Part II: Oral Microbiome and Saliva
By Karen Sheffler, MS, CCC-SLP, BCS-S. SwallowStudy.com
I was out in the beautiful pacific northwest the summer of 2014, learning about the region’s flora, fauna, volcanos and glaciers. Especially interesting was visiting Mount Saint Helens in Washington state. After 34 years, the destructive power of the 1980 volcanic eruption is still evident. However, this ecosystem or ecobiome is recovering. The ash-filled pumice plain is finally being recolonized. My then seven-year-old son asked: “What is an ecosystem?” We described the miraculous balance that is created in a complex inter-dependent system like the temperate rainforests of Washington state. These systems work to achieve a homeostasis. (Read More: previously, I discussed homeostasis in the elderly.)
Now, as I turn my attention back to oral hygiene and aspiration pneumonia, I am realizing the volcano is a good analogy for what happens in our mouth when we are critically ill and institutionalized. Our mouth is it’s own complex ecosystem (aka, the oral microbiome). My research on saliva alone has left me astounded and inspired by it’s complexity. Can an acute illness, hospitalization and poor oral hygiene act like a volcano, disrupting the balance or homeostasis of the oral microbiome?
What can cause the oral microbiome to spiral out of balance?
In the case of a volcanic eruption like Mount Saint Helens, it is easy to imagine the ash’s impact on the environment. Ash lowers the pH of the soil, causing harsh acidification. This causes oxygen deprivation and decreased availability of essential minerals. The soil’s characteristics change, and the once healthy plants will not survive. This sounds very similar to my readings on the oral microbiome, in terms of an illness or stress causing a disruption. That can change the pH and the once healthy flora.
What starts the vicious cycle in the mouth?
- What changes the balanced diversity of gram-positive healthy oral microflora to gram-negative bacteria?
- How does the chemistry of the saliva change (i.e., bicarbonates, cortisol, proteins, etc)?
- What changes the salivary pH?
- What causes the harmful bacteria to proliferate?
- How does that bacteria get into the lungs to make a patient sick?
We know from Part I of Oral Hygiene and Aspiration Pneumonia Prevention that bacteria adheres to sticky plaques and that is a primary site of infection. However, not all people with this plaque biofilm spiral down this vicious cycle. What is the “straw that broke the camel’s back” – spiraling the ecosystem out of control?
The patient’s salivary flow and salivary composition may be root causes. Let’s look at the roles and immune properties of saliva.
Why do we need saliva? Saliva’s top 10:
- Digestive process begins (via amylase, lipase and proteolytic enzymes)
- Taste (via the protein gustin)
- Lubricates the bolus of food for swallowing and the oral cavity for speech (via mucin)
- Anti-viral, anti-bacterial, anti-fungal with delicate balance of anti-microbials
- Cleansing – continuous mechanical removal of bacteria, plaque and microorganisms as we swallow our saliva. The higher the saliva flow, the better the cleansing action.
- Protects and repairs oral mucosa
- Dental remineralization – tooth enamel integrity is maintained by mineral concentrations of salivary bicarbonate and calcium phosphates, as well as a complex salivary protein layer. This is all dependent on enough saliva flow to keep the salivary pH neutral and balanced at 6-7. Low salivary flow may drop the pH to an average of 5.3 (Fennoll-Palomares, 2004). Acids in our foods and the acidic waste biproducts of bacteria can further alter the pH.
- Caries prevention – if the saliva becomes more acidic, it will harm the tooth enamel and cause decay.
- Shelters microorganisms that form a biofilm on the dental surfaces and tongue. Molecular studies have shown over 700 microbial species. Streptococcus salivarius colonizes the mouth within 18 hours of birth. The protein layer provides an environment for a balanced microbial community. It reaches a homeostasis, which helps to eliminate invader species. Periera (2012) found that the “mature” biofilm has a higher proportion of anaerobic microorganisms and non-culturalble bacteria.
- Buffering capacity:
- Selectively prevents bacterial colonization.
- Manages thickness of biofilm and amount of bacteria
- Maintenance of salivary pH
- Neutralizes acids from bacterial waste
It is such a complex puzzle that it is easy to see how the equilibrium could be disrupted.
Saliva’s immune factors:
If disrupted –> bacterial adherence, colonization and overgrowth
- Secretory Immunoglobulin A (IgA) – a primary component – adaptive immune factor. Neutralizes viruses, bacteria and enzyme toxins. Prevents absorption and penetration of respiratory pathogenic bacteria (Holmgren, 1991).
- Lactoferrin – innate immune factor. This can inhibit proliferation of microorganisms by taking away iron from the bacteria that need iron for survival. It is a bactericidal against S aureus, P aeruginosa, and H influenzae.
- Lysozyme and Sialoperoxidase – enzymes that are present in secretions that can interfere with the cell walls of bacteria and kill bacteria.
- Cystatins and Histatins – antimicrobial against bacteria and yeasts
- Proline-rich proteins and Statherins – prevention of plaque and dental calculus
- Mucins – protection against viruses and bacteria. Aids in viscous quality of saliva.
Read even more about SALIVA in this blog.
“Much is known about critical illness on systemic immunity, but less is known about specific effects on oral immunity,” per Munro and Grap (2004, page 28). They noted that critically ill patients have decreased salivary flow and decreased salivary immune components (i.e., IgA, lactoferrin, cortisol, and neopterin).
- Decreased production of IgA leaves a patient susceptible to upper respiratory tract infections.
- Bardow et al (2000) found low salivary flow was the best predictor of mineral loss and therefore increased caries risk.
- Umazume et al (1995) found both salivary IgA and saliva volume were in significantly lower amounts in patients with oral cancer versus healthy controls.
- Umazume et al found that high Lactoferrin levels in saliva were correlated with inhibited growth of candida albicans (oral thrush).
- Immunocompromised patients also have an increased number of fungal infections, which may be due to decreased levels of IgA and Lactoferrin.
Salivary Flow (SF): measured in quantity per minute stimulated or unstimulated. Unstimulated salivary flow is from the submandibular, parotid, and sublingual glands.
- Normal salivary flow (unstimulated): approximately 0.25-0.35 ml/minute (1-3 ml/minute stimulated)
- Low salivary flow (unstimulated): < 0.16 ml/minute per Bardow et al (2000) and Navazesh et al (1992).
What could cause a low salivary flow (hyposalivation)?
- Iatrogenic causes: Medication, irradiation
- Disease: Sjogren’s syndrome, salivary gland disease, salivary aplasia, sarcoidosis, cystic fibrosis. Patients with Sjogren syndrome (autoimmune attack on the salivary glands causing dry mouth) experience mircrobial overgrowth, increased caries, and some have an increased risk for pneumonia.
- Infections: HIV, Hep C
Is low salivary flow caused by the stress of acute illness?
Naumova et al (2014) found the stress of 1 1/2 hours of public speaking can cause salivary chemistry changes in young healthy males, namely increased protein concentrations, increased pH, and increased cortisol. The pH in the stress group was higher than the control group. An earlier study by Naumova et al (2012) found no changes in salivary flow rate with stress of public speaking. However, Naumova et al speculated that the feeling of dry mouth when under stress may be due to changes in the composition and properties of the saliva, rather than the flow rate. This is an area for further study, especially when under prolonged stress of chronic illness and hospitalization. Critical illness is a much greater stressor than public speaking!
Low salivary flow and changes in saliva chemistry or composition may be root causes in an oral microbiome spiraling out of control, but this is accelerated by institutionalized patients who have poor oral hygiene and are critically ill.
The accumulation of dental plaque creates a thick biofilm that is less penetrable by saliva. Then, the immune properties of saliva cannot do their work. Additionally, a lack of saliva flow will cause a decrease in the amount of salivary bicarbonate and other helpful minerals and proteins. This will start to acidify the saliva. Less saliva also means less protective buffering. It is the buffering action of saliva that neutralizes the acidic waste from the bacteria. Once the enamel is exposed to pH of 5.5 or lower, the demineralization is initiated. Demineralization leads to more decay and more adherence of bacteria. One can image the vicious cycle. Again, it comes down to prevention. Provide good oral care, with brushing a patient’s teeth. Not only will this remove the harmful bacteria that sticks to the plaque, but it will also stimulate saliva flow and potentially stop the disruption of an ecosystem.
Thank you once again for reading and traveling with me to different ecosystems to see what can disturb the homeostasis. With this topic, we may continue to ask more questions than we are answering.
My other blogs in this series will cover microorganisms from the mouth that can colonize the lungs –> We will explore how and why these pathogens from an altered oral microbiome can make the trip to the lungs (in Part III).
We will cover interventions for improved oral hygiene and comfort in critically ill patients and in cancer patients (Part IV). This is often called “oral care,” but we should start documenting it as “oral infection control” and “oral decontamination for aspiration pneumonia prevention.”
Travel with me in my fun 5th blog on the topic: “It’s Alive! Oral Microbiome.”
Check out my guest bloggers: Joanne Yee, MS, CF-SLP & Dr Nicole Rogus-Pulia, PhD, CCC-SLP, who wrote “The Saliva Puzzle: Saliva Production & Swallowing.”
- Bardow, A., Nyvad, B. & Nauntofte, B. (2001). Relationships between medication intake, complaints of dry mouth, salivary flow rate and composition, and the rate of tooth demineralization in situ. Archives of Oral Biology, 46 (5), 413-423. https://dx.doi.org/10.1016/S0003-9969(01)00003-6
- Fennoll-Palomares, C, Munoz-Montagud, J.V., Sanchiz, V., Herreros, B, Hernandez, B., Minguez, M. & Benages, A. (2004). Unstimulated salivary flow rate, pH and buffer capacity of saliva in healthy volunteers. Revista Espanola De Enfermedades Digestivas, 96 (11), 773-783.
- Holmgren J. (1991). Mucosal immunity and vaccination. FEMS Microbiology Immunology, 4, 1-9.
- Munro, C.L. & Grap, M. (2004). Oral health and care in the intensive care unit: State of the science. American Journal of Critical Care, 13, 25-34.
- Naumova, E. A. et al. (2012). Acute short-term mental stress does not influence salivary flow rate dynamics. PLOS ONE. DOI: 10.1371/journal.pone.0051323 https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3521772/
- Naumova, E.A et al (2014). Dynamic changes in saliva after acute mental stress. Scientific Reports, 4 (article 4884). doi:10.1038/srep04884. https://www.nature.com/srep/2014/140508/srep04884/full/srep04884.html
- Navazesh, M., Christensen, C. & Brightman, V. (1992). Clinical criteria for the diagnosis of salivary gland hypofunction. Journal of Dental Research, 71 (7), 1363-9.
- Pereira, J.V., Leomil, L., Robrigues-Albuquerque, F., Pereira, J.O. & Astolfi-Filho, S. (2012). Bacterial diversity in the saliva of patients with different oral hygiene indexes. Brazilian Dental Journal, 23 (4), https://dx.doi.org/10.1590/S0103-64402012000400017
- Umazume, M., Ueta, E, Osaki, T. (1995). Reduced inhibition of candida albicans adhesion by saliva from patients receiving oral cancer therapy. Journal of Clinicial Microbiology, 33, 432-439.
Powerpoints that assisted my research:
1. Chemical Compositions and Functions of Saliva, by Dennis E Lopatin, PhD. Downloaded 7/31/14. https://www.google.com/urlsa=t&rct=j&q=&esrc=s&source=web&cd=1&ved=0CB8QFjAA&url=http%3A%2F%2Fwww.umich.edu%2F~bmsteach%2Flopatin%2Fsalivarygland%2Flectures%2Fdownload%2FChem_Comp_%26_Funct.ppt&ei=VpjaU8X9EIKoyATy6YLwAg&usg=AFQjCNF6o7cWICGhCj1V1rwhE-ZY_eWBng&sig2=Vhaz_y3iC6BviL4SFuO-Mw&bvm=bv.72185853,d.aWw
2. Structure and Function of Salivary Proteins, by Sompop Bencharit, DDS, MS, PhD (2008). Downloaded 7/31/14.