in Aged Mice Improves Health via Enhanced Autophagy and PPARα Activity.

The NLRP3 inflammasome has emerged as an important regulator of metabolic disorders and age-related diseases in NLRP3-deficient mice. In this article, we determine whether, in old mice C57BL6J, the NLRP3 inflammasome inhibitor MCC950 is able to attenuate age-related metabolic syndrome to providing health benefits. We report that MCC950 attenuates metabolic and hepatic dysfunction in aged mice. In addition, MCC950 inhibited the Pi3K/AKT/mTOR pathway, enhanced autophagy, and activated peroxisome proliferator-activated receptor-α in vivo and in vitro. The data suggest that MCC950 mediates the protective effects by the mammalian target of rapamycin inhibition, thus activating autophagy and peroxisome proliferator-activated receptor-α. In conclusion, pharmacological inhibition of NLRP3 in aged mice has a significant impact on health. Thus, NLRP3 may be a therapeutic target of human age-related metabolic syndrome.

NLRP3 inflammasome suppression improves longevity and prevents cardiac aging in male mice.

While NLRP3-inflammasome has been implicated in cardiovascular diseases, its role in physiological cardiac aging is largely unknown. During aging, many alterations occur in the organism, which are associated with progressive impairment of metabolic pathways related to insulin resistance, autophagy dysfunction, and inflammation. Here, we investigated the molecular mechanisms through which NLRP3 inhibition may attenuate cardiac aging. Ablation of NLRP3-inflammasome protected mice from age-related increased insulin sensitivity, reduced IGF-1 and leptin/adiponectin ratio levels, and reduced cardiac damage with protection of the prolongation of the age-dependent PR interval, which is associated with atrial fibrillation by cardiovascular aging and reduced telomere shortening. Furthermore, old NLRP3 KO mice showed an inhibition of the PI3K/AKT/mTOR pathway and autophagy improvement, compared with old wild mice and preserved Nampt-mediated NAD+ levels with increased SIRT1 protein expression. These findings suggest that suppression of NLRP3 prevented many age-associated changes in the heart, preserved cardiac function of aged mice and increased lifespan.

Fibroblasts Collagen Production and Histological Alterations in Hereditary Gingival Fibromatosis.

Hereditary gingival fibromatosis is a disorder for which the etiology remains unknown. We aimed to evaluate the fibroblasts and histological alterations to give new clues. A father and a daughter of a family showing gingival hereditary fibromatosis were treated, and gingival biopsies were obtained. A histological study revealed dense fibrous tissue, basal lamina disruption, and epithelial cell migration into the connective tissue. Fibroblasts were cultured from the father and daughter and compared with those from a healthy control patient. The results of the biochemical analysis showed increased collagen synthesis, reduced antioxidant CoQ10 content, and high levels of lipid peroxidation. Additionally, fibroblasts culture incubation with the oxidant H2O2 increased collagen levels that have been reduced by the addition of the antioxidant CoQ10. We conclude that some fibroblasts metabolic alterations play a significant role in initiating and maintaining persistent fibrotic tissue. Oxidative stress influences the fibroblasts collagen production and could play a particular role in the pathogenesis of hereditary gingival fibromatosis.

A review of the influence of periodontal treatment in systemic diseases.

The effects and consequences of periodontal diseases might not be confined to the oral cavity. A great body of evidence has arisen supporting the claim demonstrating an association with several systemic conditions and diseases. With different levels of evidence, an association between periodontal disease and cardiovascular disease, diabetes, psoriasis, rheumatoid arthritis, pregnancy outcomes and respiratory diseases has been established. However, the true nature of this association, if it is causal, still remains elusive. For a better understanding of the complex relationships linking different conditions, interventional studies now begin to focus on the possible outcomes of periodontal treatment in relation to the events, symptoms and biomarkers of several systemic disorders, assessing if periodontal treatment has any impact on them, hopefully reducing their severity or prevalence. Therefore, we proceeded to review the recent literature on the subject, attempting to present a brief explanation of the systemic condition or disease, what proposed mechanisms might give biological plausibility to its association with periodontal disease, and finally and more importantly, what data are currently available pertaining to the effects periodontal treatment may have. Raising awareness and discussing the possible benefits of periodontal treatment on overall systemic health is important, in order to change the perception that periodontal diseases are only limited to the oral cavity, and ultimately providing better and comprehensive care to patients.

Inflammasome and Oral Diseases.

One of the main steps in the development of the life in the earth is multicellularity. It enables cell differentiation and the development of morphological structures within an organism and is an essential factor in how to recognize friendly cells that are part of the multicellular organism and which foreign organisms can be harmful. Recognition includes devices such as the major histocompatibility complex (MHC), and the pattern recognition receptors (PRRs). PRRs are a group of proteins expressed by cells of the innate immune system that identify two classes of products: pathogen-associated molecular patterns (PAMPs), related to microbial pathogens, and damage-associated molecular patterns (DAMPs), associated with cell components that are released during cell damage or death. All these activate the inflammasome, which is a multiprotein oligomer that includes caspase 1, PYCARD, NALP, and caspase 5 (also known as caspase 11 or ICH-3). It is responsible for activation of inflammatory processes and has been shown to induce cell pyroptosis, a programmed cell death distinct from apoptosis, and promotes the maturation of the inflammatory cytokines interleukin 1ß (IL-1ß) and interleukin 18 (IL-18). We review whether inflammasome is related to diseases that can occur in the oral cavity. The mouth is always a possible environment for the development of pathological conditions because of the wide variety of microorganisms. Small variations in the equilibrium of the oral flora can cause disorders that could affect the organism in a systemic form. We provide data on periodontal disease, candidiasis, herpes virus, oral cancer, caries, and other oral diseases. There are very few papers that study this issue; therefore, we need more investigation and publications about inflammatory molecular processes, and more specifically, related to the inflammasome complex.

Nutraceuticals in Periodontal Health: A Systematic Review on the Role of Vitamins in Periodontal Health Maintenance.

Periodontal disease, a relevant public health problem worldwide, is generally considered a common pathology of elderly people. In this respect, there is agreement about that nutritional status may be a modifying factor in the progression and healing of the periodontal tissues. Vitamins have been recommended as nutraceuticals for prevention and treatment of some pathological conditions, such as cardiovascular diseases, obesity or cancer. Thus, a systematic approach to determining how the different vitamin type could ameliorate periodontal risks or improve periodontal health is necessary to further the understanding of the potential benefits and risks of vitamins supplementation use. For this, a systematic review of English-written literature in PubMed until February 2018, which included both human and animal research on the relationship of each vitamin with periodontal disease, was conducted. Among all the analyzed vitamins those with antioxidant capacity and effects on immune system seem to be useful for prevention or improvement of periodontal disease, as well as those implicated in bone metabolism. In the first case, there are quite information in favor of various vitamins, mainly vitamin C, that is the most studied. In the second case, vitamin D seems to have the most relevant role.