The Human Oral Microbiome: A Mouthful of Proof for God
The Human Oral Microbiome: A Mouthful of Proof for God
It was September 17, 1683, when Antoni van Leeuwenhoek—now considered to be the “Father of Microbiology”—described the “many very little living animalcules” that he scraped from his own mouth and examined under his microscope.1 Since that time, the occupants of the oral cavity have continued to be the object of research, with a growing interest being manifested in more recent years by cell biologists, microbiologists, and immunologists.2 Though those who have engaged in intensive investigation of the oral cavity often assume an evolutionary origin for the intricacies they observe, in reality, their discoveries constitute astounding evidence for a divine Creator. What follows is but a surface perusal of a small portion of that evidence.
Microbiome and Microbiota
The term “microbiome” was coined in 2001 by Lederberg and McCray.3 With regard to the human mouth, it refers to the entire habitat of the microbial residents of every surface area of the oral cavity.4 These surfaces are many—including both the top (dorsum) and bottom (ventral) of the tongue, lip, teeth, maxillary vestibule, keratinized gingiva (gums), gingival sulcus (the shallow groove between the gum and the tooth surface), buccal mucosa,5 tonsils, hard and soft palates, the throat, saliva, salivary glands beneath the tongue, and even the plaque that forms.6 The word “microbiota” refers to the unique combination of microorganisms that exist within this complex oral topography.
Over 700?
The reader is surely surprised to learn of the sheer number of distinct bacterial species that naturally inhabit the human mouth. While the actual number of bacteria, archaea,7 fungi, viruses, and protozoa that inhabit the human mouth is unknown,8 “the oral cavity has the second largest and diverse microbiota after the gut, harboring over 700 species of bacteria”9—“one of the most heavily colonized parts of our bodies.”10
These myriad species are not undesirable intruders or invaders. The oral cavity is their permanent home—a home that normally maintains a fairly constant temperature of 98.6 degrees Fahrenheit, providing a stable environment in which to survive.11 Within the overall oral cavity are “many distinct microenvironments” that provide unique and site-specific advantages for the various species.12 The microbiota unquestionably belong there. In fact, our bodies live in harmony with literally millions of tiny micro-organisms that perform a variety of essential functions.
In Harmony?
Do these 700+ species war with each other, making the mouth a biological warzone of conflict and carnage, inflicting sickness and suffering upon the human host? Quite the opposite. In fact, “most of the microorganisms that inhabit the oral cavity live in a symbiotic relationship.”13 The symbiotic relationship that they sustain with each other and with their human host enables ongoing fulfillment of mutual benefits.14 Indeed, the microbes work in concert with each other to perform very intricate, specific tasks that are useful to the human host, thereby maintaining symbiotic equilibrium in a “mutualistic relationship.”15 That interaction and balance among oral microorganisms aids the human body in repelling the invasion of undesirable organisms from outside the body.16 Together they “form highly regulated, structurally and functionally organized communities attached to surfaces as biofilms, with interspecies collaborations as well as antagonisms that contribute to ecologic stability.”17
As noted, an extensive variety of microbiotas and biofilms, composed of hundreds of species, are scattered among multiple sites of the oral cavity. The species within each biofilm, as well as the other biofilms, all work in harmony—unmistakably designed to work together for the common good of human health. Not only do they not harm the human host, their commensal interrelationship helps keep pathogenic species in check.18 In fact, the microbes within the oral cavity can even aid the body’s immune responses outside the oral cavity.
That is not to say that the species never conflict with each other: “The relationship between the two bacterial species can be antagonistic or synergistic, depending perhaps on the composition of the remaining species in the biofilm or other environmental conditions.”19 Thus, even when a “clash” occurs, the overall well-being of the human host is the goal of the interactions and adjustments. Even when the microbiota is “disturbed” by any number of possible circumstances, nevertheless, “the relationship between the oral microbiome and its host is dynamic and…the composition of microbial communities is remarkably stable.”20
The entrance of pathogens from outside the system can cause problems—which immediately elicit the attention of the microbiota. In fact, due to “the interplay of the host’s immune system with its microbial symbionts, acute infections of the oral mucosa are rather rare.”21 Not only does the oral mucosa22 serve as a physiological barrier, “the functions of immune networks within this mucosa reflect the site-specific challenges faced within the oral cavity” with the ability to “trigger immune responses to the development of pathologic microbial communities.”23 The oral cavity is conspicuous for its “specialized immune-cell networks” that possess the exceptional capability to respond to the constantly fluctuating environmental conditions by means of “tissue-specific cues and exclusive immunologic responses that are tailored to the oral cavity.”24
However, as is typically the case, we humans are “our own worst enemy.” We can be responsible for instigating the instability of our own oral microbiome. Scientists list a number of factors that interfere with that stability and hamper the effectiveness of microbial communities. These culprits include poor oral hygiene, excessive use of antibiotics, modern diet trends, alcohol, and tobacco.25 Incredibly, researchers have come to believe that disrupting the delicate balance of our oral microorganism residents can contribute to additional bodily ailments, including asthma, diabetes, allergies, cancer, and obesity.26 What’s more, while various types of toothpaste typically reduce harmful bacteria, they can also suppress the beneficial bacteria. Likewise, mouthwashes that claim to kill 99% of bacteria would seem to be at variance with what scientists have discovered concerning the crucial role played by the oral microbiome. Mouthwashes can also significantly reduce the ability of saliva to serve as a buffer against tooth decay and disease 27 In fact, some studies suggest that the use of antibacterial mouthwash can “increase blood pressure as a result of its inhibitory effect on the oral microbiome.”28
Inter-Communication?
As researchers continue to dig deeper, they discover new layers of complexity. It turns out that the synergism among the microorganisms includes actual communication between species by means of QS—“quorum sensing”:
Bacteria within a biofilm can communicate with each other by producing, detecting and responding to small diffusible signal molecules in a process called quorum sensing, which confers benefit for host colonization, biofilm formation, defense against competitors and adaptation to changes in the environment.29
These signaling molecules are secreted by the bacteria themselves in order to engage in nutritional and signaling interactions with other bacteria, thereby acting in concert for the benefit of the human host.30 Such intelligent synergism could not have evolved via mindless happenstances of alleged eons of evolutionary time.
Their Purpose?
But what, specifically, do these millions of microorganisms do? We are in constant contact with all types of germs, bacteria, and other microorganisms—which enter our mouths. “The oral microbiome…forms an ecosystem that maintains health in a state of equilibrium,”31 making it “crucial in maintaining oral as well as systemic health.”32 Scientists have discovered that this complex ecological community performs astonishing activities that regulate oral health, contributing to “critical metabolic, physiological and immunological functions.”33 Incredibly, though only 1 out of 10 cells in our bodies is human, this prolific microbial society is responsible for performing “many biological functions that we could not perform on our own and protect[s] us from invasion by pathogenic microorganisms.”34 Hence, resident bacteria are “crucial for maintaining homeostasis.”35
Keep in mind that each human body is genetically unique and different from all others. If a supernatural Creator is responsible for the existence of human bodies as well as the multitude of living organisms that inhabit those bodies, one would fully expect to discover symbiotic harmony.36 Such is certainly the case with the interrelationships among the bacteria and between the bacteria and the human host. Complex relationships between humans and microbes facilitate human health while simultaneously providing the means for the microbes to survive and flourish. Humans and microorganisms literally depend on each other.37
Further, “the variable microbiome…is exclusive to an individual.”38 Consequently, diversity and variation of species within the microbiome are “individual specific and site specific.”39 “Rather than being fixed, the composition of the oral microbiota changes throughout life consistent with the oral cavity being a dynamic microbial environment.”40 So the oral microbiota differs from person to person.41 The microbial communities are programmed to react to varying environmental conditions by “modifying their species composition and population size.”42 Some oral bacteria species are site specific at one or multiple sites within the mouth. Others are subject-specific.43
In fact, the bacteria possess on their surface “adhesins.” Adhesins are proteins that enable the bacteria to attach to various surfaces in the mouth. Consequently, the bacteria will select for colonization those oral surfaces that possess complimentary receptors that will adhere to and bind with their own specific adhesins.44 This site specialization is essential for the formation of a biofilm in which the bacteria can colonize and grow. “Once established, the new community of bacteria then begins the process of replication, maturation, and formation of a complex biofilm that can contain hundreds of species.”45
If these striking realities were not enough to convince us of divine design, consider the fact that each species of bacteria can differ markedly in its purpose and function. As previously noted, some bacteria in the mouth specifically inhibit pathogens, i.e., those bacteria that cause disease. These bacteria resist colonization by pathogens. One species, for example, manifests “direct antagonism against oral pathogens.”46 Another such species actually produces hydrogen peroxide in large quantities which, in turn, hampers the growth of a harmful bacterial species.47 What’s more, while diet affects the oral microbiome, scientists have come to suspect that it works the other way as well. Oral cavity microorganisms can influence a person’s dietary preferences and, thus, “modulate the expression levels of taste receptors in the mouth.”48
Saliva
As an active and integral member of the oral microbiome, the origin of human saliva is inexplicable from an evolutionary standpoint. Its sophistication and complexity alone constitute proof of its divine design. Saliva provides a multi-purpose function for the human mouth and body—including lubrication, temperature, and digestion.49 Yet, apart from these vital functions, saliva is a critical and essential component in the efficient functioning of the oral microbiome. It serves as “a protective system that limits the type of bacteria that can live in the mouth.”50 “Saliva is used by oral biofilms as a delivery system, bringing nutrients, peptides, and partially dissolved carbohydrates.”51 Human saliva “keeps the bacteria hydrated and also serves as a medium for the transportation of nutrients to microorganisms.”52
Saliva contains components—including enzymes, proteins, and glycoproteins—that provide the central source of nutrition for microorganisms. As many as 108 microorganisms have been found in a single milliliter of saliva—an average of 100 million bacteria.53 At the same time, saliva also contains elements that possess antimicrobial action.54 In addition to these salivary components, the composition of the microbial communities in the mouth are affected by the “variation in the amount and velocity of salivary flow.”55 In fact, salivary flow, together with oxygen concentration, nutrient availability, and gingival crevicular fluids, creates “spatial gradients,” that further demonstrate the complicated nature of the oral cavity and its inhabitants’ interaction with the human host.56 Together, saliva and bacteria even protect tooth surfaces against acid.57 Indeed, saliva’s multi-pronged properties help regulate and maintain a balanced oral microbiome.
Conclusion
Despite the amazing number of discoveries that have accumulated through the years, despite the progress that has been made in an effort to unravel and understand the marvelous mysteries of the human oral microbiome, when all is said and done, “little is known about the microflora of the healthy oral cavity.”58 As always, the ignorance of man must bow to the intricacy and complexity of God’s handiwork.
How may such intricate, complicated, profound, extensive, mind-boggling symbiotic interrelationships be explained from an evolutionary perspective? “Well, over a period of millions of years, humans and the various organisms co-evolved a mutual dependency.” This “explanation” is nonsensical and meaningless. The myriad microorganisms and the human host needed each other from the beginning of their existence. How did the hundreds of species come into existence in the first place? How did they then “decide” to find an evolved human and gain entrance into that human’s mouth? How did species that are antagonistic to each other come to inhabit the oral cavity together? Was a microorganism convention conducted to discuss and decide the matter?
FACT: Every single one of these microorganisms—as well as their human hosts—possess concise design variables that prove the inability of gradual mutation and natural selection to function as causative agents. Can such design, complexity, order, purpose, and intelligence come out of mindless, evolutionary chaos? To ask is to answer. The Truth: God is the causative agent: “In the beginning, God created….”
Virtually with one accord, the scientists who have spent years of their lives exploring the layered intricacies of the human oral microbiome inevitably feel compelled—perhaps unwittingly—to use terminology that tacitly implies its divine intelligent design:
- “the finely-tuned equilibrium of the oral ecosystem”59
- “the complex dynamics and fitness factors of key organisms in oral microbiomes”60
- “a complex ecosystem whose equilibrium serves as a remarkable example of reciprocal adaptation”61
- “a staggering number of species”62
- “astounding diversity”63
- “a complex ecological community”64
- “exceptionally complex habitat”65
- “finely tuned…to protect from disease”66
Yet, even in the face of tremendous strides made in recent years to unravel some of the mysteries of these incredibly sophisticated, seemingly innumerable species, researchers acknowledge that the complex processes “are still not fully understood”67—an understatement if there ever was one.
“Finely-tuned”? “Complex dynamics”? “Remarkable”? “Staggering”? “Astounding”? “Exceptionally complex”? Follow the logic. To be candid, the human oral microbiome screams divine design.68 Its complex marvels could not possibly have come about gradually over millions of years via blind, sheer accident. The Creator had to have literally preprogrammed millions of microscopic creatures to live throughout the human oral cavity to perform unending, ongoing tasks for the benefit of those created in His image (Genesis 1:26). The rational, unprejudiced person will surely acknowledge the conclusion that such evidence requires. The psalmist put it this way: “I will praise You, for I am fearfully and wonderfully made; marvelous are Your works, and that my soul knows very well” (Psalm 139:14).
Endnotes
1 Antoni van Leeuwenhoek (1952), The Collected Letters of Antoni van Leeuwenhoek (Amsterdam: C.V. Swets & Zeitlinger; Committee of Dutch Scientists), 4:135, https://www.dbnl.org/tekst/leeu027alle04_01/leeu027alle04_01_0008.php#b0076; Clifford Dobell (1932), “Letter 39. 17 September 1683. To F. Aston,” Antony van Leeuwenhoek and His “Little Animals” (New York: Harcourt, Brace, & Co.), pp. 238ff.
2 J.A. Gilbert, M.J. Blaser, et al. (2018), “Current Understanding of the Human Microbiome,” Nature Medicine, 24:392-400.
3 J. Lederberg and A.T. McCray (2001), “‘Ome Sweet ‘Omics—A Genealogical Treasury of Words,” The Scientist, 15[7]:8, https://pdfs.semanticscholar.org/c06e/e544b5e87e82f7705c401e1eff5cc8e1f780.pdf?_ga=2.78678612.1501589133.1598356620-2085924697.1588006444.
4 The buccal mucosa refers to the lining of the inside of the cheek.
5 Priya Nimish Deo and Revati Deshmukh (2019), “Oral Microbiome: Unveiling the Fundamentals,” Journal of Oral Maxillofacial Pathology, 23[1]:123,125, January-April; Akshima Sahi (2020), “What Microorganisms Naturally Live in the Mouth?” News-Medical, September 16; A. Jørn, B.J. Paster, L.N. Stokes, I. Olsen, and F.E. Dewhirst (2005), “Defining the Normal Bacterial Flora of the Oral Cavity,” Journal of Clinical Microbiology, 43[11]:5730, November; M. Kilian, I. Chapple, M. Hannig, P.D. Marsh, V. Meuric, A. Pedersen, M.S. Tonetti, W.G. Wade, and E. Zaura (2016), “The Oral Microbiome: An Update,” British Dental Journal, 221:660, November 18.
6 Archaea are single-celled microorganisms with structure similar to bacteria.
7 Maria Avila, David Ojcius, and Ozlem Yilmaz (2009), “The Oral Microbiota: Living with a Permanent Guest,” DNA & Cell Biology, 28[8]:406; Deo and Deshmukh, p. 123.
8 Deo and Deshmukh, p. 122, emp. added.
9 Kilian, et al., p. 658.
10 Deo and Deshmukh, p. 123.
11 Lea Sedghi, Vincent DiMassa, Anthony Harrington, Susan V. Lynch, and Yvonne L. Kapila (2021), “The Oral Microbiome: Role of Key Organisms and Complex Networks in Oral Health and Disease,” Periodontology 2000, 87[1]:107, October; J.L. Welch, F.E. Dewhirst, and G.G. Borisy (2019), “Biogeography of the Oral Microbiome: The Site-Specialist Hypothesis,” Annual Review of Microbiology, 73[1]:335-338.
12 Akshima Sahi (2020), “What Microorganisms Naturally Live in the Mouth?” News-Medical, September 16.
13 Deo and Deshmukh, p. 124.
14 Anil Kumar and Nikita Chordia (2017), “Role of Microbes in Human Health,” Applied Microbiology Open Access, 3[2]:1; Kilian, et al., p. 655.
15 Lu Gao, Tiansong Xu, et al. (2018), “Oral Microbiomes: More and More Importance in Oral Cavity and Whole Body,” Protein Cell, 9[5]:488,496.
16 Kilian, et al., p. 659.
17 Avila, et al., p. 406.
18 Sedghi, et al., p. 107.
19 Avila, et al., p. 409.
20 P.D. Marsh, D.A. Head, D.A. Devine (2015), “Ecological Approaches to Oral Biofilms: Control Without Killing,” Caries Research, 49[Supplement 1]:46-54; Kilian, et al., p. 664, emp. added.
21 E. Zaura, E.A. Nicu, B.P. Krom, and B.J. Keijser (2014), “Acquiring and Maintaining a Normal Oral Microbiome: Current Perspec-tive,” Frontiers in Cellular and Infection Microbiology, 4:85; Kilian, et al., p. 660.
22 “The oral mucosa refers to the moist, membrane-like lining that covers the inside of the mouth, including the lips, cheeks, tongue, and floor of the mouth. It is a protective barrier that shields the underlying tissues from injury, infection, and chemical irritants”—“Oral Mucosal Diseases” (2025), UC Davis Health, Department of Dermatology (Sacramento, CA), https://health.ucdavis.edu/dermatology/specialties/medical/oral.html#:~:text=The%20oral%20mucosa%20is%20the,or%20ulcers%20on%20this%20lining.
23 N. Dutzan, T. Kajikawa, L. Abusleme, et al. (2018), “A Dysbiotic Microbiome Triggers TH17 Cells to Mediate Oral Mucosal Immunopathology in Mice and Humans,” Science Translational Medicine, 10[463]:eaat0797; Sedghi, et al., p. 110.
24 Sedghi, et al., p. 110; “Oral Mucosal Immunity and Microbiome” in Advances in Experimental Medicine and Biology, ed. G.N. Belibasakis, G. Hajishengallis, N. Bostanci, M.A. Curtis (Cham: Springer International Publishing), 1197, emp. added; R.Q. Wu, D.F. Zhang, E. Tu, Q.M. Chen, W. Chen (2014), “The Mucosal Immune System in the Oral Cavity—An Orchestra of T Cell Diversity,” International Journal of Oral Science, 6[3]:125-132; A. Esberg, S. Haworth, R. Kuja-Halkola, P.K.E. Magnusson, I. Johansson (2020), “Heritability of Oral Microbiota and Immune Responses to Oral Bacteria,” Microorganisms, 8[8]:1126.
25 Sedghi, et al., p. 113; E. Xiao, M. Mattos, G.H.A. Vieira, et al. (2017), “Diabetes Enhances IL-17 Expression and Alters the Oral Microbiome to Increase Its Pathogenicity,” Cell Host Microbe, 22[1]:120-128; Mi Klein, L. DeBaz, S. Agidi, et al. (2010), “Dynamics of Streptococcus mutans Transcriptome in Response to Starch and Sucrose During Biofilm Development,” PLoS One, 5[10]:e13478; A. Cekici, A. Kantarci, H. Hasturk, T.E. Van Dyke (2014), “Inflammatory and Immune Pathways in the Pathogenesis of Periodontal Disease,” Periodontology 2000, 64[1]:57-80; P. De Pablo, T. Dietrich, T.E. McAlindon (2008), “Association of Periodontal Disease and Tooth Loss with Rheumatoid Arthritis in the US Population,” Journal of Rheumatology, 35[1]:70-76; J. Wu, B.A. Peters, C. Dominianni, et al. (2016), “Cigarette Smoking and the Oral Microbiome in a Large Study of American Adults,” The ISME Journal, 10[10]:2435-2446; W. Pitiphat, A.T. Merchant, E.B. Rimm, K.J. Joshipura, “Alcohol Consumption Increases Periodontitis Risk,” Journal of Dental Research, 82[7]:509-513.
26 Kumar and Chordia, p. 131.
27 Sedghi, et al., p. 121.
28 Ibid., p. 113; C.P. Bondonno, A.H. Liu, K.D. Croft, et al. (2015), “Antibacterial Mouthwash Blunts Oral Nitrate Reduction and Increases Blood Pressure in Treated Hypertensive Men and Women,” American Journal of Hypertension, 28[5]:572-575.
29 Y.H. Li and X. Tian (2012), “Quorum Sensing and Bacterial Social Interactions in Biofilms,” Sensors, 12:2519-2538; Kilian, et al., p. 659.
30 W.C. Fuqua, S.C. Winans, and E.P. Greenberg (1994), “Quorum Sensing in Bacteria: The LuxR-LuxI Family of Cell Density-Responsive Transcriptional Regulators,” Journal of Bacteriology, 176:269-275; Avila, et al., p. 408; Kilian, et al., p. 662.
31 Deo and Deshmukh, p. 127.
32 Ibid., p. 122.
33 Kilian, et al., p. 659.
34 Avila, et al., p. 405.
35 Kilian, et al., p. 660.
36 However, one must keep in mind that through the six thousand years of human history, genetic degeneration has occurred and the application of the laws of thermodynamics continues to degrade the effectiveness and efficiency of all biological organisms.
37 Kumar and Chordia, p. 131.
38 Deo and Deshmukh, p. 123.
39 Ibid., p. 124.
40 Sedghi, et al., p. 110.
41 Ibid., p. 112. Also M.W. Hall, N. Singh, et al. (2017), “Interpersonal Diversity and Temporal Dynamics of Dental, Tongue, and Salivary Microbiota in the Healthy Oral Cavity,” NPJ Biofilms Microbiomes, 3[1]:1-7.
42 Avila, et al., p. 405.
43 Jørn, et al., p. 5724.
44 R.J. Gibbons (1989), “Bacterial Adhesion to Oral Tissues: A Model for Infectious Diseases,” Journal of Dental Research, 68:750-760; Jorn, et al., p. 5731; Deo and Deshmukh, p. 123.
45 P.D. Marsh (2006), “Dental Plaque as a Biofilm and a Microbial Community—Implications for Health and Disease,” BioMed Central, 6:1-7; B. Rosan and R.J. Lamont (2000), “Dental Plaque Formation,” Microbes and Infection, 2[13]:1599-1607; Sedghi, et al., pp. 115-116; Welch, et al., pp. 335-338.
46 Sedghi, et al., p. 113.
47 Ibid., p. 122.
48 Ibid., pp. 108,120.
49 Avila, et al., p. 406; Michael Wilson (2004), Microbial Inhabitants of Humans (Cambridge: Cambridge University Press), pp. 318ff.
50 Maria del Mar Ferrándiz Lorenzo (no date), “Bacteria in Our Mouths: How Many and What are They?” KIN Laboratories, https://www.kin.es/en/bacterias-que-tenemos-en-la-boca/.
51 Avila, et al., p. 406. See also P.E. Kolenbrander, N.S. Jakubovics, N.I. Chalmers, and R.J. Palmer, Jr. (2007), “Human Oral Multispecies Biofilms: Bacterial Communities in Health and Human Disease” in The Biofilm Mode of Life: Mechanisms and Adaptations, ed. S. Kjelleberg (Norfolk, VA: Horizon Bioscience), pp. 175-194.
52 Deo and Deshmukh, p. 123.
53 Kilian, et al., p. 660; Also Lorenzo.
54 W. van’t Hof, E.C. Veerman, A.V. Nieuw Amerongen, and A.J. Ligtenberg (2014), “Antimicrobial Defense Systems in Saliva,” Monographs in Oral Science, 24:40-51; Kilian, et al., p. 660.
55 Sedghi, et al., p. 115.
56 Ibid., p. 115; D.M. Proctor, J.A. Fukuyama, P.M. Loomer, et al. (2018), “A Spatial Gradient of Bacterial Diversity in the Human Oral Cavity Shaped by Salivary Flow,” Nature Communications, p. 9.
57 Kilian, et al., p. 660.
58 Jørn, et al., p. 5721.
59 Kilian, et al., p. 657, emp. added.
60 Sedghi, et al., p. 107, emp. added.
61 Kumar and Chordia, p. 131, emp. added.
62 Avila, et al., p. 408, emp. added.
63 Deo and Deshmukh, p. 123, emp. added.
64 Kilian, et al., p. 659.
65 Deo and Deshmukh, p. 122, emp. added.
66 Kilian, et al., p. 652, emp. added.
67 Ibid., p. 660, emp. added.
68 Even as the Universe “declares” (i.e., “announces/makes known”) the glory of God (Psalm 19:1). Ludwig Koehler et al. (1994-2000), The Hebrew and Aramaic Lexicon of the Old Testament (Leiden: E.J. Brill), p. 766.
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