Your question is difficult to answer because it raises at lot more questions. First of all. Measuring salivary pH is a critical matter. It should be done within the oral cavity, as it changes under experimental conditions outside the oral cavity. Secondly salivary pH varies consideably is is dependent from a lot of different factors such as CO2, bicarbonate, protein concentration and last not least from the physiological contition of the individdum (see. also Naumova et a. Sci Rep. 4:4884). Bacterial colonization and distribution in the oral cavity is not equal. It is different in different niches. Most bacteria are found on the tongue surface. Very little are fount on the mouth floor. We are just about to study the physiological differences of the bacterial colonization in different areas of the oral cavity.

Your question is difficult to answer because it raises at lot more questions. First of all. Measuring salivary pH is a critical matter. It should be done within the oral cavity, as it changes under experimental conditions outside the oral cavity. Secondly salivary pH varies consideably is is dependent from a lot of different factors such as CO2, bicarbonate, protein concentration and last not least from the physiological contition of the individdum (see. also Naumova et a. Sci Rep. 4:4884). Bacterial colonization and distribution in the oral cavity is not equal. It is different in different niches. Most bacteria are found on the tongue surface. Very little are fount on the mouth floor. We are just about to study the physiological differences of the bacterial colonization in different areas of the oral cavity.

From a microbiological point of view, decreases in pH can be caused by the proliferation of certain (acidogenic) bacteria in the saliva, hard surfaces or (as Wolfgang points out) the soft surfaces of the mouth.  Commonly-cited examples include Streptococcus mutans and Lactobacillus species, which produce lactic and acetic acids as bi-products the metabolism of sugars in the patient's diet. On the other hand, different species can counter this effect, for example production of ammonia from arginine by Streptococcus sanguinis, which might help keep the pH from dropping too far. The oral microbiome varies considerably, and it's not difficult to image a situation in which acidogenic species proliferate more readily in one host (or patient) than another, tipping the balance in favour of acidification. Add to that decreased salivary flow rates, meaning lower levels of pH buffering. Add also potential difficulties with regular and effective oral health among critically ill patients, and it is possible that prolonged levels of lowered pH might  feasibly prevail. These conditions may then select out members of the non-aciduric members of the oral microbiome, allowing further proliferation of acidogenic bacteria, exacerbating the issue.

I don't claim to know a lot about the host-factors involved, especially in critically-ill patients, but I hope this helps.

This really speaks to the power of a homeostasis in our body. This is especially true in elderly patients. You see patients who are just barely getting by at home with some balance of homeostasis, but then an acute illness tips them over and the body does not have enough functional reserve to maintain a homeostasis. It sounds like the oral microbiome is an ecosystem that has a fine balance of acidic waste producing bacteria and alkaline waste producing bacteria with lots of saliva flow as a buffer with immune properties too. We know that it just takes 48 hours of hospitalization to change from normal healthy gram-positive oral flora to gram-negative strains. We also know that the mouth gets easily colonized with bacteria in the institution, exacerbated by poor oral care in institutions. 

I went to a talk recently by Kenneth Shay, DDS, Director of the VA Geriatrics and Extended Care Service Line. He listed 12 different microflora found in periodontitis that have also been found in nosocomial pneumonia microflora. (i.e., S. Aureus, fusobacterium nucleatum, haemophilus influenzae, and more). Patients are aspirating this oral flora. Brushing the mouth is the single best action we can do to decrease bacteria adhering to plaques. Brushing just does not happen often enough in hospitals and nursing facilities, especially with dependent elders.

Would rinsing with baking soda daily in the hospital reduce the acidification and proliferation of these harmful bacteria?

I would love to keep discussing this as I am preparing my Part 2 of Oral hygiene and Aspiration Pneumonia article on my website: www.swallowstudy.com.

www.swallowstudy.com

E.g. because of xerogenic medication, salivary flow is often lowered in ill people. Under conditions of low salivary flow, the salivary bicarbonate concentration and consequently the pH are diminished too.

Still, I think that rather than pH, the lack of saliva by itself is the  underlying cause of the shift in oral microflora.  Saliva promotes the establishement of a benign stable oral microflora: it promotes the continuous removal of bacteria from the mouth as well as serves as a source of growth substrates for bacteria. In the absence of saliva, this equilibrium is disrupted, leading to an ecological shift.     

Our suggestion is to keep the pH of the saliva alkaline in Leukemia patients undergoing chemotherapy though a daily oral intake of two 500 mg capsules of marine concentrate of minerals of organic origin rich in calcium, magnesium and others importants minerals. For prevention of the microbiota (microflora) of mucositis and xerostomy. Sea minerals from "Lithothaminium Calcarium". 

I like your question but what do you mean by "critically ill patients". It is a very broad term. You need to specify patients who are terminally ill, For example; ASA ( American Society of Anesthesiologists)PS 4 or ASA PS 5 patients? If they are, then, which condition is the underlying cause of such patients being terminally ill? Secondly, Not all terminally ill patients would be taking drugs which would induce Xerostomia. On the contrary, many of these patients might be taking drugs which would induce Sialorrhoea (for example; benzodiazepines, neuroleptics, cholinesterase inhibitors etc) 

In animal studies has been shown that benzodiazepines inhibit saliva secretion (see e.g. LIFE SCIENCES 31, 1465-147). In line xerostomia is often reported as side effect of benzodiazepines. Saliva hypersecretion is very rarely reported. In the majority of the cases sialorrhoe (drooling) is caused by an inability to retain saliva within the mouth or problems with swallowing, not by excessive saliva production.    

Eci, I agree with you.

Yes, sialorrhea is rare as compared to xerostomia but my point is that xerostomia is not necessarily associated with every debilitating disease or medications used in such patients.

Here are two reference of benzodiazepines causing sialorrhea in human beings:

1) Color atlas of orofacial health and disease in children and adolescent - By Crispian Scully, Richard Welbury, Catherine Fiatz, Oslei (page 179, table 28)

2) Pediatric Otolaryngology (Section 4, Page 1290, Table 72-1)

these are the links of above mentioned references

http://books.google.co.uk/books?id=JzfCjsGFT2gC&pg=PA179&lpg=PA179&dq=benzodiazepine+causing+sialorrhea&source=bl&ots=W_svZGuTvn&sig=m9A9buqimRLMcfQi_VxkvwWlgNo&hl=en&sa=X&ei=aGrbU7SbOIWY1AXFs4HYBQ&ved=0CEUQ6AEwBjgK#v=onepage&q=benzodiazepine%20causing%20sialorrhea&f=false

http://books.google.co.uk/books?id=-D0rAwAAQBAJ&pg=PA1290&lpg=PA1290&dq=benzodiazepine+causes+sialorrhea&source=bl&ots=0UP3UPwdUr&sig=HTklxmARTBXA6JXt5frh3MHo4V8&hl=en&sa=X&ei=o23bU7_FKs2Z0QXd0oBg&ved=0CEMQ6AEwBjgK#v=onepage&q=benzodiazepine%20causes%20sialorrhea&f=false

My point was that sialorrhoe  in most cases is not due to hypersalivation, but to an inability to retain saliva or to swallow properly. Coordinated muscle activity is crucial for proper swallowing. Benzodiazepines are muscle relaxants and as such may interfere in the swallowing process, leading to drooling.

True Agreed

Sixty patients undergoing treatment at the State Institute of Hematology Arthur Siqueira Cavalcanti of Rio de Janeiro (HEMORIO) were studied. Patients with Acute Mieloide Leukemia (AML) and Acute Lymphoid Leukemia (ALL). Initially, thirty patients were part of the study. However, five of these patients died during the process. The twenty-five patients that continued in the program took two daily tablets of 500 mg each of a concentration of sea minerals of organic origin. These patients’ conditions developed quite well, with the pH of the saliva from 7.0 to 7.5, with no relevant oral complications. Six patients had light mucositis, easily controlled by the usual methods (according to the HEMORIO treatment protocol of mucositis caused by chemotherapy) and three neutropenic patients evolved without the presence of infection.

Therefore, was observed that the food supplement concentration of sea minerals of organic origin has proven to be a viable support in the control of the oral mucositis generated by chemotherapy in patients with AML and ALL, keeping the pH of the saliva of these patients alkaline and the oral microbiota unchanged.

This way, the advent of opportunist microorganisms and oral lesionsare prevented.

The other thirty patients of the control group who did not take the food supplement developed the acid pH of the saliva (pH 6.0 and 6.5) and mucositis.

Considering the results presented above, this study suggest this food supplement should be incorporated in the treatment of all the patients undergoing chemotherapy.

Key words: pH, oral lesions, sea minerals, saliva, mucosites, chemotherapy and leukemia.

Karen,

I think this is a very interesting question and train of thought. Clearly the need to understand and comparethe oral microbiome changes during illness is an important and understudied area, especially among hospital (and probably nursing home) patients. Neither salivary flow nor salivary composition are typically measured in a hospital stay. How would one advocate that that could be a powerful tool to add to the clinician's armamentarium?

Thank you to everyone for this great ongoing discussion.

Certainly the benzodiazepines (including lorazepam - Ativan) can inhibit swallowing function. If the patient is sedated and muscles relaxed, the patient will not be swallowing the quart of saliva a day that is produced. Therefore, drooling may result.  However, this may not be an actual increase in salivary flow.

In terms of "critically ill" patients: I think in terms of hospitalized elderly - particularly those in the ICU. I had a patient the other day who came in with a fall, but then developed pneumonia after 3 days. They asked me to evaluate the swallowing, which was really only minimally impaired. The issue may have been that he had not brushed his teeth during the entire hospital stay. Toothbrush and mouthwash were not opened and per pt report. In addition to that, he was bedridden with 2 rib fractures - so we know he had poor pulmonary clearance and activity due to pain. Studies have shown that it takes only 48 hours in the hospital to change oral flora to gram-negative from gram-positive. The patients I'm interested in are those who develop Hospital Acquired Pneumonia due to the hospital environment and poor oral hygiene. Medicare in the USA is not going to pay for hospitalizations anymore when a patient develops pneumonia at the hospital. We know prevention is such a big aspect of this oral issue. Hospitals here finally will have incentive to follow prevention techniques!

In addition to hosts' factors, the microbial community contributes equally to the balance and health in the oral ecosystem. Changes in the pH of saliva maybe brought about by acidic endproducts of the saccharolytic bacteria.  In critically ill patient, oral hygiene is often neglected. This allows for the accumulation of dental plaque on tooth surfaces. This dense biofilm would be less penetrable by the saliva which functions to neutralise the acidic endproducts of the bacteria. Without the buffering action of the saliva, acids will get accumulated and when the enamel is exposed to a critical pH of about 5.5, demineralisation is initiated.  Due to the low saliva flow rate of these patients, cleansing action of saliva is also impaired. In addition to that the buffering components within unstimulated saliva is low as compared to stimulated saliva.  

Thank you Fathilah Abdul razak - that is such a clear summary tying this together.

Do you have a favorite research article or articles that you would suggest to give to hospitals to reinforce this science and encourage oral hygiene? Maybe a systematic literature review?

This would help reinforce the expenses necessary (i.e., purchasing toothbrushes on suction and supplying them to all floors around the hospital for patients who are dependent on others). There would need to be training programs for staff in oral hygiene best-practices. Additionally, policies need to reflect a commitment to improving oral hygiene as a measure to reduce hospital acquired aspiration pneumonias. 

Oral decontamination by rinsing with chorhexidine can also be considered, see

help: http://www.hopkinsmedicine.org/heic/docs/VAP_prevention_best_practices.pdf

Thank you for the pdf.

Also here is a link to my website on Dysphagia and my blog on the topic: 

http://www.swallowstudy.com/?p=392

This will bring you to Part III of Oral Hygiene and Aspiration Pneumonia, where it addresses specific microflora. There are links in that blog to Part I (addressing dental plaque) and Part II (addressing saliva). Comments and questions can be posted there too. 

http://www.swallowstudy.com/?p=392