Cavity and Periodontal Disease Prevention

Written by Robert W Malone MD, MS on December 2, 2024. Posted in Current News

Our teeth are our only permanent body part, so it makes sense that they must be cared for if you are going to live a long, healthy life.

Unlike the rest of our body, once formed, they are not continually rebuilt through routine metabolism. Teeth are, under healthy conditions, essentially indestructible, as demonstrated by fossil records and forensic medicine.

Yet, as we go about our daily lives, microorganisms constantly assault our teeth. This battle results in dental infections, a universal affliction of humankind — the discomfort caused by these infections and their enormous cost. Dental infections rank third in medical expenses in the United States, right behind heart disease and cancer. Furthermore, dental disease is closely linked to the development of a variety of heart diseases.

Beginning in the 1940s, a consensus emerged (particularly in the United States) that the risks and consequences of dental disease could be prevented mainly by ensuring that children consume adequate levels of a chemical called “fluoride” in their diet so that it would then be incorporated into their developing teeth.

Based on this belief, most US municipal water systems began injecting fluoride into drinking water. In 2014, three-quarters of the US population on the public water supply received fluoridated water, representing two-thirds of the total US population.

Despite this intervention, dental disease remains near the top of US health cost drivers. It is time to revisit the mid-20th century consensus on fluoride supplementation. The metadata indicates that the mandated intervention is not curing the problem.

Recent scientific study data, including a comprehensive evaluation by the US HHS National Toxicology Program, indicate that “higher levels of fluoride exposure, such as drinking water containing more than 1.5 milligrams of fluoride per liter, are associated with lower IQ in children.”

This finding underscores a couple of central principles of pharmacology and toxicology – first, all substances (including generally beneficial supplements) are toxic at some dose. Secondly, there is no substitute for long-term studies in the species of interest (humans) because cumulative effects may not be revealed in short-term analyses. Sound familiar? Basic principles.

The key is to understand and dose according to the “therapeutic window,” and to control exposure so that toxic levels are avoided while maintaining therapeutic levels. The issue with injecting fluoride into municipal water supplies are twofold.

First, there no practical informed consent option has been available for what is essentially a medical treatment. We are just told to “trust the experts.” Second, the overall dosing of fluoride is uncontrolled- the mineral is present in various ingested materials (including toothpaste!), and people (including children) consume variable amounts of water.

These new findings demonstrate that the therapeutic window for fluoride dosing is much narrower than previously believed. In sum, recent US HHS analyses demonstrate that fluoride is toxic at levels consistent with currently supplemented municipal water supplies.

If you actually “follow the science,“ it is time to rethink the consensus public health policy position on municipal water fluoridation.

We have discovered another example of “Groupthink” among public health policy “experts.” Have we (and our children) once again become unwitting “victims” of this phenomenon?

Outside North America, water fluoridation was adopted in some European countries, but in the late 1970s and early 1980s.

Denmark and Sweden banned fluoridation when government panels found insufficient evidence of safety, and the Netherlands banned water fluoridation when “a group of medical practitioners presented evidence” that it caused negative effects in a percentage of the population.

The American Dental Association (ADA) does not mention the dangers of fluoride in its fluoride promotion literature. Likewise, the American Association of Family Practitioners (AAFP) – does not disclose the neurodevelopment issues with fluoride.

Both of these organizations are primarily acting to reinforce outdated public health “consensus” rather than keeping practitioners and the public fully informed of recent findings in a balanced and transparent fashion.

Informed by these recent findings, HHS Secretary nominee Robert F Kennedy Jr. has stated that “the Trump White House will advise all U.S​. water systems to remove fluoride from public water” on Inauguration Day has prompted widespread attacks from mainstream media and public health officials who appear to be unaware of the changes in understanding the toxicology of fluoride.

Once again, widely quoted “experts in public health” are being revealed as reflexively strident defenders of outdated groupthink consensus and are gaslighting, demeaning, and attempting to delegitimize others who are more up-to-date with recent findings. Sound familiar?

Cavities have caused tooth pain and systemic human disease for millions of years. Fossils from the Australopithecus species reveal some of the earliest dental caries from 1.1 million to 4.4 million years ago. Mesolithic skulls (8,000 years BC) also show signs of cavities.

Two leading factors contributing to increases in dental caries appear to be the consumption of plant-based foods containing carbohydrates and rice cultivation between 7,000 BC and 5,500 BC. This led to the development of the first cavity treatments in Pakistan in around the same era. In the 11th century, the appearance of sugar cane led to an increase in reported cavities.

Humans existed for millennia without supplemental fluoride. Are there better, more effective options other than functionally mandating uncontrolled treatment of children with fluoride and consequently risking cognitive damage?

The short answer is surprisingly simple and hauntingly familiar to those who have “followed the science” of COVID early treatment protocols: reduce exposure to refined sugar and simple carbohydrate-rich diets and ensure adequate Vitamin D levels.

Caries (tooth decay) and periodontal disease are the two most prevalent oral health conditions, affecting millions worldwide. The impact of these diseases extends beyond oral health; they have profound implications for overall well-being, quality of life, and healthy functioning of many other parts of the body, including the heart.

The mouth, particularly the junction between tooth and gum, is a common portal of entry for a range of pathogens, mainly bacteria and fungi. Our mouths are typically colonized by 200 to 300 bacterial species, but only a limited number of these species participate in dental decay (caries) or periodontal disease.

The main bad actors are the bacteria Streptococcus mutans, and the fungus Candida albicans.

These two species cooperate with each other to form biofilms, which create a protected microenvironment that covers teeth and gums. You can think of this as like an umbrella that protects these two from assault by your oral immune system.

The biofilms then enable the two species (and other camp followers) to manipulate that protected space to support their own metabolic needs – at the expense of underlying teeth and gums. All of this is greatly facilitated by dietary simple sugars and carbohydrates, which Streptococcus and Candida consume as food. But what is the biofilm “umbrella” protecting these opportunists from? Our oral (mucosal) immune system.

The oral immune system is a complex network of defense mechanisms that work together to protect the oral cavity from pathogens and maintain oral health. A key component of mucosal immunity, the oral immune system plays a vital component of the body’s defense against pathogens and other foreign substances.

It plays a crucial role in protecting the oral cavity, including the teeth, gums, tongue, and lips, from infection and inflammation.

The oral immune system has four major components. Innate immunity: The oral epithelium and resident immune cells (e.g., macrophages, dendritic cells) recognize and respond to pathogens through pattern recognition receptors (PRRs) and Toll-like receptors (TLRs). Adaptive immunity:

T-cells and B-cells recognize and respond to specific oral antigens, leading to the production of cytokines and antibodies. Cytokine networks: The oral immune system relies on complex cytokine networks, including IL-1β, IL-6, IL-8, TNF-α, and IFN-γ, to coordinate the immune response. Saliva: Saliva contains antimicrobial factors, such as lysozyme, lactoferrin, and histatin, which help to neutralize pathogens and maintain oral health.

We have briefly summarized the emerging consensus on the narrowing therapeutic window for fluoride, as well as the role of sugar, simple carbohydrates, biofilms, bacteria and yeast in promoting tooth decay. But what about vitamin D?

The following is an AI-generated summary of the current state of vitamin D deficiency in American children and adults:

“A more comprehensive analysis using NHANES data from 2001 to 2018 found that 2.6% of Americans have severe vitamin D deficiency (<25 nmol/L) and 22.0% have moderate deficiency (25-50 nmol/L. Some studies report higher rates, with one estimating that 41.6% of US adults are vitamin D deficient.”

“9% of the pediatric population, representing 7.6 million US children and adolescents, were vitamin D deficient (defined as 25(OH)D levels <15 ng/mL). 12.1% of children in a sample of healthy infants and toddlers were vitamin D deficient (defined as ≤20 ng/mL). Approximately 15% of children ages 1 through 11 and 14% of children and teens ages 12 through 19 are estimated to be vitamin D deficient.”

Adequate vitamin D levels are essential for immunologic function and health. The oral immune system plays a crucial role in protecting oral health and resisting the development of dental caries and periodontal disease. So, it is reasonable to ask whether vitamin D has any role in protecting against dental disease.

The short answer is absolutely yes! The emerging data suggest that adequate levels of Vitamin D3 provide huge benefits in preventing dental disease in both adults and children.

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References on Vitamin D3, dental caries in adults and children, and periodontal disease.

1. Al-Jubori, S. H., M. A. Al-Murad, and F. A. Al-Mashhadane. “Effect of Oral Vitamin D3 on Dental Caries: An in-Vivo and in-Vitro Study.” Cureus 14, no. 5 (May 2022): e25360. https://dx.doi.org/10.7759/cureus.25360.

Aim: Vitamin D3 plays an important role in affecting the overall remineralization process of the dentition. The use of supplements help to keep the levels at optimum and thus reduce the chances of treating very early lesion of caries. Hence the aim was to investigate the indirect effects of oral vitamin D3 on microhardness and elemental weight percentage of Calcium (Ca) and Phosphorous (P) in enamel surface with an artificially initiated carious lesion.

Results: For all specimens, there was a significant decrease in both (Ca and P weight %) after demineralization and then they significantly increased after receiving vitamin D3. The microhardness and elemental analysis provide confirmed results that were represented as a statistically significant difference at (P≤ 0.05) between groups that received vitamin D3 and those without vitamin D3 dosage.

Conclusions: Oral vitamin D3 has a significant potential in motivating remineralization of early lesions on the enamel surfaces representing improved surface microhardness and minerals content (Ca and P weight %) of demineralized tooth surfaces.

2. Behm, C., A. Blufstein, J. Gahn, A. Moritz, X. Rausch-Fan, and O. Andrukhov. “25-Hydroxyvitamin D(3) Generates Immunomodulatory Plasticity in Human Periodontal Ligament-Derived Mesenchymal Stromal Cells That Is Inflammatory Context-Dependent.” Front Immunol 14 (2023): 1100041. https://dx.doi.org/10.3389/fimmu.2023.1100041.

Conclusion: These data indicate that 25(OH)D₃ influences the immunomodulatory activities of hPDL-MSCs. This modulatory potential seems to have high plasticity depending on the local cytokine conditions and may be involved in regulating periodontal tissue inflammatory processes.

3. Blufstein, A., C. Behm, B. Kubin, J. Gahn, X. Rausch-Fan, A. Moritz, and O. Andrukhov. “Effect of Vitamin D(3) on the Osteogenic Differentiation of Human Periodontal Ligament Stromal Cells under Inflammatory Conditions.” J Periodontal Res 56, no. 3 (Jun 2021): 579-88. https://dx.doi.org/10.1111/jre.12858.

Objectives: Vitamin D₃ is known to activate osteogenic differentiation of human periodontal ligament stromal cells (hPDLSCs). Recently, inflammatory stimuli were shown to inhibit the transcriptional activity of hPDLSCs, but their effect on vitamin D₃-induced osteogenic differentiation is not known.

The present study aimed to investigate whether the effects of 1,25-dihydroxvitamin D₃ (1,25(OH)₂D₃) and 25-hydroxvitamin D₃ (25(OH)D₃) on the osteogenic differentiation of hPDLSCs are also altered under inflammatory conditions. Furthermore, the expression of osteogenesis-related factors by hPDLSCs under osteogenic conditions was assessed in the presence of inflammatory stimuli.

Conclusion: The results of this study indicate that inflammatory stimuli also diminish the 1,25(OH)₂D₃-induced expression of osteogenesis-related factors in hPDLSCs under osteogenic conditions, while having no effect on the osteogenic differentiation.

4. Buzatu, R., M. M. Luca, and B. A. Bumbu. “A Systematic Review of the Relationship between Serum Vitamin D Levels and Caries in the Permanent Teeth of Children and Adolescents.” Dent J (Basel) 12, no. 4 (Apr 22 2024). https://dx.doi.org/10.3390/dj12040117.

Abstract: This systematic review critically evaluates the association between serum Vitamin D levels and dental caries incidence in the permanent teeth of children and adolescents.

The search strategy comprised three databases (PubMed, Scopus, Embase), up to November 2023, targeting studies on the correlation between Vitamin D and dental caries in permanent dentition. The eligibility criteria focused on observational studies involving children and adolescents aged 12 to 19 years with permanent dentition. The screening process, guided by the PRISMA guidelines and the Newcastle–Ottawa Scale for quality assessment, resulted in the inclusion of eight studies conducted across various global regions from 2013 to 2023.

The analysis revealed that Vitamin D insufficiency and deficiency were prevalent among the study populations, ranging from 17.3% to 69.4%. Specifically, children and adolescents with Vitamin D insufficiency (<50 nmol/L) were found to have significantly higher odds of developing caries, with odds ratios (ORs) ranging from 1.13 to 2.57. Conversely, two studies indicated a protective effect of higher Vitamin D levels, with an OR of 0.80 and 0.59, respectively, for caries among children and adolescents with serum levels ≥ 50 nmol/L, suggesting an inverse relationship between Vitamin D status and caries risk.

The results indicate both the protective role of adequate serum levels of Vitamin D above 20 ng/mL and the increased risk associated with insufficient levels below this threshold. However, the variations in study quality, methodologies and geographic settings underscore the challenges in drawing universal conclusions.

Despite these limitations, our review suggests that improving Vitamin D status could be a beneficial component of preventive strategies against dental caries in children and adolescents, warranting further research to clarify the clinical significance of our findings.

5. Dietrich, T., K. J. Joshipura, B. Dawson-Hughes, and H. A. Bischoff-Ferrari. “Association between Serum Concentrations of 25-Hydroxyvitamin D3 and Periodontal Disease in the Us Population.” Am J Clin Nutr 80, no. 1 (Jul 2004): 108-13. https://dx.doi.org/10.1093/ajcn/80.1.108.

Background: Periodontal disease (PD) is a common chronic inflammatory disease and an important risk factor for tooth loss. Vitamin D might affect periodontal disease risk via an effect on bone mineral density (BMD) or via immunomodulatory effects.

Objective: The objective was to evaluate whether serum 25-hydroxyvitamin D₃ [25(OH)D₃] concentrations are associated with PD in the third National Health and Nutrition Examination Survey.

Design: We analyzed data on periodontal attachment loss (AL) and serum 25(OH)D₃ concentrations from 11 202 subjects aged ≥20 y. Mean AL was modeled in a multiple linear regression with quintile of serum 25(OH)D₃ concentration as an independent variable. The model was stratified by age and sex and was adjusted for age within age groups, race or ethnicity, smoking, diabetes, poverty income ratio, body mass index, estrogen use, and gingival bleeding.

Results: 25(OH)D₃ concentrations were significantly and inversely associated with AL in men and women aged ≥50 y. Compared with men in the highest 25(OH)D₃ quintile, those in the lowest quintile had a mean AL that was 0.39 mm (95% CI: 0.17, 0.60 mm) higher; in women, the difference in AL between the lowest and highest quintiles was 0.26 mm (0.09, 0.43 mm). In men and women younger than 50 y, there was no significant association between 25(OH)D₃ and AL. The BMD of the total femoral region was not associated with AL and did not mediate the association between 25(OH)D₃ and AL.

Conclusions: Low serum 25(OH)D₃ concentrations may be associated with PD independently of BMD. Given the high prevalence of PD and vitamin D deficiency, these findings may have important public health implications.

6. Dura-Trave, T., and F. Gallinas-Victoriano. “Dental Caries in Children and Vitamin D Deficiency: A Narrative Review.” Eur J Pediatr 183, no. 2 (Feb 2024): 523-28. https://dx.doi.org/10.1007/s00431-023-05331-3.

Dental caries represents one of the most prevalent health problems in childhood. Numerous studies have assessed that vitamin D deficiency is highly related to dental caries in primary and permanent teeth in children.

The aim of this study is to elaborate a narrative review about proposed mechanisms by which vitamin D deficiency interacts with dental caries process in children. Vitamin D deficiency during pregnancy may cause intrauterine enamel defects, and through childhood is accompanied by insufficient activity of antibacterial peptides, decreased saliva secretion, and a low level of calcium in saliva.

Conclusion: In conclusion, vitamin D deficiency would increase the risk of caries in the primary and/or permanent dentition. Relationship between vitamin D deficiency and dental caries is evident enough for vitamin D deficiency to be considered as a risk factor for dental caries in children. Optimal levels of vitamin D throughout pregnancy and childhood may be considered an additional preventive measure for dental caries in the primary and permanent dentition.

6. Govindharajulu, R., N. K. Syed, B. Sukumaran, P. R. Seshadri, S. Mathivanan, and N. Ramkumar. “Assessment of the Antibacterial Effect of Vitamin D3 against Red Complex Periodontal Pathogens: A Microbiological Assay.” J Contemp Dent Pract 25, no. 2 (Feb 1 2024): 114-17. https://dx.doi.org/10.5005/jp-journals-10024-3642.
7. Kalra, G., Y. Kumar, C. Langpoklakpam, T. Chawla, T. Thangaraju, and R. Singhania. “Relationship between Maternal Prenatal Vitamin D Status and Early Childhood Caries in Their Children: A Cross-Sectional Survey.” Int J Clin Pediatr Dent 17, no. 8 (Aug 2024): 860-63. https://dx.doi.org/10.5005/jp-journals-10005-2836.
8. Li, Z., X. Wei, Z. Shao, H. Liu, and S. Bai. “Correlation between Vitamin D Levels in Serum and the Risk of Dental Caries in Children: A Systematic Review and Meta-Analysis.” BMC Oral Health 23, no. 1 (Oct 19 2023): 768. https://dx.doi.org/10.1186/s12903-023-03422-z.
9. Liu, K., H. Meng, R. Lu, L. Xu, L. Zhang, Z. Chen, D. Shi, X. Feng, and X. Tang. “Initial Periodontal Therapy Reduced Systemic and Local 25-Hydroxy Vitamin D(3) and Interleukin-1beta in Patients with Aggressive Periodontitis.” J Periodontol 81, no. 2 (Feb 2010): 260-6. https://dx.doi.org/10.1902/jop.2009.090355.
10. Patil, V. S., R. S. Mali, and A. S. Moghe. “Evaluation and Comparison of Vitamin D Receptors in Periodontal Ligament Tissue of Vitamin D-Deficient Chronic Periodontitis Patients before and after Supplementation of Vitamin D3.” J Indian Soc Periodontol 23, no. 2 (Mar-Apr 2019): 100-05. https://dx.doi.org/10.4103/jisp.jisp_173_18.
11. Pu, R., M. Fu, N. Li, and Z. Jiang. “A Certain Protective Effect of Vitamin D against Dental Caries in Us Children and Youth: A Cross-Sectional Study.” J Public Health Dent 83, no. 3 (Jul 2023): 231-38. https://dx.doi.org/10.1111/jphd.12571.
12. Sahin, M., and I. R. Toptanci. “Evaluation of Serum Levels in Children with Delayed Eruption.” BMC Oral Health 24, no. 1 (Nov 21 2024): 1418. https://dx.doi.org/10.1186/s12903-024-05210-9.
13. Tapalaga, G., B. A. Bumbu, S. R. Reddy, S. D. Vutukuru, A. Nalla, F. Bratosin, R. M. Fericean, C. Dumitru, D. C. Crisan, N. Nicolae, and M. M. Luca. “The Impact of Prenatal Vitamin D on Enamel Defects and Tooth Erosion: A Systematic Review.” Nutrients 15, no. 18 (Sep 5 2023). https://dx.doi.org/10.3390/nu15183863.
14. Wang, Q., X. Zhou, P. Zhang, P. Zhao, L. Nie, N. Ji, Y. Ding, and Q. Wang. “25-Hydroxyvitamin D(3) Positively Regulates Periodontal Inflammaging Via Socs3/Stat Signaling in Diabetic Mice.” Steroids 156 (Apr 2020): 108570. https://dx.doi.org/10.1016/j.steroids.2019.108570.
15. Wojcik, D., A. Krzewska, L. Szalewski, E. Pietryka-Michalowska, M. Szalewska, S. Krzewski, E. Pels, and I. Ben-Skowronek. “Dental Caries and Vitamin D3 in Children with Growth Hormone Deficiency: A Strobe Compliant Study.” Medicine (Baltimore) 97, no. 8 (Feb 2018): e9811. https://dx.doi.org/10.1097/MD.0000000000009811.
16. Wojcik, D., L. Szalewski, E. Pietryka-Michalowska, J. Borowicz, E. Pels, and I. Ben-Skowronek. “Vitamin D(3) and Dental Caries in Children with Growth Hormone Deficiency.” Int J Endocrinol 2019 (2019): 2172137. https://dx.doi.org/10.1155/2019/2172137.
17. Zameer, M., S. Wali Peeran, S. Nahid Basheer, S. Ali Peeran, G. Anwar Naviwala, and S. Badiujjama Birajdar. “Molar Incisor Hypomineralization: Prevalence, Severity and Associated Aetiological Factors in Children Seeking Dental Care at Armed Forces Hospital Jazan, Saudi Arabia.” Saudi Dent J 36, no. 8 (Aug 2024): 1111-16. https://dx.doi.org/10.1016/j.sdentj.2024.06.003.
18. Zhang, C., K. Liu, and J. Hou. “Extending the Vitamin D Pathway to Vitamin D(3) and Cyp27a1 in Periodontal Ligament Cells.” J Periodontol 92, no. 7 (Jul 2021): 44-53. https://dx.doi.org/10.1002/JPER.20-0225.
19. Zhang, P., W. Zhang, D. Zhang, M. Wang, R. Aprecio, N. Ji, O. Mohamed, Y. Li, Y. Ding, and Q. Wang. “25-Hydroxyvitamin D(3) -Enhanced Ptpn2 Positively Regulates Periodontal Inflammation through the Jak/Stat Pathway in Human Oral Keratinocytes and a Mouse Model of Type 2 Diabetes Mellitus.” J Periodontal Res 53, no. 3 (Jun 2018): 467-77. https://dx.doi.org/10.1111/jre.12535.

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