259

Oral Health Effects of Combat Stress

Chapter 17

ORAL HEALTH EFFECTS OF COMBAT 

STRESS

GEORGIA dela CRUZ, DMD, MPH*; and PAUL COLTHIRST, DDS, MS†

INTRODUCTION

STRESS AND ORAL HABITS 

STRESS AND DENTAL HARD-TISSUE DISEASES

Dental Caries

Dental Erosion

Eating Disorders

Prevention

Treatment

STRESS AND PERIODONTAL DISEASES

Gingivitis

Periodontitis

Necrotizing Ulcerative Gingivitis

Prevention

Treatment

TEMPOROMANDIBULAR DYSFUNCTION

Prevention

Treatment

SUMMARY

*Lieutenant Colonel, Dental Corps, US Army; Office of The Surgeon General, US Army, 5109 Leesburg Pike, Suite 682, Falls Church, Virginia 22041 

† Major, Dental Corps, US Army; Dental Public Health, Department of Leadership Development, US Army Medical Department Center and School, 2250 

Stanley Road, Fort Sam Houston, Texas 78234-6100; formerly, Staff Officer, Dental Command Headquarters, Fort Sam Houston, Texas
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Combat and Operational Behavioral Health

The average American, if not prepared, will cope with distress by eating more junk food, drinking more alcohol, smoking 

more cigarettes, taking more over-the-counter drugs, or under-the-counter drugs. We are a society that copes with distress 

with some form of oral behavior.

—JO Prochaska, PhD, developer of the Trans-Theoretical Model of Behavior Change 

(interview available at: mms://mediastream.buffalo.edu/content/nur/Part1a.wmv, accessed July 13, 2010)

INTRODUCTION

Approximately 5% to 10% of disease and nonbattle 

injuries among service members result from oral diseases 

or injuries.1

 The rate of dental emergencies is higher for 

units whose soldiers deploy with poor oral health. Oral 

diseases can cause impaired duty performance, work loss, 

restricted activity, poor diet, difficulty pronouncing words, 

inability to sleep, and excruciating pain. If they are not 

prevented or treated early, oral diseases can cause severe, 

life-threatening illness and may even require medical 

evacuation from theater. One recent study of US Army 

soldiers (regular Army, reserve, and National Guard) 

medically evacuated from the Central Command area 

of responsibility during 2003 and 2004 found that oral 

disease accounted for 42% of oral-facial evacuations.2

STRESS AND ORAL HABITS

Many Americans have a low level of health literacy 

and perceive oral health as less important and separate 

from general health.3

 Advances in dental research since 

the 1950s have shown that nearly all oral disease is 

preventable, yet many people continue to have a fatalistic view that “dental problems” are inevitable, of 

mysterious origin, and can be ignored as long as they 

are not unaesthetic or painful. Many service members 

join the military with these erroneous beliefs about oral 

diseases, viewing oral hygiene as mainly cosmetic and 

unnecessary during field training or operations. 

The primary causes of oral diseases during deployment are bacterial or viral infections that are initiated 

or exacerbated by the effects of poor oral hygiene, poor 

diet, or substance use. Self-care and hygiene habits are 

often the first things to break down when a soldier is 

deployed to an austere environment or experiences 

overwhelming stress. Many of these soldiers also turn 

to harmful oral habits such as using tobacco or eating 

and drinking nutrient-poor beverages and foods that 

are high in simple carbohydrates. 

According to the 2006 Department of Defense 

Survey of Health-Related Behaviors in the Reserve 

Component,4

 nearly 45% of service members admitted 

to eating as a way to cope with stress. Women were 

significantly more likely than men to eat as a coping 

strategy (51.8% vs 42.5%), while more men than women reported using cigars or smokeless tobacco (11.4% 

vs 3.6%). Reserve-component men and women were 

similar in their use of cigarettes (19.4%) and alcohol 

(24.9%) for coping. Results of the 2008 Department of 

Defense Survey of Health-Related Behaviors Among 

Active Duty Military Personnel5

 shows that men were 

significantly more likely to smoke cigarettes (28.6%) 

or drink alcohol (34.5%) for coping than were women 

(21.0% and 25.2%, respectively). Comparisons between 

the services show that more service members in the 

Marine Corps (39.9%), the Army (35.6%), and the Navy 

(33.7%) have a drink to cope with stress than do service 

members in the Air Force (25.0%). The same pattern is 

seen for smoking, with 33.2% of Marine Corps, 30.8% 

of Army, 27.9% of Navy, and 18.8% of Air Force service 

members lighting up a cigarette to cope with stress. 

Women, on the other hand, are still significantly more 

likely to use eating as a coping mechanism (56.2%) 

than are men (45.7%). Service members in the Navy 

and Army are significantly more likely to use eating as 

a coping mechanism (49.6% and 48.2%, respectively) 

than those in the Air Force or Marine Corps (45.1% 

and 44.5%, respectively). The combination of poor oral 

hygiene with harmful oral habits such as tobacco use 

and increased intake of refined carbohydrates causes 

oral disease (Figure 17-1). 

Figure 17-1. Plaque accumulation, tobacco staining, gingival inflammation, and generalized caries resulting from a 

combination of inadequate oral hygiene, tobacco use, and 

refined carbohydrate intake.
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Oral Health Effects of Combat Stress

Changes in diet during deployment or other stressful situations can cause service members to suffer from 

dehydration and micronutrient deficiencies that can 

lead to skin conditions, stress fractures, anemia, and 

other conditions.6–11 Because the oral epithelium has a 

high rate of cellular turnover, these same deficiencies 

can affect oral health by preventing the oral epithelium 

from renewing or repairing itself. As a result, the first 

signs of micronutrient deficiency can appear in the 

mouth, and may present as glossitis, angular cheilitis, 

stomatitis, and gingivitis. Undernutrition can also exacerbate oral infections and has been associated with 

increased progression of periodontal disease.12 Vitamins A, C, D, E, B2

, B6, B12, niacin, and folic acid, and 

minerals such as zinc, iron, magnesium, and calcium 

are essential for repairing oral epithelium, maintaining 

periodontal attachment, preventing demineralization 

of bones and teeth, and ensuring an adequate amount 

of saliva of sufficient quality to protect the oral cavity. 

In addition to enabling taste, mastication, and digestion, saliva is critical for defense against oral diseases. 

Compromised saliva composition or flow impairs or 

eliminates its antifungal, antiviral, and antibacterial 

activities and prevents it from protecting the teeth 

from demineralization by acids from oral bacteria or 

foods and beverages. 

STRESS AND DENTAL HARD-TISSUE DISEASES

When eating is used as a coping mechanism for 

stress, it often involves the frequent consumption 

of foods containing organic acids and simple carbohydrates such as sugar and starch. Between-meal 

consumption of these foods or beverages (ie, sports 

drinks, energy drinks, or soda) promotes dental caries 

and dental erosion. 

Dental Caries

 The majority of dental emergencies during deployment have been for conditions resulting from dental 

caries.13–18 Exact incidence of new disease is unknown, 

but a pilot study19 of soldiers deployed in Operation 

Iraqi Freedom for 6 months during 2003 found that 

the number of carious lesions increased by 156%, and 

the severity of disease, as measured by the number 

of tooth surfaces involved, increased by 183% over 

predeployment statistics. 

Dental caries is caused when poor oral hygiene 

allows uncontrolled growth of bacteria in dental 

plaque on tooth surfaces (Figure 17-2). The bacteria 

rapidly metabolize the simple carbohydrates (starches 

or sugars) in the diet into destructive acids (lactic acid). 

Fermentable carbohydrate metabolism supports the 

colonization of more bacteria on the tooth surface, 

further increasing the amount of acid produced. Following exposure to fermentable carbohydrates, plaque 

pH falls below 5.5, the critical pH for maintaining the 

structural integrity of the mineralized dental tissue. 

It can take 30 to 40 minutes for the pH to rise again, 

depending on the flow rate and buffering capacity 

of the individual’s saliva. As a result, the amount of 

bacterial acid produced in any 24-hour period mirrors 

the frequency and duration of exposure to fermentable 

carbohydrates more closely than the total amount of 

carbohydrate consumed. 

Starches do not directly serve as substrate for oral 

bacterial fermentation. Starch granules in grains, vegetables, potatoes, and beans are damaged when they 

are subjected to heat and mechanical forces, producing 

a gelatinized starch. This starch is further broken down 

by salivary and bacterial amylases into sucrose, maltose, and maltotriose—substances that are available 

for bacterial acid production.20 As a result, untreated 

whole grains and raw vegetables have lower cariespromoting potential than heat-processed foods like 

white breads, crackers, chips, snacks, and dry cereal. 

Foods that contain sugar plus starch destroy dental 

enamel more rapidly than pure sugar foods because 

the starch acts like digestible glue, keeping the sugar in 

close contact with the tooth surface for longer periods 

of time. Teeth that have low levels of fluoride in the 

enamel are more vulnerable to these acids, and decay 

can begin and progress quite rapidly. Without regular 

exposure to fluoride, sugar consumption is a strong 

indicator of caries risk.21

Figure 17-2. Extensive accumulation of bacterial plaque after 

cessation of oral hygiene. Gingiva is inflamed and several 

carious lesions are evident. 

Photograph: Courtesy of Captain Andrew Marshall, US 

Army Dental Corps.
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Combat and Operational Behavioral Health

Dental Erosion

Dental erosion, or erosive tooth wear, is described 

as “the loss of dental hard tissue either through 

chemical etching and dissolution by acids of nonbacterial origin or by chelation.”22(p243) The prevalence of 

dental erosion is increasing, particularly in younger 

populations.23,24 Nonbacterial acids that cause erosion 

primarily come from two sources: gastric acids or diet. 

Caffeinated sodas, sports drinks, and energy drinks are 

commonly used in theater for hydration, to maintain 

alertness, or for simple enjoyment. These flavored 

beverages often contain polybasic organic acids such 

as citric acid, phosphoric acid, malic acid, and tartaric 

acid. Popular beverages that fall into this category 

include soft drinks, sports drinks, energy drinks, and 

sweetened, bottled tea blends. Other types of acidic 

drinks include apple or citrus fruit juice. Acidic foods 

include citrus, pineapple, and sour candies. Any of 

these acidic foods and beverages can accelerate the 

progression of dental caries. Organic acids accelerate 

the progression of decay by chemically eroding the 

dental enamel25 (Figure 17-3). Polybasic acids have a 

unique buffering capacity and can maintain an acidic 

pH even with marked dilution. This high titratable acid 

level multiplies the actual number of hydrogen ions 

available for interaction with the tooth surface, and 

is thought to be an important reason for their erosive 

properties. The chemical structure of polybasic organic 

acids also gives them the ability to chelate calcium at 

higher pHs, so they can erode dental enamel even in 

a neutral environment.26

Exposure to gastric acids is caused by either gastroesophageal reflux disease (GERD) or eating disorders that involve self-induced vomiting. Exposure to 

gastric acids is one of the most destructive processes 

that can affect the teeth. Stomach acids demineralize 

the outer layers of tooth enamel, leaving behind the 

protein matrix, which is then easily removed with 

brushing. GERD is the most common gastrointestinalrelated diagnosis given during office visits, and affects somewhere between 10% to 20% of the Western 

population.27 The disorder causes erosion of the lingual 

and occlusal surfaces of the teeth, affecting the posterior teeth most severely. In the early stages, affected 

teeth exhibit a smooth, glazed appearance. Damage 

generally progresses to the development of a “dished 

out” appearance and the exposure of the dentin layer 

(Figure 17-4). Over time the affected teeth can become 

weakened and may develop thermal sensitivity.28 Patients with GERD are usually prescribed proton pump 

inhibitors and must avoid eating certain foods, as well 

as sleeping within a few hours of eating, exercising, 

or bending over. Disruption of dietary or medication 

routines by high operations tempo or combat situations may cause recurrence of GERD symptoms and 

repeated exposure of the dentition to gastric acids. 

Figure 17-3. Generalized demineralization and loss of 

enamel on the facial surfaces of teeth just above the gingival 

margin in the absence of gingival inflammation is often an 

indication of frequent use of sugared beverages that contain 

organic acids.

Photograph: Courtesy of Captain Andrew Marshall, US 

Army Dental Corps.

Figure 17-4. Erosion of enamel and exposure of the dentin 

layer in a patient with gastroesophageal reflux disease. 

Photograph: Courtesy of Bennett T Amaechi, Associate Professor and Director of Cariology, University of Texas Health 

Science Center at San Antonio.
263

Oral Health Effects of Combat Stress

Eating Disorders

In most cases, dental hard-tissue damage is unlikely 

to signify anorexia or bulimia, except in those with 

an already established diagnosis who experience a 

recurrence under stress. Oral manifestations associated with eating disorders may include one or more 

of the following29:

	 • smooth erosion of the enamel or perimylolysis,

	 • traumatized oral mucosal membranes and

pharynx,

	 • variations in the periodontium,

	 • enlargement of the parotid or submandibular

salivary glands,

	 • xerostomia (dry mouth due to reduced salivary

flow), and

	 • dental caries.

When vomiting occurs repeatedly over time, 

tooth enamel becomes thin and eroded, resulting in a 

smooth, glassy appearance. In the case of eating disorders, these changes are most commonly seen on the 

lingual, occlusal, and incisal surfaces of the maxillary 

teeth. When confined to these areas, the condition is 

termed “perimylolysis” (Figures 17-5 and 17-6). These 

areas of the teeth are more susceptible to erosion due 

to the combined chemical and mechanical effects of 

regurgitated gastric acids and their retention on the 

surface of the tongue. Erosion is usually not clinically 

detectible until vomiting behavior has occurred for 

about 2 years. However, the daily frequency of selfinduced vomiting is one of the main determinants of 

the rate of progression and degree of dental erosion. 

As is the case with GERD, erosion may eventually affect the occlusal and facial surfaces of teeth, resulting 

in exposure of the underlying dentin and decreased 

vertical dimension (overclosure; Figure 17-7). 

Patients with eating disorders may also develop 

diet-caused dental erosion in other areas of the 

teeth. Several studies have reported that people with 

restrictive anorexia tend to favor highly acidic, lowFigure 17-5. Erosion of the lingual, occlusal, and incisal surfaces of the maxillary teeth in a patient with bulimia. 

Photograph: Courtesy of cosmetic dentist Dr Craig Mabrito, 

Houston, Texas.

Figure 17-6. Translucency of the maxillary central incisors 

due to erosion in a patient with bulimia.

Photograph: Courtesy of cosmetic dentist Dr Craig Mabrito, 

Houston, Texas.

Figure 17-7. Occlusal wear and dentin exposure due to erosion in a patient with bulimia. 

Photograph: Courtesy of cosmetic dentist Dr Craig Mabrito, 

Houston, Texas.
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Combat and Operational Behavioral Health

calorie foods, particularly raw citrus.29–31 If exposure 

is frequent, these foods tend to cause erosion on the 

buccal or facial surfaces of the tissue, in contrast to 

perimylolysis (Figure 17-8).

Stomach acids may irritate the gingival tissue if 

exposure is frequent, but controlled studies of gingival 

inflammation in patients with eating disorders have 

produced conflicting results.32,33 A more common cause 

of gingival inflammation in patients with eating disorders appears to be a lack of interest in oral hygiene, 

which can accompany depression. Also, alveolar bone 

support of the teeth may be compromised in some 

patients. Patients with severe disease experience early 

bone loss or osteoporosis as a result of changes in their 

estrogen and cortisol levels, and are probably at risk 

for accelerated alveolar bone loss.

Trauma to the oral mucous membranes or the 

oropharynx may also occur in patients who engage in 

binge eating or self-induced vomiting. The rapid ingestion of food associated with binge eating may cause 

trauma, as may the force of regurgitation. Objects used 

to induce vomiting may also injure the soft palate.

Salivary gland enlargement is seen in approximately 10% to 50% of patients who binge eat and purge 

by vomiting. The gland most frequently involved is 

the parotid gland, and swelling usually occurs 2 to 6 

days after bingeing/purging behavior. The enlargement often becomes persistent as the eating disorder 

progresses. The swelling may give a square, widened 

appearance to the mandible. However, the involved 

Figure 17-8. Erosion of the facial enamel and exposure of 

the underlying dentin. 

Photograph: Courtesy of Bennett T Amaechi, Associate 

Professor and Director of Cariology, Department of Community Dentistry, University of Texas Health Science Center 

at San Antonio.

gland is usually soft and painless upon palpation and 

has a patent duct, normal salivary flow, and an absence 

of inflammation, both clinically and histologically. 

Other histological characteristics include greater acinar 

size, increased secretory granules, fatty infiltration, 

and fibrosis. The exact cause of the enlargement is not 

known, but individuals who purge by methods other 

than vomiting do not experience salivary gland enlargement. Hypothesized reasons include autonomic 

stimulation of the glands by activation of the taste 

buds or cholinergic stimulation of the glands during 

vomiting.29

Antidepressants, which are frequently used to 

treat anorexia nervosa, usually cause xerostomia, 

and patients with xerostomia are more susceptible to 

developing carious lesions. Risk for dental caries may 

also be increased in patients whose bingeing episodes 

frequently involve high-calorie, high-carbohydrate 

foods. As a general rule, however, patients with eating disorders who primarily practice restriction or 

self-induced vomiting do not experience an increase 

in caries rates.29

Prevention

Nearly all dental caries is preventable with the use 

of good personal health habits (proper diet and nutrition, oral hygiene, and avoiding substance use). Daily 

oral hygiene is essential for the removal of harmful microorganisms and maintenance of oral health. Soldiers 

must be trained in proper field oral hygiene. Brushing 

after meals with fluoride toothpaste is the most effective caries prevention method. Soldiers who have been 

diagnosed with GERD should attempt to maintain or 

reestablish medication and dietary restrictions. 

To prevent tooth decay, soldiers must use combat 

stress control techniques to help cope with the stresses 

of deployment, rather than relying on harmful dietary 

habits. Techniques such as talking, exercise, quick relaxation, deep relaxation, and cognitive exercises can 

all be used to relieve combat stress without harming 

oral health.34,35

Use of gum or mints that contain xylitol as the first 

ingredient, three to five times a day, between meals 

or after snacks also prevents dental decay.36 Xylitol 

is a naturally occurring sweetener found in fruits, 

vegetables, and some other plants. It has about half 

the calories of sugar but is just as sweet. Xylitol prevents harmful bacteria from using starchy or sugary 

food particles to create acids that cause dental caries. 

It works synergistically with fluoride to prevent decay and promote remineralization of damaged tooth 

structure. Xylitol gum is distributed in theater dining facilities in the accessory pack of the MRE (meal, 
265

Oral Health Effects of Combat Stress

ready-to-eat). Chewing xylitol gum for about 5 minutes 

regularly after meals and snacks should help prevent 

decay. 

For both oral health and weight management, free 

sugar intake from foods and beverages should be less 

than 10% of energy intake (less than 41 g/day).37 On 

average, people who consume over 55 grams of sugar 

a day are at high risk for dental caries. The frequency 

of free sugar intake should be less than five times a 

day. Cariogenic foods and beverages can be combined 

with protective foods (cheese, tea, protein, high-fiber 

foods, etc) to prevent dental caries.38 Soldiers should be 

encouraged to drink fluoridated water for hydration 

between meals, and limit consumption of foods and 

drinks that contain harmful polybasic organic acids 

to mealtimes. Soldiers can also mitigate the effects of 

foods and beverages that have a high organic-acid or 

refined-carbohydrate content by rinsing their mouths 

with water after ingestion. 

Patients who experience xerostomia are at increased 

risk for dental caries, and should be advised to use artificial saliva preparations to lubricate the oral tissues, 

avoid cariogenic foods or drinks, and use sugarless or 

xylitol-containing candies or mints. Sucking on these 

items can stimulate increased salivary flow, which may 

buffer oral acids. Increased saliva flow also increases 

the concentration of calcium, phosphate, and hydroxyl 

ions, which may aid remineralization of early carious 

lesions. Xylitol may also be beneficial because of its 

bacteriostatic properties. 

Treatment

Patients should be referred to a dentist for treatment 

of dental caries. Soldiers who experience recurrence of 

GERD symptoms for any reason should be seen by a 

dentist as soon as possible. To prevent chemical damage to dental hard tissues by stomach acids, dentists 

may fabricate a thin plastic stent that covers the dentition. The stent is to be worn at night or at times when 

reflux symptoms are most likely to occur. Early referral 

of eating-disorder patients to a psychiatric therapist 

can reduce the risk of further damage to the teeth and 

the oral cavity. Patients should be referred to a dentist 

for an evaluation of dental erosion, salivary flow rate, 

and oral mucosa condition. Comprehensive dental 

procedures should not be performed until vomiting 

behavior is significantly improved or the patient has 

recovered completely; until then, proper home care is 

the best treatment.

All patients whose oral cavity is exposed to gastric 

acid should be counseled on several important principals of home care29,33: 

	 •	 Toothbrushing should never be performed

immediately after the mouth is exposed to 

stomach acid because demineralized enamel 

has been shown to be vulnerable to removal 

by abrasive forces.

	 •	 Following acid exposure, patients should

rinse with a buffering or alkaline solution 

to neutralize the acid and allow the saliva to 

remineralize the teeth, thereby reducing damage from demineralization. Options include 

0.5% sodium fluoride sodium bicarbonate in 

water, liquid antacids, slightly alkaline mineral water, or plain water. 

	 •	 If acid exposure happens repeatedly on a daily

basis, a neutral sodium fluoride mouth rinse 

or prescription fluoride gel may be necessary 

to prevent dental erosion. 

	 •	 Acidic foods and drinks should be avoided,

including citrus, pineapple, and lemon 

candies; apple or citrus fruit juice; alcohol 

(particularly white wine); and drinks that 

contain polybasic organic acids such as citric, 

phosphoric, malic, and tartaric.10,11

	 •	 Patients who experience xerostomia should

be advised to use artificial saliva preparations 

to lubricate the oral tissues, avoid cariogenic 

foods or drinks, and use sugarless or xylitolcontaining candies or mints. Sucking on these 

items can stimulate increased salivary flow, 

which may buffer oral acids. 

Stress and Periodontal Diseases

Gingivitis

Neglect of oral hygiene is common in stressful operational environments. Failure to properly remove 

plaque from the teeth and gums for a week or more 

usually results in the development of gingivitis in 

response to bacteria (Figure 17-9). The previously mentioned evaluation of soldiers deployed to Iraq showed 

that these service members experienced a significant 

worsening of their average periodontal screening and 

recording scores after 6 months of deployment.19 If left 

untreated, gingivitis associated with tenderness and 

bleeding gums may discourage soldiers from performing normal oral hygiene. 

Acute presentations of gingivitis can be managed by 

improved oral hygiene and the use of an antimicrobial 

mouth rinse. Soldiers with extreme gingival tenderness 

may be encouraged to reestablish oral hygiene proce-
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Combat and Operational Behavioral Health

Figure 17-9. A case of gingivitis.

Photograph: Courtesy of Colonel Dave Reeves, US Army 

Dental Corps, Consultant to The Surgeon General for Periodontology, and Chief, Periodontics, Fort Hood, Texas.

dures using viscous lidocaine on their toothbrushes 

rather than a dentifrice.

Periodontitis

Untreated gingivitis may progress to periodontal 

disease (Figure 17-10). The risk of periodontal disease 

has been studied for both men and women (Figure 17-

11), and several risk factors have been identified,39–42

such as gram-negative anaerobic bacteria, smoking, 

diabetes mellitus, a genetic tendency to produce increased levels of proinflammatory mediators, and use 

of hormone-mimicking medications. 

Periodontitis has been described as “a complex disease in which disease expression involves 

intricate interactions of the oral biofilm with the 

host immunoinflammatory response and subsequent alterations in bone and connective tissue 

homeostasis.”43(p1560) Classification of periodontal 

disease is based on two clinical factors: inflammation and loss of supporting tissue.44 Inflammation 

features typically seen are redness, edema, and 

bleeding on probing. Loss of supporting tissue 

is usually measured as increased probing depth, 

decreased attachment level, or alveolar bone loss. 

Even with the presence of periodontal pathogens, the 

pathogenesis of periodontitis cannot occur without 

immune and inflammatory responses, which are 

in turn shaped by both intrinsic (eg, genetics, age, 

systemic disease) and extrinsic (eg, toxins, tobacco, 

plaque) host factors45 (Figure 17-12). How much bone 

loss occurs depends largely on the level of inflammatory mediators present in gingival tissue. 

Alveolar bone destruction occurs after activation 

of the pathogenesis pathways and the penetration of 

inflammatory mediators deep into gingival tissue, near 

alveolar bone. Several proinflammatory cytokines are 

responsible for bone resorption, such as interleukin-1, 

-6, -11, and -17; tumor necrosis factor-α; leukemia 

inhibitory factor; and oncostatin M.45 When an inflammatory response occurs, periosteal osteoblasts 

are stimulated by proinflammatory cytokines and 

other mediators. Once the osteoblasts are stimulated, 

Figure 17-10. Gingival erythema, edema, and recession in 

conjunction with blunting of the interdental papilla are 

evident in this patient with periodontal disease. 

Photograph: Courtesy of Lieutenant Colonel Georgia dela 

Cruz, US Army Dental Corps, Falls Church, Va.

Female Male

Age Group

25–34 35–44 45–54 55–64 65–74 75+

40

35

30

25

20

15

10

5

0

Percentage of People With Disease Figure 17-11. Prevalence of periodontal disease. Males are 

more likely than females to have at least one tooth site with 

6 mm or more of periodontal loss of attachment.

Adapted from: US Department of Health and Human Services. The Surgeon General’s Report on Oral Health. Washington, 

DC: USDHHS; 2000: 65.
267

Oral Health Effects of Combat Stress

changes in the overall cell surface occur that increase 

the expression of a protein called “receptor activator 

of nuclear factor-κ B ligand (RANKL).”45 RANKL can 

be found on the surface of many other cells, including fibroblasts, T lymphocytes, and B lymphocytes. In 

the noninflammatory state, there is a balance between 

osteoclastic and osteoblastic processes determined by 

the proportion of RANKL. However, during an active 

inflammatory response, the proinflammatory mediators increase the expression of RANKL while at the 

same time decreasing other surface protein production 

in osteoclast precursor cells, triggering the formation 

of mature osteoclasts. Alveolar bone resorption by 

these osteoclasts leads to destruction of the supporting structures of the teeth, which, in the absence of 

intervention, leads to tooth loss.45

Women’s risk of developing gingival inflammation 

or periodontal problems may be increased by the 

higher levels of estrogen and progesterone associated 

with the menstrual cycle and use of oral contraceptives.46,47 Gingival tissues may become tender and 

swollen, and may bleed during brushing. Human 

gingiva has specific high-affinity estrogen receptors 

and can function as an estrogen target tissue. The 

stratified squamous epithelium of the oral mucosa 

Environmental and Acquired Risk Factors

(poor oral hygeniene, subgingival calculus, tobacco 

smoking)

Connective 

tissue and bone 

metabolism

Clinical signs of 

disease 

initiation and 

progression

Host Factors

Genetic risk factors, age, systemic disease

Antigens,

lipopolysaccharides, 

other virulence 

factors

Antibodies

PMNs

Cytokines

Prostanoids

Matrix 

metalloproteinases

Host immunoinflammatory 

response

Microbial 

challenge

(gram-negative 

anaerobic 

bacteria)

Figure 17-12. Model of periodontitis depicting the multifactorial nature of periodontal disease. A change in any one factor 

can result in clinical signs of the disease. 

PMN: polymorphonuclear leukocytes

Data sources: (1) Page RC, Kornman KS. The pathogenesis of human periodontitis: an introduction. Periodontology 2000. 

1997;14:9–11. (2) US Department of Health and Human Services. The Surgeon General’s Report on Oral Health. Washington, DC: 

DHHS; 2000. (3) Gluck G, Morganstein W. Jong’s Community Dental Health. 5th ed. St Louis, Mo: Mosby; 2003: 185–187.

and gingiva responds to ovarian hormone levels, with 

alterations in maturation and keratinization. Estrogen 

is involved in the regulation and maintenance of collagen synthesis and has been associated with gingival 

hyperplasia.

Estrogen and progesterone also promote changes 

in the microcirculatory system of the gingiva. The 

endothelial cells and pericytes of the venules swell, 

granulocytes and platelets adhere to the vessel walls, 

microthrombi form, and perivascular mast cells are 

disrupted.46 The microvasculature proliferates and 

becomes more permeable, causing gingival edema 

and increasing the flow of gingival crevicular fluid. 

The resulting fluid also contains elevated levels of 

sex hormones, polymorphonuclear leukocytes, and 

increased levels of prostaglandin E2. Anaerobic bacteria 

(eg, Bacteroides melaninogenicus, Prevotella intermedia, 

and Porphyromonas gingivalis) may be present and 

proliferate under these conditions.

The increase in bacteria production is a result of 

two factors: (1) some bacteria associated with gingival 

inflammation are able to metabolize steroid hormones 

and use them for energy production, thereby directly 

increasing their numbers; and (2) increased estrogen 

and progesterone levels also depress T-cell responses 
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Combat and Operational Behavioral Health

and decrease neutrophil chemotaxis and phagocytosis. 

This impaired immune response allows bacteria in the 

gingival crevice to proliferate without restraint.

Proliferating bacteria can cause increased levels of 

bacterial endotoxins, which can increase inflammation 

and trigger bone loss from the periodontium. Oral 

contraceptives, especially those containing progesterone, have been associated with an increased risk of 

periodontal bone loss.47,48 No studies have been done 

on Depo-Provera (medroxyprogesterone acetate [the 

Upjohn Company, Kalamazoo, Mich]) and periodontal 

bone loss.

Necrotizing Ulcerative Gingivitis

When soldiers are placed under severe stress, increased cortisol levels can compromise immune function. Under these conditions, gingivitis can progress 

to acute necrotizing ulcerative gingivitis, an extremely 

painful inflammation accompanied by necrosis of the 

interdental gingiva and a fetid odor (Figure 17-13).

Prevention

Noncommissioned officers should ensure that the oral 

hygiene routine of all troops includes the following:

	 •	 toothbrushing, once daily at a minimum, preferably twice daily, with fluoride toothpaste to 

prevent dental caries and gingival problems;

	 •	 flossing daily, which is also effective in preventing gingival or periodontal problems; 

and

	 •	 rinsing several times a week with an antimicrobial mouthwash containing thymol 

or chlorhexidine gluconate (for those with 

chronic periodontal conditions).

Treatment

Acute presentations of necrotizing periodontitis 

should be referred to a dental professional. In addition 

to reestablishing oral hygiene procedures with viscous 

lidocaine hydrochloride and an antimicrobial mouthwash, acute periodontal disease usually requires the 

removal of plaque-retentive factors, such as calculus 

or defective restorations, from the crown and root 

surfaces of the teeth. 

Stress can produce temporomandibular dysfunction 

(TMD) symptoms when it causes patients to clench 

or brux their teeth more frequently, either at night or 

during the day. Masticatory muscle spasms and pain 

may result. Other known causes of TMD symptoms 

include injury to the temporomandibular joint from 

blunt force to the face, arthritis, joint overload, or 

repetitive loading (usually because of bruxism or 

grinding of the teeth). 

Although the overall incidence of the condition is 

low, TMD affects both men and women. According 

to a 1994 triservice recruit comprehensive oral health 

survey,49 approximately 3.5% of female recruits were 

found to have some type of orofacial pain or limited 

mandibular movement sufficient to require referral 

or treatment for TMD. The incidence for women was 

significantly higher than that for men (1.5%). Civilian 

studies50,51 have consistently shown an increased incidence of TMD (1.5- to 2-fold higher) in women compared with men, and most patients treated for TMD

are women (80%). Age plays a strong role in women. 

Symptoms begin after puberty and peak during the 

reproductive years, with prevalence highest among 

women aged 20 to 40. Gender and age distributions of 

TMD expression strongly suggest a link to the female 

hormonal system. Some studies51–53 have shown that 

women who use oral contraceptives may be at increased risk compared with women who do not. TMD

pain levels increase during menstruation.54,55 Current 

studies investigating the relationship of increased risk 

with the presence of estrogen receptors in the temporomandibular joint structures (particularly the synovial 

Figure 17-13. Gingival edema, erythema, and cratering of the 

interdental papilla and purulent exudate are visible in this 

patient with acute necrotizing ulcerative gingivitis. 

Photograph: Courtesy of Dr Carl Allen, Professor and Director, Oral and Maxillofacial Pathology, Ohio State University 

College of Dentistry.

Temporomandibular Dysfunction
269

Oral Health Effects of Combat Stress

lining cells, the articular disc, and the chondrocytes) 

have produced contradictory results.56,57

Prevention

TMD can be prevented by avoiding opening the 

mouth too wide during eating or yawning, and avoiding frequent, prolonged masticatory activity associated 

with pervasive oral habits such as jaw clenching, gum 

chewing, cheekbiting, or nailbiting.

Treatment

Acute open lock (an internal joint derangement 

that prevents closing the mouth) can cause extreme 

pain and should be immediately referred to a dental 

provider for reduction of the dislocation. If the provider is unable to reduce the dislocation due to severe 

muscle spasm or extreme pain, then the patient must 

be referred to an oral and maxillofacial surgeon for 

sedation prior to reduction of the dislocation. An acute 

closed lock (where the mouth is prevented from opening) warrants an immediate referral for evaluation by 

an oral and maxillofacial surgeon or an orofacial pain 

specialist because early intervention beyond conservative therapy (such as arthrocentesis) may be necessary. 

For all other cases, conservative therapy for an acute 

condition should focus on reducing joint loading and 

inflammation. Attempts should be made to relax the 

muscles as much as possible. The patient should use 

ice or cold packs for the first 24 to 48 hours, adhere 

to a soft diet, and avoid gum chewing. After the first 

24 to 48 hours, the patient should apply moist heat 

several times a day. Gentle stretching exercises of the 

mastication muscles should be performed after heat 

application. The patient should continue to avoid gum 

chewing and adhere to a soft diet for several days to 

limit masticatory activity. 

Pharmacological interventions should begin as 

soon as possible with analgesics, preferably nonsteroidal antiinflammatory analgesics. Patients with 

more severe TMD may also require short-term use of 

skeletal muscle relaxants. Because low-dose tricyclics 

improve sleep, they may be effective in decreasing 

pain from nocturnal bruxism. If symptoms recur, the 

patient should initiate moist heat application, stretching therapy, and use of nonsteroidal antiinflammatory 

drugs. Normally, this treatment prevents the development of more severe problems. 

Ideally, TMD patients should be referred to a dentist 

for a comprehensive evaluation of contributing factors 

from diet, occlusion, oral habits, and stress. However, 

because no national standards exist for TMD curricula 

at the predoctoral level, finding a knowledgeable practitioner may be difficult.58 Initial evaluation for acute 

TMD pain from trauma must rule out fractures, tears, 

and articular disc displacement. Examination of the occlusion and oral habits may show whether the patient 

would benefit from wearing an appliance (eg, a bite 

plate) every night to prevent or minimize the effects 

of jaw movements during sleep. 

If symptoms do not resolve, patients should be 

referred to an orofacial pain specialist, who can 

determine if the patient would also benefit from 

cognitive-behavioral skills training and biofeedback 

(eg, relaxation techniques) to decrease muscle jaw tension, decrease stress, increase awareness, and prevent 

diurnal tooth grinding or clenching incidents. Studies 

have shown that early intervention using a biopsychosocial approach is effective in reducing TMD pain and 

decreasing the progression of the disorder to chronic 

stages, as well as decreasing depression, increasing 

positive coping behaviors, and significantly reducing 

TMD-related healthcare costs.59,60

REFERENCES

1. Darakjy S, Marin RE, Knapik JJ, Jones BH. Injuries and illnesses among armor brigade soldiers during operational 

training. Mil Med. 2006;171(11):1051–1056.

2. Mitchener TA, Hauret KG, Hoedebecke EL, Darakjy S, Jones BH. Air medical evacuations of soldiers due to oral-facial 

disease and injuries, Operations Enduring Freedom/Iraqi Freedom. Mil Med. 2008;173(5):465–473.

SUMMARY

The stress of deployment can cause serious oral 

health problems. Soldiers should be trained in stressreducing techniques to avoid these problems (as 

well as the many other negative effects of combat 

stress). However, once problems occur, they should 

be treated with self-care techniques; more serious 

conditions necessitate attention from oral care practitioners.
270

Combat and Operational Behavioral Health

3. US Department of Health and Human Services. National Call to Action to Promote Oral Health. Rockville, Md: USDHHS, 

Public Health Service, National Institutes of Health, National Institute of Dental and Craniofacial Research; 2003. NIH 

Publication 03-5303.

4. Hourani LL, Bray RM, Marsden ME, et al. 2006 Department of Defense Survey of Health Related Behaviors in the Reserve 

Component. Research Triangle Park, NC: RTI International; 2007.

5. Bray RM, Hourani LL, Rae-Olmsted KL, et al. 2008 Department of Defense Survey of Health Related Behaviors Among Active Duty Military Personnel. Research Triangle Park, NC: RTI International; 2009.

6. McClung JP, Marchitelli LJ, Friedl KE, Young AJ. Prevalence of iron deficiency and iron deficiency anemia among 

three populations of female military personnel in the US Army. J Am Coll Nutr. 2006;25(1):64–69.

7. McClung JP, Scrimgeour AG. Zinc: an essential trace element with potential benefits to soldiers. Mil Med.

2005;170(12):1048–1052. Review.

8. Halliday AW, Vukelja SJ. Neurologic manifestations of vitamin B-12 deficiency in a military hospital. Mil Med.

1991;156(4):201–204.

9. Friedl KE, Evans RK, Moran DS. Stress fracture and military medical readiness: bridging basic and applied research. 

Med Sci Sports Exerc. 2008;40(11 suppl):S609–S622.

10. Lappe J, Cullen D, Haynatzki G, Recker R, Ahlf R, Thompson K. Calcium and vitamin D supplementation decreases 

incidence of stress fractures in female navy recruits. J Bone Miner Res. 2008;23(5):741–749.

11. Scrimgeour AG, Lukaski HC. Zinc and diarrheal disease: current status and future perspectives. Curr Opin Clin Nutr 

Metab Care. 2008;11(6):711–717. Review.

12. Moynihan PJ. The role of diet and nutrition in the etiology and prevention of oral diseases. Bull World Health Organ. 

2005;83:694–699.

13. Dunn WJ, Langsten RE, Flores S, Fandell JE. Dental emergency rates at two expeditionary medical support facilities 

supporting Operations Enduring and Iraqi Freedom. Mil Med. 2004;169(7):510–514.

14. Simecek JW. Estimation of nonpreventable dental emergencies in US Marine Corps personnel. Mil Med. 2008;173(11):

1104–1107.

15. Deutsch WM, Simecek JW. Dental emergencies among Marines ashore in Operations Desert Shield/Storm. Mil Med. 

1996;161(10):620–623.

16. Moss DL. Dental emergencies during SFOR 8 in Bosnia. Mil Med. 2002;167(11):904–906.

17. Mahoney GD, Coombs M. A literature review of dental casualty rates. Mil Med. 2000;165(10):751–756.

18. Teweles RB, King JE. Impact of troop dental health on combat readiness. Mil Med. 1987;152(5):233–235.

19. dela Cruz G. US Army Center for Health Promotion and Preventive Medicine. Unpublished study on degradation of 

oral health of soldiers deployed to Iraq, March 2004. 

20. Mobley CC. Nutrition and dental caries. Dent Clin North Am. 2003;47(2):319–336. Review.

21. Burt BA, Satishchandra P. Sugar consumption and caries risk: a systematic review. J Dent Educ. 2001;65(10):1017–

1023.

22. Amaechi BT, Higham SM. Dental erosion: possible approaches to prevention and control. J Dent. 2005;33(3):243–252.

23. Lussi A, Hellwig E, Zero D, Jaeggi T. Erosive tooth wear: diagnosis, risk factors and prevention. Am J Dent. 2006;19(6):

319–325.
271

Oral Health Effects of Combat Stress

24. Young A, Amaechi BT, Dugmore C, et al. Current erosion indices—flawed or valid? Summary. Clin Oral Invest. 2008;12 

(suppl 1):S59–S63.

25. von Fraunhofer JA, Rogers MM. Effects of sports drinks and other beverages on dental enamel. Gen Dent. 2005;53(1):28–

31.

26. von Fraunhofer JA, Rogers MM. Dissolution of dental enamel in soft drinks. Gen Dent. 2004;52(4):308–312.

27. Sharma P, Wani S, Romero Y, Johnson D, Hamilton F. Racial and geographic issues in gastroesophageal reflux disease. 

Am J Gastroenterol. 2008;103(11):2669–2680.

28. Huber MA. Gastrointestinal illnesses and their effects on the oral cavity. Oral Maxillofacial Surg Clin N Am. 2008;20:625–

634.

29. Studen-Pavlovich D, Elliott MA. Eating disorders in women’s oral health. Dent Clin North Am. 2001;45(3):491–511.

30. Hurst PS, Lacey LH, Crisp AH. Teeth, vomiting and diet: a study of the dental characteristics of seventeen anorexia 

nervosa patients. Postgrad Med J. 1977;53(620):298–305.

31. Brown S, Bonifazi DZ. An overview of anorexia and bulimia nervosa, and the impact of eating disorders on the oral 

cavity. Compendium. 1993;14(12):1594, 1596–1602, 1604–1608; quiz 1608. Literature review. 

32. Montecchi PP, Custureri V, Polimeni A, et al. Oral manifestations in a group of young patients with anorexia nervosa. 

Eat Weight Disord. 2003;8(2):164–167. 

33. Sundaram G, Bartlett D. Preventative measures for bulimic patients with dental erosion. Eur J Prosthodont Restor Dent. 

2001;9(1):25–29. 

34. US Department of the Army. Combat Stress. Washington, DC: DA; 2009. Field Manual 6-22.5.

35. US Army Center for Health Promotion and Preventive Medicine. Guide to Coping With Combat and Deployment Stress. 

Aberdeen Proving Ground, Md: USACHPPM; 2008. TG 320.

36. Ly KA, Milgrom P, Rothen M. Xylitol, sweeteners, and dental caries. Pediatr Dent. 2006;28(2):154–163.

37. Sheiham A. Dietary effects on dental diseases. Public Health Nutr. 2001;4(2B):569–591. Review. 

38. Moynihan P. Foods and dietary factors that prevent dental caries. Quintessence Int. 2007;38(4):320–324.

39. Page RC, Kornman KS. The pathogenesis of human periodontitis: an introduction. Periodontol 2000. 1997;14:9–11.

40. US Department of Health and Human Services. Oral Health in America: A Report of the Surgeon General. Washington, 

DC: USDHHS, National Institute of Dental and Craniofacial Research, National Institutes of Health; 2000: 39–42.

41. US Department of Health and Human Services. Healthy People 2010: Understanding and Improving Health. 2nd ed. 

Washington, DC: US Government Printing Office; November 2000: 41.

42. Gluck GM, Morganstein WM, eds. Jong’s Community Dental Health. 5th ed. St Louis, Mo: Mosby; 2003: 185–187.

43. Kornman KS. Mapping the pathogenesis of periodontitis: a new look. J Periodontol. 2008;79(8):1560–1568.

44. Offenbacher S, Barros SP, Beck JD. Rethinking periodontal inflammation. J Periodontol. 2008;79:1577–1584.

45. Cochrane DL. Inflammation and bone loss in periodontal disease. J Periodontol. 2008;79:1569–1576.

46. Krejci CB, Bissada NF. Women’s health issues and their relationship to periodontitis. J Am Dent Assoc. 2002;133:323–

329.
272

Combat and Operational Behavioral Health

47. Knight GM, Wade AB. The effects of hormonal contraceptives on the human periodontium. J Periodont Res. 1974;9:18–

22.

48. Tilakaratne A, Soory M, Ronasinghe AW, Corea SM, Ekanayake SL, de Silva M. Effects of hormonal contraceptives on 

the periodontium, in a population of rural Sri-Lankan women. J Clin Periodontol. 2000;27:753–757.

49. Tri-Service Comprehensive Oral Health Survey Working Group. 1994 Tri-Service Comprehensive Oral Health Survey—

Active-Duty Report. Washington, DC: Department of Defense, Office of the Assistant Secretary of Defense for Health 

Affairs; June 1995. Naval Dental Research Institute. PR 9503. 

50. Dworkin SF, Huggins KH, LeResche L, et al. Epidemiology of signs and symptoms in temporomandibular disorders: 

clinical signs in cases and controls. J Am Dent Assoc. 1990;120:273–281. 

51. Warren MP, Fried JL. Temporomandibular disorders and hormones in women. Cells Tissues Organs. 2001;169:187–

192. 

52. Bragdon EE, Light KC, Costello NL, et al. Group differences in pain modulation: pain-free women compared to painfree men and women with TMD. Pain. 2002;96:227–237. 

53. Nekora-Azak A. Temporomandibular disorders in relation to female reproductive hormones: a literature review. J 

Prosthet Dent. 2004;91:491–493. 

54. LeResche L, Mancl L, Sherman JJ, Gandara B, Dworkin SF. Changes in temporomandibular pain and other symptoms 

across the menstrual cycle. Pain. 2003;106:253–261. 

55. Isslee H, De Laat A, De Mot B, Lysens R. Pressure-pain threshold variation in temporomandibular disorder myalgia 

over the course of the menstrual cycle. J Orofac Pain. 2002;16:105–117. 

56. Campbell JH, Courey MS, Bourne P, Odziemiec C. Estrogen receptor analysis of human temporomandibular disc. J 

Oral Maxillofac Surg. 1993;51:1101–1105. 

57. Abubaker AO, Raslan WF, Sotereanos GC. Estrogen and progesterone receptors in temporomandibular joint discs of 

symptomatic and asymptomatic persons: a preliminary study. J Oral Maxillofac Surg. 1993;51:1096–1100.

58. Klasser GD, Greene CS. Predoctoral teaching of temporomandibular disorders: a survey of US and Canadian dental 

schools. J Am Dent Assoc. 2007;138:231–237.

59. Gatchel RJ, Stowell AW, Wildenstein L, Riggs R, Ellis E 3rd. Efficacy of an early intervention for patients with acute 

temporomandibular disorder-related pain: a one-year outcome study. J Am Dent Assoc. 2006;137(3):339–347.

60. Stowell AW, Gatchel RJ, Wildenstein L. Cost-effectiveness of treatments for temporomandibular disorders: biopsychosocial intervention versus treatment as usual. J Am Dent Assoc. 2007;138:202–208.