The Fundamentals of Oral & Systemic Health

The first questions we should ask are always how, when, and why. This discussion is about the how, when, and why of chronic systemic disease and, until only recently, the truth hiding in “plain sight.” The association of oral health to systemic health has a very long history, starting at least 3200 years ago with murals depicting Ramses II before the battle of Kadesh (1274 BC) inspecting captured Sashu spies with their mouths forced open for oral inspection.1 A healthy oral cavity meant a healthy captive for enslavement. The Roman historian Tacitus, in his Annals and Agricola writings, also referred to the oral inspections of the captured Celtic and Germanic peoples sold into slavery at the Roman Forum (14-98 AD).2

The knowledge of oral health affecting systemic health was widely known throughout history until recently when it mysteriously vanished. Oddly, the great G.V. Black, the eminent Dean of Northwestern University Dental School, who was so instrumental in Dental education, often emphasized treating dental disease medically, – “The day is surely coming and perhaps within the lifetime of you young men before me, when we will be engaged in practicing preventive, rather than reparative, dentistry”.3 He also recognized the systemic health connection to dental health well. He pioneered the use of the microscope for studying dental disease. His work in microbiology and cellular pathology led to a better understanding of dental caries, periodontal disease, and other pathological conditions and subsequently contributed to improved treatment methods.4 But that was then, and now we, as oral health care professionals, must somehow regain the great wisdom of the past. We can start by asking key questions and applying the known science to build a foundation of knowledge that will advance oral medicine into its next “Golden Age.”

Does oral health affect systemic health? Where is the data? Good oral health definitely correlates with systemic health. There has always been a “retort’ that there are biases due to the overall “healthy living” individual scenario. But, after removing all other con-founders and just considering good oral health due to good oral hygiene practices, those who brush their teeth live longer and healthier, regardless of exercise and diet.5 The risk of any chronic diseases (OR = 1.27, 95% CI: 1.18–1.37), cardiovascular diseases (CVD, OR = 1.30, 95% CI: 1.21–1.39), and endocrine or nutritional metabolic disorders (OR = 1.11, 95% CI: 1.01–1.22) was higher in those who with poor oral health behavior.6 Poor oral hygiene practices were associated with a higher risk of chronic diseases, CVD, and diabetes mellitus (DM) among middle-aged and older adults.6 In another study of toothbrushing and total systemic health, Participants who rarely or never brushed their teeth had adjusted HR of 1.12 (95% CI: 1.09, 1.15) for MVE, with similar HRs for stroke (1.08, 1.05-1.12), intracerebral hemorrhage (1.18, 1.11-1.26) and pulmonary heart disease (1.22, 1.13-1.32) compared with those who brushed teeth regularly.7 In addition, it was reported that those who did not brush their teeth also had an increased risk of cancer (1.09, 1.04-1.14), chronic obstructive pulmonary disease (COPD) (1.12, 1.05-1.20), liver cirrhosis (1.25, 1.09-1.44) and all-cause death (1.25, 1.21-1.28) 7. So even the simple act of tooth brushing increases survivability, making the connection between systemic oral health and oral health rock solid.8

But how does this happen, and why? The how is now well confirmed: keystone pathogens initiate chronic disease, and these keystone pathogens are well-studied periodontal bacteria. Porphyromonas gingivalis is a causative agent of periodontal disease, arteriosclerosis, and inflammatory Alzheimer’s.9,10 Because Porphyromonas gingivalis can be considered a foremost or “keystone” initiator of periodontal disease, it is reasonable to describe Porphyromonas gingivalis as a causal agent of NAGS, a single disease with all of its downstream comorbidities.11,12

Porphyromonas gingivalis has also been called a “guerilla” for its notable tactics of slowly subverting the host’s defensive mechanisms.13 It does this in three ways: 1) the host’s immunity is bypassed by the ability of Porphyromonas gingivalis fimbriae to attach to host cells, like gingival epithelial cells or endothelial cells, and then invade the cell itself;14 2) Porphyromonas gingivalis can genomically shift into different strains to specifically target different host cells, making it particularly infectious15 and 3) the epigenetic influence of Porphyromonas gingivalis allows it to open the tight junctions between cells and to modulate the immune response.16 All told, Porphyromonas gingivalis undermines a massive host immune response but does not normally overwhelm the host because that would effectively limit the pathogen’s spread. A dead host does not help a pathogen flourish.

With the new concept of Porphyromonas gingivalis infection causing a single disease with multiple symptoms, it is easy to understand the processes involved. The oral component houses the initial infection, where the immune system is alerted and subverted, creating an inflammatory environment. Circulating leukocytes carry Porphyromonas gingivalis and associated lipopolysaccharides, which affect the endothelial cells of arteries and pass into the neural component.17 This eventually diminishes the cognitive ability of the host, resulting in reduced oral hygiene and further spreading of the pathogen amongst all contacts.18

We have answered how, albeit with only one example, Porphyromonas gingivalis, as there are definitely other keystone pathogens, but why does this happen? Now we have to explore the evolution and the development of gateway microbiomes,” a very important concept describing homo sapiens’ close relationship to the microbiome and its genetic material, i.e., the development of the holobiont and our survival as a species. The biology of this success is intertwined with the coevolution of homo sapiens and the associated holobiome.19,20 Chronic illnesses and debilitations appear to be increasing, requiring reflection into the evolutionary process and the perturbations that have recently occurred, creating this environment of now-declining health.21 Current research would point to the “Hygiene hypothesis,” overuse of anti-microbials, dietary shifts, and the resultant decrease in human microbiome diversity.22,23 The old model of looking for an increase in pathogens is flawed. Indeed, the fault lies with the decrease in commensals that not only compete directly with the pathogens but also modulate the immune response of the host.24

The oral microbiome is considered a “gateway” to the body, rapidly adjusting to environmental and dietary changes to protect the host and further process the host’s nutritional needs. The host and microbiome evolve in concert, both influencing the development of the other and creating a dependency on each other for survival. Dysbiosis, maladaptation or imbalance of microbiota, of the oral microbiome systematically affects the human host, most seriously impairing the host’s immune response, and initiates serious pathologic conditions, including hypertension, diabetes, obesity, and cardiovascular disease.25 There are other important “gateways,” such as the nasal gateway microbiome, which is also important in disease prevention and health. And, of course, the placental gateway microbiome, as in the case of the nasal gateway, these other gateways are closely related to the oral gateway.26-29

And now, as to the when, the ideal time to influence the oral microbiome is actually before birth. The literature reports positive results with pre-natal intervention through supplementing the mother with probiotics and polyols.30,31 Published studies using xylitol that involved the nursing mother and child demonstrate a decrease in the maternal transmission of Mutans streptococci.32 The maternal microbiome can also be influenced in numerous ways, including diet, exercise, and probiotic supplementation. 33-36 Limiting added dietary sugar and the regular addition of polyols can help decrease the prevalence of pathogens before they are passed on to the child. 32, 37-39 Erythritol and xylitol are polyols that have been extensively researched and demonstrated to have notable anti-cariogenic and anti-periodontal disease properties.40 In addition, studies demonstrate that xylitol decreases the levels of cariogenic bacteria while having little effect on beneficial bacteria.41

Viewing the oral microbiome as a gateway to the body makes sense since the connection of oral health to systemic health is now well-established.42 Intervention is so necessary, but when is the ideal time? Pre-natal intervention has been studied with positive results reported by supplementing the mother with probiotics or polyols. Certainly, intervention may be desired even earlier, preferably before pregnancy, because it is also reported that antecedent use of antibiotics by the mother will affect the maternal microbiome.43 The placental microbiome is most closely related to the maternal oral microbiome.44 The presence of commensal bacteria in the placenta and developing fetus is considered to be essential to fetal immunological maturation.45 The expectant mother’s oral health should then be considered primarily important to the oral-systemic health of the fetus and, later, the child. In addition, the placental microbiome appears to be developed quite early in the pregnancy by maternal imprinting.44 This maternal imprinting involves the transportation of viable commensals via circulating monocytes, correctly creating a fetal microbiome to program the developing child.46 Animal studies have demonstrated the transmission of maternal breast commensals into the amniotic fluid.47

All this depends upon the mother actually having a healthy microbiome.48 In the case of Early Childhood Caries, the reduction of maternal Candida albicans will reduce the biofilm formation by Streptococcus mutans, potentially reducing the incidence of dental caries.49,50 Some Lactobacilli, all probiotics such as Lactobacilli rhamnoses, have been demonstrated to inhibit Candida albicans.51-54

Complicating this developed scenario is the effect of the airway, which has a bi-directional relationship with both the oral and the nasal microbiomes.55 It is indeed the classic vicious cycle whereby gut dysbiosis disturbs the respiratory and immune response to environmental challenges, creating mucosal discharge that plugs the nares, especially in the case of small children.55,56 This creates mouth breathing that then affects the oral microbiome, increasing gingival pathology and dental caries. The disturbed oral microbiome also increases lymphoid tissue growth; tonsils swell, further inhibiting proper respiration.56 Nasal dysbiosis also causes mucosal irritation, further swelling the nasal tissue and reducing nasal patency, enhancing the pathologic effect further as the facial development is altered in a compensatory manner, causing long “face syndrome” 57-59.

The appropriate treatment is to correct the dysbiosis with probiotic therapy, use prebiotics to support normal commensals and reduce inflammation. Key to all of this (pun intended) are the “keystone” commensals, probiotics that moderate inflammation and inhibit the pathogens. The most recent research has discovered several keystone probiotics, including strains of Lactobacilli caseiLactobacillus rhamnoses, and Akkermansia muciniphila (research recently completed and submitted for publication) that are present in the nasal and oral cavity.28 Pesticide agricultural use results in pesticides being consumed by people eating produce, and the pesticide may reduce the commensals and keystone probiotics.60 Some Lactobacilli strains recently investigated are also facial skin and vaginal probiotics.27 Time will tell, but we are on the threshold of finally comprehending what GV Black (deceased 1915) attempted to tell us over a century ago.4 

Oral Health welcomes this original article.

  1. Wikipedia contributors. (2023, November 21). Battle of Kadesh. In Wikipedia, The Free Encyclopedia. Retrieved 22:20, January 3, 2024, from
  2. Wikipedia contributors. (2023, November 2). Tacitus. In Wikipedia, The Free Encyclopedia. Retrieved 22:30, January 3, 2024, from
  3. Joseph R. The father of modern dentistry – Dr. Greene Vardiman Black (1836-1915) J Conserv Dent. 2005;8:5–6. [Google Scholar]
  4. Singh H. Remembering Sir G.V. Black. Indian J Dent. 2015;6:147–48. [PMC free article] [PubMed] [Google Scholar]
  5. Hwang, S. Y., Shim, J. L., Kang, D., & Choi, J. (2018). Poor Oral Health Predicts Higher 10-Year Cardiovascular Risk: A Propensity Score Matching Analysis. The Journal of cardiovascular nursing, 33(5), 429–436.
  6. Guo, D., Shi, Z., Luo, Y., Ding, R., & He, P. (2023). Association between oral health behavior and chronic diseases among middle-aged and older adults in Beijing, China. BMC oral health, 23(1), 97.
  7. Zhuang, Z., Gao, M., Lv, J., Yu, C., Guo, Y., Bian, Z., Yang, L., Du, H., Chen, Y., Ning, F., Liu, H., Chen, J., Chen, Z., Huang, T., Li, L., & China Kadoorie Biobank (CKB) Collaborative Group (2021). Associations of toothbrushing behaviour with risks of vascular and nonvascular diseases in Chinese adults. European journal of clinical investigation, 51(12), e13634.
  8. Ehrenzeller S, Klompas M. Association Between Daily Toothbrushing and Hospital-Acquired Pneumonia: A Systematic Review and Meta-Analysis. JAMA Intern Med. Published online December 18, 2023. doi:10.1001/jamainternmed.2023.6638
  9. Kim H. J., Cha G. S., Kim H. J., Kwon E. Y., Lee J. Y., Choi J., & Joo, J. Y. (2018). Porphyromonas gingivalis accelerates atherosclerosis through oxidation of high-density lipoprotein. Journal of periodontal & implant science, 48(1), 60-68. doi:10.5051/jpis.2018.48.1.60
  10. Bale, B.F., Doneen A.D., Vigerust, D.J. (2016) High-risk periodontal pathogens contribute to the pathogenesis of atherosclerosis. Postgrad Med J. November 29, 2016 as 10.1136. Open Access
  11. Hussain M., Stover C. M., Dupont A., P. gingivalis in Periodontal Disease and Atherosclerosis – Scenes of Action for Antimicrobial Peptides and Complement. Front Immunol. 2015 Feb 10;6:45.
  12. Cannon M.L. Peldyak J.N. The prevention and treatment of neural arterial gingival simplex (2019) Dental Res Manag 3: 32-37
  13. Hajishengallis G, Darveau R.P., Curtis MA. The keystone-pathogen hypothesis. Nat Rev Microbiol. 2012;10(10):717–725. doi:10.1038/nrmicro2873
  14. Hajishengallis G. (2009). Porphyromonas gingivalis-host interactions: open war or intelligent guerilla tactics?. Microbes and infection, 11(6-7), 637–645. doi:10.1016/j.micinf.2009.03.009.
  15. Moreno, S., & Contreras, A. (2013). Functional differences of Porphyromonas gingivalis Fimbriae in determining periodontal disease pathogenesis: a literature review. Colombia medica (Cali, Colombia), 44(1), 48–56.
  16. Tribble, G. D., Kerr, J. E., & Wang, B. Y. (2013). Genetic diversity in the oral pathogen Porphyromonas gingivalis: molecular mechanisms and biological consequences. Future microbiology, 8(5), 607–620. doi:10.2217/fmb.13.30.
  17. Guo, W., Wang, P., Liu, Z. H., & Ye, P. (2018). Analysis of differential expression of tight junction proteins in cultured oral epithelial cells altered by Porphyromonas gingivalis, Porphyromonas gingivalis lipopolysaccharide, and extracellular adenosine triphosphate. International journal of oral science, 10(1), e8. doi:10.1038/ijos.2017.51.
  18. Hajishengallis G. Periodontitis: from microbial immune subversion to systemic inflammation Nature Reviews Immunology volume 15,pages 30–44 (2015)
  19. Zilber-Rosenberg I., Rosenberg E. (2008) Role of microorganisms in the evolution of animals and plants: the hologenome theory of evolution. FEMS Microbiol Rev 32:723-735.
  20. Huitzil, S., Sandoval-Motta, S., Frank, A., & Aldana, M. (2018). Modeling the Role of the Microbiome in Evolution. Frontiers in physiology, 9, 1836. doi:10.3389/fphys.2018.01836.
  21. Ley R.E., Peterson D.A., Gordon J.I. Ecological and evolutionary forces shaping microbial diversity in the human intestine. Cell. 2006;124(4):837–848.
  22. Blaser M.J., Falkow S. What are the consequences of the disappearing human microbiota? Nat Rev Microbiol. 2009;7(12):887–894.
  23. Okada, H., Kuhn, C., Feillet, H., & Bach, J. F. (2010). The ‘hygiene hypothesis’ for autoimmune and allergic diseases: an update. Clinical and experimental immunology, 160(1), 1–9. doi:10.1111/j.1365-2249.2010.04139.x
  24. Abt, M. C., & Artis, D. (2013). The dynamic influence of commensal bacteria on the immune response to pathogens. Current opinion in microbiology, 16(1), 4–9. doi:10.1016/j.mib.2012.12.002
  25. Li, C., Yu, R., & Ding, Y. (2022). Association between Porphyromonas Gingivalis and systemic diseases: Focus on T cells-mediated adaptive immunity. Frontiers in cellular and infection microbiology, 12, 1026457.
  26. Lazarini, F., Roze, E., Lannuzel, A., & Lledo, P. M. (2022). The microbiome-nose-brain axis in health and disease. Trends in neurosciences, 45(10), 718–721.
  27. De Boeck, I., Spacova, I., Vanderveken, O. M., & Lebeer, S. (2021). Lactic acid bacteria as probiotics for the nose?. Microbial biotechnology, 14(3), 859–869.
  28. De Boeck, I., van den Broek, M. F. L., Allonsius, C. N., Spacova, I., Wittouck, S., Martens, K., Wuyts, S., Cauwenberghs, E., Jokicevic, K., Vandenheuvel, D., Eilers, T., Lemarcq, M., De Rudder, C., Thys, S., Timmermans, J. P., Vroegop, A. V., Verplaetse, A., Van de Wiele, T., Kiekens, F., Hellings, P. W., … Lebeer, S. (2020). Lactobacilli Have a Niche in the Human Nose. Cell reports, 31(8), 107674.
  29. Ozkan, J., Willcox, M., & Coroneo, M. (2022). A comparative analysis of the cephalic microbiome: The ocular, aural, nasal/nasopharyngeal, oral and facial dermal niches. Experimental eye research, 220, 109130.
  30. Baldassarre, M. E., Palladino, V., Amoruso, A., Pindinelli, S., Mastromarino, P., Fanelli, M., … Laforgia, N. (2018). Rationale of Probiotic Supplementation during Pregnancy and Neonatal Period. Nutrients, 10(11), 1693. doi:10.3390/nu10111693.
  31. Luoto R., Laitinen K., Nermes M., Isolauri E. Impact of maternal probiotic-supplemented dietary counselling on pregnancy outcome and prenatal and postnatal growth: a double-blind, placebo-controlled study. Br J Nutr. 2010 Jun;103(12):1792-9. doi: 10.1017/S0007114509993898. Epub 2010 Feb 4.
  32. Söderling E., Isokangas P., Pienihäkkinen K., Tenovuo J., Alanen P. Influence of maternal xylitol consumption on mother-child transmission of mutans streptococci: 6-year follow-up. Caries Res. 2001 May-Jun;35(3):173-7.
  33. Nørrisgaard P.E., Haubek D., Kühnisch J., et al. Association of High-Dose Vitamin D Supplementation During Pregnancy With the Risk of Enamel Defects in Offspring: A 6-Year Follow-up of a Randomized Clinical Trial. JAMA Pediatr. Published online August 05, 2019. doi:10.1001/jamapediatrics.2019.2545
  34. Ley, R. E., Turnbaugh, P. J., Klein, S. & Gordon, J. I. Microbial ecology: human gut microbes associated with obesity. Nature 444, 1022–1023 (2006).
  35. Brown K., DeCoffe D., Molcan E., Gibson D.L. Diet-induced dysbiosis of the intestinal microbiota and the effects on immunity and disease. Nutrients 4: 1095–1119, 2012.
  36. Clarke S.F., Murphy E.F., O’Sullivan O., Lucey A.J., Humphreys M., Hogan A., Hayes P., O’Reilly M., Jeffery I.B., Wood-Martin R., Kerins D.M., Quigley E., Ross R.P., O’Toole P.W., Molloy M.G., Falvey E., Shanahan F., Cotter P.D. Exercise and associated dietary extremes impact on gut microbial diversity. Gut 63: 1913–1920, 2014.
  37. Caufield P.W., Cutter G.R., Dasanayake A.P: Initial acquisition of mutans streptococci by infants: Evidence for a discrete window of infectivity. J Dent Res 1993;72:37–45.
  38. Isokangas P., Söderling E., Pienihäkkinen K., Alanen P. Occurrence of dental decay after maternal consumption of xylitol chewing gum, a follow–up from 0 to 5 years of age. J Dent Res 2000;79:1885–1889.
  39. Loesche W.J., Grossman N.S., Earnest R., Corpron R: The effect of chewing xylitol gum on the plaque and saliva levels of Streptococcus mutans. J Am Dent Assoc 1984;108:587–592.
  40. Janakiram C., Deepan Kumar C. V., Joseph J., Xylitol in preventing dental caries: A systematic review and meta-analyses. J Nat Sci Biol Med. 2017 Jan-Jun; 8(1): 16–21.
  41. Bahador, A., Lesan, S., & Kashi, N. (2012). Effect of xylitol on cariogenic and beneficial oral streptococci: a randomized, double-blind crossover trial. Iranian journal of microbiology, 4(2), 75–81.
  42. Kim, J., & Amar, S. (2006). Periodontal disease and systemic conditions: a bidirectional relationship. Odontology, 94(1), 10–21. doi:10.1007/s10266-006-0060-6
  43. Prince, A. L., Ma, J., Kannan, P. S., Alvarez, M., Gisslen, T., Harris, R. A., Aagaard, K. M. (2016). The placental membrane microbiome is altered among subjects with spontaneous preterm birth with and without chorioamnionitis. American journal of obstetrics and gynecology, 214(5), 627.e1–627.e16. doi:10.1016/j.ajog.2016.01.193
  44. Aagaard, K., Ma, J., Antony, K. M., Ganu, R., Petrosino, J., & Versalovic, J. (2014). The placenta harbors a unique microbiome. Science translational medicine, 6(237), 237ra65. doi:10.1126/scitranslmed.3008599
  45. Romano-Keeler, J., & Weitkamp, J. H. (2015). Maternal influences on fetal microbial colonization and immune development. Pediatric research, 77(1-2), 189–195. doi:10.1038/pr.2014.163
  46. Pablo F. Perez, Joël Doré, Marion Leclerc, Florence Levenez, Jalil Benyacoub, Patrick Serrant, Iris Segura-Roggero, Eduardo J. Schiffrin, Anne Donnet-Hughes. Bacterial Imprinting of the Neonatal Immune System: Lessons From Maternal Cells? Pediatrics Mar 2007, 119 (3) e724-e732; DOI: 10.1542/peds.2006-1649
  47. Yajima M1, Nakayama M, Hatano S, Yamazaki K, Aoyama Y, Yajima T, Kuwata T. Bacterial translocation in neonatal rats: the relation between intestinal flora, translocated bacteria, and influence of milk. J Pediatr Gastroenterol Nutr. 2001 Nov;33(5):592-601.
  48. Nyangahu, D. D., Lennard, K. S., Brown, B. P., Darby, M. G., Wendoh, J. M., Havyarimana, E., Jaspan, H. B. (2018). Disruption of maternal gut microbiota during gestation alters offspring microbiota and immunity. Microbiome, 6(1), 124. doi:10.1186/s40168-018-0511-7
  49. Nørrisgaard P.E., Haubek D., Kühnisch J., et al. Association of High-Dose Vitamin D Supplementation During Pregnancy With the Risk of Enamel Defects in Offspring: A 6-Year Follow-up of a Randomized Clinical Trial. JAMA Pediatr. Published online August 05, 2019. doi:10.1001/jamapediatrics.2019.2545
  50. Falsetta M.L., Klein M.I., Colonne P.M., et al. : Symbiotic relationship between Streptococcus mutans and Candida albicans synergizes virulence of plaque biofilms in vivo. Infect Immun. 2014;82(5):1968–1981.
  51. Koo H., Bowen W.H: Candida albicans and Streptococcus mutans: a potential synergistic alliance to cause virulent tooth decay in children. Future Microbiol. 2014;9(12):1295–1297.
  52. Hatakka K., Ahola A.J., Yli-Knuuttila H., Richardson M., Poussa T., Meurman J.H., Korpela R. (2007) Probiotics reduce the prevalence of oral Candida in the elderly—a randomized controlled trial. J Dent Res 86(2):125–130
  53. Hasslof P., Hedberg M., Twetman S., Stecksen-Blicks C. (2010) Growth inhibition of oral mutans streptococci and Candida by commercial probiotic lactobacilli—an in vitro study. BMC Oral Health 10:18.
  54. Kohler G.A., Assefa S., Reid G. (2012) Probiotic interference of Lactobacillus rhamnosus GR-1 and Lactobacillus reuteri RC-14 with the opportunistic fungal pathogen Candida albicans. Infect Dis Obstet Gynecol 2012:636474.
  55. Pathak, J. L., Yan, Y., Zhang, Q., Wang, L., & Ge, L. (2021). The role of oral microbiome in respiratory health and diseases. Respiratory medicine, 185, 106475.
  56. Saafan, M. E., Ibrahim, W. S., & Tomoum, M. O. (2013). Role of adenoid biofilm in chronic otitis media with effusion in children. European archives of oto-rhino-laryngology : official journal of the European Federation of Oto-Rhino-Laryngological Societies (EUFOS) : affiliated with the German Society for Oto-Rhino-Laryngology – Head and Neck Surgery, 270(9), 2417–2425.
  57. Bredun, O., Tymchenko, M., Faraon, I., & Melnikov, O. (2020). Cytokine and immunoglobulin spectra of tissue extracts from tonsils of children with hypertrophy and chronic tonsillitis. Wiadomosci lekarskie (Warsaw, Poland : 1960), 73(1), 156–160.
  58. Tourne L. P. (1990). The long face syndrome and impairment of the nasopharyngeal airway. The Angle orthodontist, 60(3), 167–176.<0167:TLFSAI>2.0.CO;2
  59. Zhang, X., Li, X., Xu, H., Fu, Z., Wang, F., Huang, W., Wu, K., Li, C., Liu, Y., Zou, J., Zhu, H., Yi, H., Kaiming, S., Gu, M., Guan, J., & Yin, S. (2023). Changes in the oral and nasal microbiota in pediatric obstructive sleep apnea. Journal of oral microbiology, 15(1), 2182571.
  60. Salazar-Flores, J., Lomelí-Martínez, S. M., Ceja-Gálvez, H. R., Torres-Jasso, J. H., Torres-Reyes, L. A., & Torres-Sánchez, E. D. (2022). Impacts of Pesticides on Oral Cavity Health and Ecosystems: A Review. International journal of environmental research and public health, 19(18), 11257.

Dr. Mark L. Cannon has received his Diplomate status by the American Board of Pediatric Dentistry, and is a Professor of Otolaryngology, Division of Dentistry at Northwestern University, Feinberg School of Medicine. He has been a long-time member of the International Association of Pediatric Dentistry. In addition to founding a large multi-specialty highly respected private practice in the suburbs of Chicago, he is the Research Coordinator of the residency program at Ann and Robert Lurie Children’s Hospital, Chicago, Illinois. Most of all, Dr. Cannon is the proud father of five, all of whom are very accomplished. He is also a very proud grandfather of five beautiful children!

Source link

Leave a Reply

Your email address will not be published. Required fields are marked *