Saliva, Chewing Gum, and Oral Health

Although the average American will chew about 300 sticks of gum a year, in the past a chewing gum habit has been criticized by some clinicians as harmful. For example, in 1869 a physician wrote that chewing gum would "exhaust the salivary glands and cause the intestines to stick together."1 Today, we recognize that chewing gum does not cause those maladies, nor does it lead to clicking and popping of the TMJ.

More than $2 billion of gum is sold in the United States each year, with worldwide sales in excess of $5 billion. Current research has indicated a number of positive oral benefits to be realized from chewing gum, mainly focusing on the stimulation of saliva, control of oral pH, and remineralization of enamel.2-4 Realizing the popularity of chewing gum, dental health professionals need to recognize the potential dental health benefits of these products when used as an adjunct to routine oral healthcare.

 

 

Table. Components of Saliva and Their Function. 2,4

Salivary Component
Function
Amylas
Digestion
Bicarbonate Buffering
Calcium Remineralization
Histatins Antimicrobial effects
IgA Antimicrobial; inhibits microbial adherence
IgM Antimicrobial; inhibits microbial adherence
Lactoferrin Antimicrobial; hydrolysis of bacterial cell membranes
Lactoperoxidase Antibacterial; hydrolysis of bacterial cell membranes
Lysozyme Antimicrobial; hydrolysis of cell membrane
Mucins Antibacterial, digestion, lubrication, pellicle formation
Protease Digestion
Phosphates Buffering
Proline rich proteins Antimicrobial, lubrication, remineralization
Statherin Antimicrobial, remineralization
Water Cleansing, digestion, lubrication, mucosal integrity
Urea Buffering



In humans, saliva is generated by 3 pairs of major and numerous minor salivary glands. The minor glands are located within the oral mucosa, including lips, buccal mucosa, and soft palate. The major salivary glands produce 93% of all saliva.4 The salivary glands are under the control of the autonomic nervous system and respond to hormonal influences. Saliva is formed in the acinar cells of the glands via an osmotic mechanism. Saliva is 99% water. The remaining components are macromolecules, which are formed within the endoplasmic reticulum of the acinar cells2,3 and secreted by the ducts into the lumen (Table).

Daily saliva output is in the range of 500 to 1,500 mL, although the average resting volume of saliva in the oral cavity at any one time is only 1 mL.2,3 Saliva output may either be resting (basal) or stimulated, and stimulation increases the flow rate. Mean resting saliva output (whole saliva) is 0.4 mL/minute and is highest in the morning.2 Stimulated saliva output, which is driven by masticatory or gustatory signals, is between 1 to 2 mL/minute. When the saliva is stimulated, there is an increase in the concentration of bicarbonate ions, which consequently causes a rise in the pH, increasing the buffering capacity of saliva against the acids formed after carbohydrate ingestion.2-5

Adequate saliva is critical for good oral health. Aside from lubricating the tissues, saliva helps maintain a pH environment that promotes tooth remineralization via deposition of ionic minerals available in solution and serves an antimicrobial function as a result of the immunoglobulins and proteins present in the fluid. Saliva assists in digesting, diluting, and clearing dietary carbohydrates as well as buffering of acid that is a byproduct of the metabolism of sugar. Due to the presence of histatins (proline-rich proteins including cystatins and statherin), calcium and phosphate are maintained in supersaturation and are available for remineralization of tooth structure.3 In addition, saliva aids in maintaining mucosal integrity and aids in digestion as a result of enzymes in the fluid. Saliva also is integral to the formation of the pellicle, which protects the tooth after eruption (Table).

Saliva's buffering capacity maintains the health of the dentition. For the 2 hours after carbohydrate ingestion and acid production by oral bacteria, there is a drop in pH. Following ingestion of a dietary sugar, the stimulated production of saliva ceases after the sugar clears the mouth, and salivary output returns to a resting state within a short time.5,6 The tooth is most susceptible to demineralization and white spot production during the period of lowered pH. The need for protection afforded by salivary buffers is highest after carbohydrate consumption.


The importance of saliva is clearly observed after salivary flow is reduced. Since saliva aids in mechanically removing food debris and bacteria from the oral cavity and teeth, a diminished saliva flow will adversely affect the oral tissues. Xerostomia has many etiologies, including simple mouth breathing, side effects of drug usage, hormonal fluctuations, autoimmune diseases, and neurological or psychogenic disorders. There are more than 400 drugs that will affect salivary flow and possibly cause xerostomia, including anticholinergics, antidepressants, antihistamines, antihypertensives, diuretics, and sedatives. Most drug-induced xerostomia is reversible.3 Patients may also exhibit compromised salivary gland function as a result of a neoplasm, trauma, and surgical intervention, or as a sequela of radiation therapy.2-4,6-9 The main immediate consequence of xerostomia is the dry, burning mouth, which will impact on the ability to swallow, taste food, speak, and maintain oral tissue integrity. Longer-term consequences are demineralization of enamel, an increased caries rate with rapid progression of the carious lesions, and an overgrowth of Candida.2-3

Saliva must be present in the oral cavity to preserve the integrity of both oral hard and soft tissues. Therefore, methods should be examined to increase salivary flow. Cholinergic agonists, such as pilocarpine (Salagen) and cevimeline (Evoxac), may be prescribed to stimulate salivary flow in postradiation patients and those with Sjogrens syndrome.3 Maintaining the salivary flow during normal waking hours is imperative. As there is a rapid decrease in pH after ingestion of sugar with a concomitant return to the basal flow rate of saliva when the stimulating signals have ceased, approaches to decrease or balance the detrimental effect of this decrease in pH should be considered. Stimulation of saliva by non-food products such as sugarless chewing gum can increase the salivary flow rate with no detrimental effects on the oral tissues.

Initially, chewing gums were produced from mastiche, a resin from the mastic tree, and were first used by the Greeks in 50 AD. The term masticate is a derivative of this Greek word. South American Mayans chewed chicle, while North American Indians chewed spruce resin. Paraffin and other waxes were also chewed but were not as popular as the resins. The first commercial spruce resin gum appeared in 1848. In 1869, dentist Dr. William F. Semple patented the first rubber-based chewing gum. Sugar was not added to gum until the 1880s. Sugarless gum was introduced in the 1950s by Dr. Bruno Petrulis1, a Naperville, Ill, dentist.

Masticatory stimulation such as gum chewing causes the salivary glands to produce more fluid. This stimulated saliva contains more ions, including neutralizing bicarbonate, calcium, and phosphorous, which are available to remineralize dental enamel. When a sweetness or flavor is added to chewing gum, there is a 10-fold increase in flow rate compared to stimulation by mastication alone. Even after 20 minutes of chewing, saliva output is elevated 3-fold.10

Several studies have concluded that chewing sugarless gum containing polyols such as sorbitol or xylitol will increase salivary flow.8,10-20 The production of stimulated saliva increases the presence of bicarbonate ions and thereby increases the buffering capacity of saliva, raising the pH after carbohydrate consumption. The 20-minute to 30-minute acidogenic challenge after carbohydrate ingestion can be counteracted by the increased volume of saliva, the increase in bicarbonate ion concentration, and the concomitant rise in pH. The increased availability of bicarbonate ions will decrease the harmful effects of organic acids on the hydroxyapatite crystals of enamel. The increase in fluid volume assists in oral clearance, thereby removing more of the challenge created by the ingestion of acidogenic food or drink.

Chewing gum for 20 minutes after consuming carbohydrates promotes remineralization by raising the pH and the amount of available calcium and phosphate ions in the saliva.6,8-18 The lower pH generated after carbohydrate consumption causes the hydroxyapatite crystals to dissolve, resulting in tooth demineralization. The demineralization/remineralization cycle needs to be in equilibrium; loss of mineral without replacement will lead to tooth damage. Stimulated salivary flow will enable more ions to be available in solution for remineralization.

A mechanical cleansing effect on the teeth adds to the anticaries effect of sugarless gum. Food is cleared from the oral cavity, and plaque is removed from the occlusal tooth surfaces. Although smooth surface plaque will not be affected, a reduction of as much as 44% of the accumulated plaque has been reported.20 The normal oral movements of chewing and swallowing will cleanse the buccal, occlusal, and lingual surfaces of the teeth, but the gingival margin may be unaffected.12 Therefore, in these areas there is a need for proper oral hygiene. As occlusal surfaces are the most susceptible to caries, oral debris clearance and plaque removal from these areas would be very beneficial.

Sugarless gum can also be used as a vehicle to deliver medicaments that may benefit oral and systemic health. Chewing gum products can be formulated to assist caries reduction by remineralization or neutralization of plaque acid. Other formulations can assist in tooth-whitening and breath-freshening. Chewing gums formulated with sodium fluoride, chlorhexidine, carbamide, bicarbonate, calcium phosphate lactate, calcium phosphate, and zinc compounds are on the market in the United States and overseas.10-12 Chewing gums formulated to deliver systemic medicaments such as nicotine, methadone, acetylsalicylic acid, miconazole, and vitamin C are also available.

Volatile sulfur-containing compounds are released from anaerobic bacteria associated with periodontal disease as well as metabolism of host cells and are the cause of halitosis.21 Cinnamic aldehyde from plant essential oils has been shown to kill these bacteria on a short-term basis; hence cinnamon flavor might be useful in eliminating halitosis.21 Nicotine-containing gums are currently available as part of smoking cessation programs. All these products will increase salivary stimulation while delivering specific active substances into the oral cavity, which then are available systemically.

 

CONCLUSIONS

Stimulation of saliva increases the level of bicarbonate ions in the oral cavity, which raises the pH to neutralize acids produced as a byproduct of the metabolism of fermentable carbohydrates. The concentration of calcium and phosphate ions available in supersaturated salivary fluid is increased, promoting tooth remineralization. Mastication allows for clearance of fermentable carbohydrates from the oral cavity. Chewing sugarless gum can provide all 3 of these oral health benefits. Under certain conditions, recommending chewing of sugarless gum after acidogenic exposures can promote oral health, producing an environment that favors tooth remineralization and facilitates clearance of fermentable carbohydrates.


References

1. Fascinating facts about the invention of chewing gum by Thomas Adams in 1845. The Great Idea Finder Web site. Available at: http://www.ideafinder.com/history/inventions/story056.htm. Accessed May 22, 2004.
2. A Symposium on the Endogenous Benefits of Saliva in Oral Health. March 21, 1989. LSU School of Dentistry, New Orleans, LA. Compend Suppl. 1989;(13):S448-S488.
3. Diaz-Arnold AM, Marek CA. The impact of saliva on patient care: a literature review. J Prosthet Dent. 2002;88:337-343.
4. Dowd FJ. Saliva and dental caries. Dent Clin North Am. 1999;43:579-597.
5. Edgar WM. A role for sugar free gum in oral health. J Clin Dent. 1999;10:89-93.
6. Lenander-Lumikari M, Loimaranta V. Saliva and dental caries. Adv Dent Res. Dec 2000;14:40-47.
7. Edgar WM. Saliva and dental health. Clinical implications of saliva: report of a consensus meeting. Br Dent J. Aug 11-25 1990;169:96-98.
8. Edgar WM. The clinical implications of salivary stimulation. Gen Dent Practitioner. Jul/Aug 1989:9-12.
9. Navazesh M, Denny P, Sobel S. Saliva: a fountain of opportunity. J Calif Dent Assoc. 2002;30:783-788.
10. Itthagarun A, Wei SH. Chewing gum and saliva in oral health. J Clin Dent. 1997;8(6):159-162.
11. Imfeld T. Chewing gum—facts and fiction: a review of gum-chewing and oral health. Crit Rev Oral Biol Med. 1999;10:405-419.
12. Simons D. Chewing gum: trick or treat? A review of the literature. Dent Update. 1996;23:162-169.
13. Koparal E, Ertugrul F, Sabah E. Effect of chewing gum on plaque acidogenicity. J Clin Pediatr Dent. 2000;24:129-132.
14. Creanor SL, Strang R, Gilmour WH, et al. The effect of chewing gum use on in situ enamel lesion remineralization. J Dent Res. 1992;71:1895-1900.
15. Leach SA, Lee GT, Edgar WM. Remineralization of artificial caries-like lesions in human enamel in situ by chewing sorbitol gum. J Dent Res. 1989;68:1064-1068.
16. Jensen ME. Effects of chewing sorbitol gum on human salivary and interproximal plaque pH. J Clin Dent. 1988;1:6-19.
17. Szoke J, Banoczy J, Proskin HM. Effect of after-meal sucrose-free gum-chewing on clinical caries. J Dent Res. 2001;80:1725-1729.
18. Dawes C, Macpherson LM. Effects of nine different chewing-gums and lozenges on salivary flow rate and pH. Caries Res. 1992;26:176-182.
19. Polland KE, Higgins F, Orchardson R. Salivary flow rate and pH during prolonged gum chewing in humans. J Oral Rehabil. 2003;30:861-865.
20. Hanham A, Addy M. The effect of chewing sugar-free gum on plaque regrowth at smooth and occlusal surfaces. J Clin Periodontol. 2001;28:255-257.
21. Zhu M, Carvalho RHR, Scher A, et al. Short-term germ-kill effect of chewing gum containing plant essential oils. Paper presented at: IADR/AADR 82nd General Session; March 10-13, 2004; Honolulu, Hawaii. Available at: http://iadr.confex.com/iadr/2004Hawaii/techprogram/abstract_45849.htm. Accessed July 15, 2004.



Dr. Doniger has been in private practice of family and preventive dentistry for almost 20 years. She is currently focusing on women's health and well-being issues. She can be contacted at (847) 677-1101 or This e-mail address is being protected from spambots. You need JavaScript enabled to view it .



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