The Impact of Oral Health on Systemic Conditions

Kristin Hofer, RDH, MSDH; Marija Cahoon, RDH, MS; Stefania Moglia Willis, DMH, RDH; and Ivianie Exinor, RDH, MPH

June 2016 Course - Expires June 30th, 2019

American Dental Hygienists' Association


The oral-systemic link has been well established through evidence-based research. The oral environment is both a likely source of pathogens responsible for some diseases, as well as acting as an early indicator for others as manifestations of other conditions first show up in the oral cavity. As first-line oral healthcare providers, dental hygienists should be versed in the common systemic diseases, such as cardiovascular disease and diabetes, in order to help identify their patients who may be at risk for these conditions, but they should also be aware of some less common diseases that patients may present with that hygienists may need to take specific diagnostic steps and precautions when treating.

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By Kristin Hofer, RDH, MSDH

Significant effort has been made to retain our teeth for as long as possible. We are well aware of the negative implications associated with tooth loss. But what if the teeth that we have been successful retaining become periodontally involved? The consequences can present systemic health risks for the elderly. Much of this population is medically compromised and/or resides in nursing homes where their oral hygiene is inadequate and they lack access to dental care.1

Aspiration pneumonia is an infection that causes inflammation in the lungs or bronchial tubes after regurgitated gastric contents or oropharyngeal secretions make their way through the respiratory tract.2 It is a prominent cause of mortality among individuals aged 60 years and older in both independent homes and institutional facilities, accounting for nearly 15,000 deaths annually.3 Aspiration pneumonia is common in older adults who are medically at risk. This compromised population may have decreased lung function; recent gastrointestinal procedures such as nasogastric tube placement; complex dental procedures; gastroesophageal reflux disease; diabetes; poor immune response; and neurologic issues such as multiple sclerosis, Parkinson’s disease, and dementia.4

The oral environment has been identified as a likely source of the pathogens responsible for aspiration pneumonia, which research has also linked to poor oral hygiene, dental decay, periodontal disease, and dysphagia. Of these risk factors, poor oral hygiene and dysphagia have been identified as having the most significant link to aspiration pneumonia.4 An individual with dysphagia has difficulty swallowing, or the swallow may be followed by nasal regurgitation, coughing, or choking, possibly due to significant delay and longer oral bolus transport time.1 The swallowing reflex also weakens during sleep, which allows the aspiration of toxic saliva into the lungs. Due to an elderly person’s weakened immune system, bacteria in the saliva then enter the bronchi and lungs, proliferating and strengthening enough to cause pneumonia.

The microorganisms responsible for aspiration pneumonia include Streptococcus pneumoniae, Haemophilus influenza, Staphylococcus aureus, and other gram-negative bacteria. While aspiration of these microbes may go unnoticed at first, their pernicious nature will often result in pneumonia.5 In the presence of poor oral hygiene, the growth of the deleterious bacteria and candida multiplies to an extent that allows for increased oropharyngeal colonization of pathogens, making the host much more susceptible.1 Signs and symptoms are often similar to pneumonia and include difficult or shallow breathing, fever, weight loss, frequent throat clearing, and a productive cough with foul smelling and/or tasting sputum.5 For patients who present with the signs and symptoms of aspiration pneumonia, a chest radiograph is taken to assess infiltrate in the lung. However, for a more specific and detailed image of the lung, a contrast-enhanced computed tomography scan is used.

Upon diagnosis, patients with known gastric aspiration are treated with supplemental oxygen, use of a mechanical ventilator, and antibiotics. These patients should also be tested for any underlying swallowing disorder to help prevent future aspiration. If the condition is serious enough, some patients may need to be hospitalized.6 The Infectious Diseases Society of America guidelines recommend clindamycin or a carbapenem antibiotic for a duration of 1 to 2 weeks.5 Carbapenem antibiotics are a beta-lactam class of antibiotics that are used to treat multidrug-resistant bacteria.

So then, what can be done to prevent aspiration pneumonia from recurring in the elderly, at-risk, population? Patients with dysphagia may be taught how to swallow using techniques such as a chin-tuck strategy or adopting a diet with food textures less likely to be aspirated. For those with a severe form of dysphagia, a percutaneous gastrostomy tube can be used. Additionally, understanding the importance of proper oral health and implementing regularly scheduled dental care will help to prevent the recurrence of aspiration pneumonia.

In conclusion, anyone responsible for the care of an at-risk elderly person must ensure that every effort is made to safeguard their oral health, including biannual or quarterly dental visits, as well as assistance with daily flossing and toothbrushing.

About the Author

Kristin Hofer, RDH, MSDH, is a clinical instructor of dental hygiene at the New York University College of Dentistry.



By Marija Cahoon, RDH, MS

Crohn’s disease (CD) is an immune-mediated inflammatory disorder of the gastrointestinal tract; CD and ulcerative colitis comprise the two major subsets of inflammatory bowel disease.1,2 As the second most common inflammatory bowel disease, CD has an estimated incidence rate of one to four persons per 100,000 in North America, primarily affecting whites and females in early adulthood.1 The granulomatous inflammation of CD may affect any site along the gastrointestinal tract from the mouth to the anus, with oral lesions often preceding any symptoms of intestinal disease.1 Oral manifestations of CD are referred to as oral CD or orofacial CD, and they often serve as early indicators of the condition;1,2 for this reason, the dental hygienist and dental team play a key role in identifying, detecting, and referring patients who may otherwise be asymptomatic.2

With no cure, CD manifests as periods of disease activity followed by asymptomatic intervals of remission.3 While the etiology of CD is not fully known, accepted theories suggest defects in mucosal immunity and intestinal epithelial barrier function in a genetically susceptible individual, causing an inappropriate inflammatory response to intestinal microbes.2 Common symptoms for patients presenting with CD include abdominal pain adjacent to the navel, diarrhea, recalcitrant fevers, malaise, anorexia, and fatigue.2 While some research hypothesizes environmental risk factors, the most current independent risk factor for CD is a positive family history of the disease.2 Management of CD depends on disease location and activity, with medications such as anti-inflammatory agents and steroids, immunosuppressants such as thiopurines and methotrexate, and biologic agents such as infliximab for treatment.2 Patients suffering from severe intestinal manifestations of the disease may require resective surgery.3

The prevalence rate of oral cavity involvement for adults with CD ranges from 20% to 50%.4 Oral manifestations may be associated with the disease itself, with nutritional deficiencies due to lack of absorption or with complications from current medications and therapies.4 Oral CD may precede or predict future intestinal disease and, while affecting all ages, tends to be more common in children.4 Oral CD may present as mucosal cobblestoning, mucosal tags, deep linear ulcerations, gingival hyperplasia, lip fissuring, aphthous ulcers, and angular cheilitis.5 Upon histopathological examination, the typical linear fissures and ulcerations from the oral cavity appear the same as intestinal CD.4 Persistent, firm, painless, diffuse swelling of lips, buccal mucosa, and facial soft tissues also appear as symptoms of oral CD.1 Lips are the most frequent site of oral CD followed by the buccal mucosa, gingiva, and vestibular and retromolar areas.5 Often these symptoms present as nonspecific, especially in children; therefore, thorough and frequent intra- and extraoral examination of recurring lesions by the dental hygienist and dental team plays a critical role in proper referral for timely diagnosis and treatment.4

Patients with CD present many challenges for the dental hygienist, ranging from pain management of oral lesions and caries risk assessment to nutritional counseling. Patients with recurring oral manifestations of CD may suffer from pain, persistent swelling, and sometimes cosmetic disfigurement, making daily functions such as eating, drinking, and oral hygiene routines difficult to perform.2,4 Topical corticosteroids, such as beclomethasone rinses, or intralesional injections have been reported for use, but bring only short-term relief and carry the risk of systemic steroid absorption.1 Recent studies indicate established risk factors for dental caries in patients suffering from CD due to decreased salivary flow, insufficient oral hygiene, and poor dietary habits, as well as increased lactobacilli and Streptococcus mutans present in the oral cavity.4 These studies also identify higher plaque scores and decayed, missing, and filled surface scores in patients with CD, especially patients with a history of resective surgery.3 A high rate of sugar consumption has been observed in patients with CD, especially higher consumption of sugary drinks.4 Nutritional malabsorption, such as zinc deficiency, which alters sweet taste perceptions, may relate to high sugar consumption in patients with CD.3 For the dental hygienist, frequent review of oral hygiene routines and nutritional assessment with a patient with CD allows for more thorough management of the dental hygiene process of care and assessment of risk factors relating to oral health.

Due to the range and severity of oral manifestations associated with CD, patients with an existing diagnosis of CD require frequent evaluation from the dental professional, as well as thorough discussion of the patient’s history and management of the disease. For patients with recurring oral lesions or orofacial symptoms with an otherwise noncontributory medical history, the dental professional plays an investigatory role in identifying family history as a risk factor for any underlying systemic relationship. The management of a patient with CD requires a multidisciplinary approach, with the dental hygienist at the forefront in identifying early indicators of disease and active secondary manifestations of the disease as well as providing essential patient education for optimal long-term oral health.

About the Author

Marija L. Cahoon, RDH, MS, is a clinical instructor of dental hygiene at the New York University College of Dentistry. She also works in private practice as a clinician.



By Stefania Moglia Willis, DMH, RDH

Research has identified between 80 and 100 types of autoimmune diseases, and the National Institutes of Health estimates that 5% to 8% of the US population is affected,1 while another 10% to 20% has early-stage autoimmune symptoms and imbalances.2 About 80% of these cases occur in women, most notably during their childbearing years.3

It is hypothesized that the primary pathogenic elements involved in the development of autoimmune disease are innate genetic predisposition and environmental factors or triggers. A review of the literature implicates microbial agents, trauma, and toxic substances as triggers of the immune response that precede the manifestation of autoimmune diseases.4-7 Also, inflammatory processes may enhance the possibility of autoimmune disease developing in individuals with a genetic susceptibility. It is well established that having one autoimmune disease increases the risk for developing another, and certain autoimmune diseases overlap — such as celiac disease, inflammatory bowel disease, and Addison’s disease — resulting in a need for polypharmacy and creating multiple concerns in patient treatment.

Most of the drugs used in the treatment of autoimmune diseases are anti-inflammatory medications and immunosuppressive drugs. These medications reduce pain and improve function but come with side effects such as susceptibility to opportunistic infections, adrenal insufficiency, mouth sores, nausea, vomiting, and decreased appetite. Additionally, the medications have adverse interactions with vitamins, lipids, and minerals that play a significant role in a patient’s ability to respond to inflammatory insult as well as to maintain health and well-being.

Pathogenesis of Autoimmune Diseases

Autoimmune disease is a type of immune dysregulation whereby what should be a beautifully orchestrated response against a pathogen becomes a disease process involving the self. Autoimmune disease occurs when specific immune responses (activated self-reactive T-cells and antibodies) are directed against the body, leading to chronic inflammation and injury to cells, tissues, organs, and blood vessels. Autoimmunity reactions are common to all people. Self-reactive immune cells that are normally eliminated in the bone marrow or thymus sometimes escape into the circulation. The body has several protective programs in place to limit autoimmune responses against its organs, tissues, and cells and to minimize harm. In a healthy immune system, the body knows the difference between a foreign infiltrant and itself, or it can regulate the intensity of the body’s response. The body’s ability to avoid aggressive maneuvers by the immune system against itself is called “tolerance.” Regulatory T-cells (Tregs) help to prevent immune responses against the self by monitoring and inhibiting the activity of other T-cells.8

Autoimmune diseases—like antibodies—are not limited to one body part but cross over, often impacting multiple body systems. As a result, comorbidity among several autoimmune diseases often occurs in genetically susceptible individuals, targeting many areas of the body and presenting challenges to general and oral healthcare. Because autoimmune disease impacts so many aspects of the body, patients suffering from these diseases are often diagnosed and managed by multiple providers, including those in oral healthcare.

Types of Autoimmune Diseases with Oral Manifestations

Many autoimmune diseases impact oral tissues and patients’ ability to manage their oral health. In Sjögren’s syndrome, the body attacks and damages the secretory glands—involved with the production of tears and saliva—putting patients at risk for dental caries. Crohn’s disease results in the impaired absorption of nutrients leading to pallor, angular cheilitis, and glossitis.9 Scleroderma affects the connective tissues, resulting in a painful tightening of the skin, dryness of the mouth, and an inability to move the fingers and hands easily.10 An autoimmune disease that affects 50% of adults over the age of 65 and similarly impacts movement and ability to perform home care is rheumatoid arthritis (RA).11 A group of autoimmune diseases with oral mucosal involvement resulting in blistering, erosions, and ulcers are lichen planus, pemphigus vulgaris, pemphigoid, erythema multiforme, systemic lupus erythematosus (SLE), and linear IgA disease. Another type is Behçet’s disease (BD) known as “the triple syndrome complex” because of its multiple organ involvements. BD has implications for dental management because the first clinical signs are mucocutaneous lesions.12

Management of Medicine Risks Through Diet

Patients with autoimmune disease often suffer from side effects of medications and side effects commonly present with xerostomia and mucocutaneous lesions. Management includes advising patients to eat a nutrient-dense, bland, and soft diet that will not put them at increased risk for dental caries or cause pain and exacerbate their disease. In particular, the diet should contain the following: moderate amounts of protein (1.5 g/Kg/day of proteins); low fat levels (less than 30% of calories, obtained mostly from unsaturated fatty acids); and high-fiber complex carbohydrates (80%) providing 50% of the caloric intake. The diet should be low in sodium and contain high amounts of calcium, fluoride, magnesium, and potassium to maintain bone and teeth health.13 Including vitamins B2, B3, B6, B12, folic acid, and vitamin C as well as A, D, and E14 is useful for maintaining healthy mucous membranes as well as in wound healing. Finally, zinc plays a significant role in cell growth and reproduction and healthy immune function. Also, zinc enhances taste and appetite, so its inclusion reduces the likelihood of recurring malnutrition problems; ie, patients avoiding healthy food choices because of decreased taste sensation and appetite.14 According to the 2015–2020 Dietary Guidelines for Americans, we need 15 mg per day of zinc.15 Foods rich in zinc that may be easy to consume are oysters (6 oysters contain 32 mg zinc), chickpeas (1.3 mg in one half cup cooked), chicken (2.4 mg in 3 ounces), Swiss cheese (1.2 mg in 1 ounce), oatmeal (1.1 mg in a packet of instant) and wheat germ (4.7 mg per ounce).15

Dietary Preventive and Therapeutic Approaches to Autoimmune Diseases

There is a growing body of evidence to support an association between vitamin D and autoimmune diseases such as RA, multiple sclerosis (MS), SLE, Type 1 diabetes and inflammatory bowel disease.16,17 It is suggested that vitamin D may prevent or ameliorate autoimmune disease activity because it supports self-tolerance and improves the immunological response.18 For example, a birth-cohort study published in The Lancet in 2001 followed 10,821 children (born in 1966) for 30 years.19 The study showed that “ensuring adequate vitamin D supplementation for infants could help to reverse the increasing trend in the incidence of Type 1 diabetes.” A recent meta-analysis examined evidence from epidemiological studies regarding the relationship between vitamin D and RA. Data from 24 reports involving 3,489 patients were analyzed.20 The authors concluded that RA patients had lower vitamin D values than healthy controls, and there was a negative association between vitamin D and RA disease activity. Another study identified low levels of vitamin D as a risk factor in MS because its presence helps shape T-cell response and induces T-cells with immunosuppressive properties.21 According to Holick in Modern Nutrition and Health and Disease, MS risk is 40% lower among women taking 400 IU/day of vitamin D supplements.16

There is much interest in and mixed evidence to support newer dietary applications for prevention and control of autoimmune diseases. Examples include using omega-3 fatty acids, particularly those found in fish oil, to modulate inflammatory cytokines; incorporating antioxidants (such as vitamin A and E) in the diet to protect against oxidative damage and prevent tissue damage; and restricting calories to lessen oxidative stress caused by adipose tissues.22-24 Other promising compounds with anti-inflammatory and immune-modulatory properties are polyphenols that are micronutrients present in vegetables, cereals, legumes, spices (curry, turmeric, ginger), herbs, fruits, wine, fruit juices, chocolate, tea, and coffee.25 Dietary probiotics is the newest area of research into therapeutic approaches to inflammation and modulation of immune dysregulation. Preliminary studies suggest the use of probiotics to control gut bacteria may have benefit in colitis and inflammatory bowel disease because the composition and function of the gut microbe community can modulate the innate and adaptive immune system.26 There are promising trends in the nutritional management of autoimmune diseases; however, further studies with larger sample sizes are needed in this area.

The overall goal of therapy in patients with autoimmune diseases is to relieve discomfort, reduce the inflammatory process during relapses, and maintain disease remission and improve quality of life.27 While referral and consultation with the patient’s physician are necessary to provide optimum dental hygiene care for patients with autoimmune disease, the inclusion of sound dietary recommendations in the dental treatment plan may help provide comprehensive oral healthcare to the patient.

About the Author

Stefania Moglia Willis, DMH, RDH, is a clinical assistant professor of dental hygiene at the New York University College of Dentistry.



By Ivianie Exinor, RDH, MPH

Sarcoidosis is a rare condition that stems from unresolved inflammatory responses in the body. As such, it can potentially lead to pervasive nonencased systemic granulomas. Sarcoidosis can be acute or chronic, extrinsic, or intrinsic. Although causation has not been established, many factors and/or agents have been suggested to influence sarcoidosis. This section addresses the etiology, incidence, prevalence, and intervention for systemic and oral healthcare maintenance to further empower the dental hygienist with information to treat patients experiencing sarcoidosis.

Sarcoidosis is listed as ORPHA797 on the list of rare diseases.1 It was reported initially in 1875 by Jonathan Hutchinson, an English surgeon-dermatologist.2 In 1899, however, Boeck reintroduced the term sarcoidosis and was credited with naming it “flesh like condition” based on its Greek root of word origin.2 Sarcoidosis is characterized by the buildup of exposed granulomas in systemic organs and tissues. Its most common sites of manifestation are the lungs and the lymphatic systems.3 Although orofacial involvement is rare, occurring in 10% to 15% of affected individuals, when it does manifest, it involves the maxilla, mandible, the parotid glands, salivary glands, and the cervical chain.2,4 The signs and symptoms are bilateral swollen parotid glands, intraoral/extraoral lesions, and periodontal involvement.2,4

Incidence and Prevalence

The incidence of this disease varies with age, sex, race, and geographic location.5 It is estimated to be at approximately 1:6,300 men and 1:5,300 women; the prevalence is 1–5:10,000 in the US population.5,6 Additionally, the disease affects more African Americans than Caucasians, occurring in 39:100,000 African Americans compared to 5:100,000 Caucasians.7

Manifestation, Symptoms, and Treatment of Sarcoidosis

Sarcoidosis can manifest as an acute/benign or chronic illness.4 The acute form of the condition, also known as Lofgren Syndrome, is visible on chest radiographs and seen as bilateral hilar lymphadenopathy, tender red nodules, or erythema nodosum and arthritis of the lower limbs.3,4 This mode of manifestation is most often asymptomatic and resolves on its own, sometimes without the affected person’s knowledge.3

The chronic mode of the disease manifests as bilateral hilar lymphadenopathy with lung infiltration that causes malfunction of the pulmonary organs.8-10 Common symptoms are dry cough, dyspnea, chest pain, and fatigue as well as symptoms affecting or resulting from other systemic organs.8,10 The chronic stage of the disease requires long-term intervention with different types of medications, corticosteroids (glucocorticoids) being the most widely used.8-10 Other medications are methotrexate, azathioprine, and chlorambucil hydroxychloroquine.8,9


The true cause of sarcoidosis is not known, but it has been attributed to genetic predisposition, environmental factors (dust, clay, and mold), Mycobacterium tuberculosis, Epstein-Barr virus, organ transplant, and human herpes.3,4,8,11


The American Thoracic Society, European Respiratory Society, and the World Association of Sarcoidosis and Other Granulomatous Disorders’ Statement on Sarcoidosis revealed that diagnosis should address the following four goals:3

• Provide histologic confirmation of the disease

• Assess the extent and severity of organ involvement

• Assess whether the disease is stable or is likely to progress

• Determine if therapy will benefit the patient

Sarcoidosis is reported as being challenging to diagnose.12 For instance, the disease has a tendency to mimic the symptoms of tuberculosis13 and Sjögren’s syndrome.10 As such, it tends to take time to eliminate the confounders in order to decipher the true condition.10 A series of tests are required to diagnose sarcoidosis accurately, including a complete medical history and comprehensive physical examination to rule out comorbidities and to isolate sarcoidosis.9,10 Bronchoscopy, mediastinoscopy and skin biopsy, eye examination, computed tomography scan, and chest radiography are all instrumental in helping to diagnose this condition as there is no blood test that can do so conclusively.13,14


Prognosis depends on whether the sarcoidosis is acute or chronic.2 If acute, the prognosis is very good.2 If chronic, the prognosis depends on the organs involved and how advanced the disease is.2 Multiple courses of intervention with medication may be necessary to help the affected individual cope with the condition.2,8 In the presence of radiological signs of irreversible fibrosis, prognosis is said to be unfavorable.2

How Sarcoidosis Affects Oral Health

The disease compromises oral health greatly due to the related orofacial lesions.10,15-18 Extraoral manifestations include bilateral enlargement of the parotid and submandibular glands, cervical lymphadenopathy and lip lesion resembling widespread chronic herpetic lesions.10,15-18 Intraorally, sarcoidosis adversely affects the salivary glands and sublingual glands and leads to gingival proliferation, gingivitis, gingival recession, ulcers, xerostomia, and enlargement of the labial and palatal minor.10,15-18 The buccal mucosa, tongue, and palate may also be affected.2,15-20

The Oral Healthcare Appointment

Successfully managing the oral healthcare of patients with sarcoidosis requires interdisciplinary care, defined by the American Dental Hygienists’ Association (ADHA) as “Two or more healthcare providers working within their respective disciplines who collaborate with the patient and/or caregiver to develop and implement a care plan (ADHA Policy Manual, Interdisciplinary Care 3-10). An interdisciplinary approach requires healthcare providers working within their respective disciplines to collaborate with the patient and/or caregivers to develop and implement a care plan. For the sarcoidosis patient, this may include the primary care physician, gastroenterologist, pulmonologist, dentist, dental hygienist, the patient, and the rest of the office team.”

The initial visit begins with a comprehensive medical and dental history data collection. Communication with the other specialists will help to ensure that it is safe to proceed with dental hygiene care.15 Then, intraoral and extraoral examinations and assessments are performed to completion. The dental hygiene care plan should include:

• Home care instruction or modification

• Capturing oral radiograph and digital images

• Pain management medications (consult with specialists for clearance)

• Prophylaxis

• Scaling and root planing if/when needed

• Alcohol-free antiseptic rinses

• Fluoride treatment

• Enamel protection toothpaste

• Oral moisturizing rinse

• Frequent recall appointment

Additional oral treatment may vary from no treatment to removal of excess tissue growth through curettage.15 Gingivitis and periodontitis may be resolved with scaling, polishing, and diligent oral hygiene home care.15


Sarcoidosis exists in both acute and chronic phases independently. Alleviation can be self-resolved or achieved with pharmacological intervention. Although the confounding effects of the disease can make diagnosis challenging, once it is completed, moving forward for a positive outcome requires the concerted effort of all stakeholders.

About the Author

Ivianie Exinor, RDH, MPH, is a clinical instructor at New York University College of Dentistry and an adjunct assistant professor at Hostos Community College and New York City College of Technology. She also works in private practice at Safferstein Dental, Bronx, New York.



1. Marik PE, Kaplan D. Aspiration pneumonia and dysphagia in the elderly. Chest. 2003;124(1):328-336.

2. Pace CC, McCullough GH. The association between oral microorganisms and aspiration pneumonia in the institutionalized elderly: review and recommendations. Dysphagia. 2010;25(4):307-322.

3. Terpenning MS, Taylor GW, Lopatin DE, et al. Aspiration pneumonia: dental and oral risk factors in an older veteran population. J Am Geriatr Soc. 2001;49(5):557-563.

4. Swaminathan A, Varkey B, Stearns DA. Aspiration pneumonitis and pneumonia. Medscape. 2015. Available at:

5. Sethi S. Aspiration pneumonitis and pneumonia. Merck Manuals. 2014. Available at:

6. Terpenning MS. Geriatric oral health and pneumonia risk. Clin Infect Dis. 2005;15(40):1807-1810.



1. Padmavathi B, Sharma S, Astekar M, et al. Oral Crohn’s disease. J Oral Maxillofac Pathol. 2014;18(Suppl):S139-S142.

2. Woo VL. Oral manifestations of Crohn’s disease: a case report and review of the literature. Case Rep Dent. 2015;1-7.

3. Szymanska S, Lordal M, Rathnayake N, et al. Dental caries, prevalence and risk factors in patients with Crohn’s disease. PLoS ONE. 2014;9(3):E91059.

4. Katsanos KH, Torres J, Roda G, et al. Review article: Non-malignant oral manifestations in inflammatory bowel diseases. Aliment Pharmacol Ther. 2015;42(1):40-60.

5. Anderson WD 3rd, Treister NS, Mayeaux E JR, Nalilah RP. Oral lesions you can’t afford to miss. J Fam Pract. 2015;64(7):392-399.



1. Department of Health and Human Services, National Institutes of Health (NIH), National Institute of Allergy and Infectious Diseases (NIAID). FY 2014 Budget, p.23. Available at: Accessed January 18, 2016.

2. Palmer S. Is there a link between nutrition and autoimmune disease? Today’s Dietitian. 2011; 13(11):36. Available at: Accessed January 18, 2016.

3. Department of Health and Human Services, National Institutes of Health (NIH), National Institute of Allergy and Infectious Diseases (NIAID). Gender specific health challenges facing women: autoimmune diseases. Available at: Accessed January 16, 2016.

4. Abbas AK, Lichtman AH. Diseases caused by humoral and cell-mediated immune reactions. In: Abbas AK and Lichtman AH (eds.). Cellular and Molecular Immunology. Philadelphia: WB Saunders–Harcourt Brace Jovanovich; 2003:357-379.

5. Janeway CA Jr, Travers P. Autoimmunity and transplantation. In: Janeway CA Jr, Travers P (eds.). Immunobiology: The Immune System in Health and Disease. 5th ed. New York: Current Biology–Garland; 2001.

6. Schwartz RS. Autoimmunity and autoimmune diseases. In: Paul WE (ed.). Fundamental Immunology. 3rd ed. New York: Raven Press, 1993:1033-1097.

7. Bellone M. Autoimmune disease pathogenesis. Available at: Accessed January 16, 2016.

8. Immune cell clustering suppresses autoimmunity in healthy tissues. Available at: Accessed January 18, 2016.

9. Siegel M. Diseases of the gastrointestinal tract. In: Greenberg MS, Glick M, Ship JA (eds.). Burket’s Oral Medicine. 11th ed. Hamilton (Ontario): BC Decker; 2002.

10. Tolle SL. Treatment planning for patients with scleroderma. Dimens Dent Hyg. 2012;10(9):50-53.

11. Centers for Disease Control and Prevention. Prevalence of doctor-diagnosed arthritis and arthritis-attributable activity limitation—United States, 2010–2012. MMWR Morb Mortal Wkly Rep. 2013;62(44):869-873.

12. Rotondo C, Lopalco G, Iannone F, et al. Mucocutaneous involvement in Behçet’s disease: how systemic treatment has changed in the last decades and future perspectives. Mediators Inflamm. 2015. Available at: Accessed January 18, 2016.

13. Miggiano GA, Migneco MG. Diet and chronic corticosteroid therapy. Clin Ter (La Clinica Terapeutica). 2004;155(5):213-220.

14. Thomas DM, Mirowski GW. Nutrition and oral mucosal diseases. Clin Dermatol. 2010;28(4):426-431.

15. Office of Disease Prevention and Health Promotion. 2015–2020 Dietary Guidelines for Americans. Available at: Accessed January 19, 2016.

16. Holick M. Vitamin D. In Shils ME, Shike M, Ross AC, et al. (eds.): Modern Nutrition in Health and Disease. Philadelphia: Williams and Wilkins; 2006;376-395.

17. Hayes CE, Nashold FE, Spanier JA, et al. Vitamin D and multiple sclerosis. In: Feldman D, Pike JW, Adams JS (eds). Vitamin D. San Diego: Elsevier; 2011:1843-1877.

18. Arnson Y, Amital H, Shoenfeld Y. Vitamin D and autoimmunity: new aetiological and therapeutic considerations. Ann Rheum Dis. 2007;66:1137-1142.

19. Hyppönen E, Läärä E, Reunanen A, et al. Intake of vitamin D and risk of type 1 diabetes: a birth-cohort study. Lancet. 2001;358(9292):1500-1503.

20. Lin J, Liu J, Davies ML, Chen W. Serum vitamin D level and rheumatoid arthritis disease activity: review and meta-analysis. Plos One. 2016;11(1):e0146351.

21. Correale J, Gaitán MI. Multiple sclerosis and environmental factors: the role of vitamin D, parasites, and Epstein-Barr virus infection. Acta Neurol Scand. 2015;132(Suppl 199):46-55.

22. Flores-Alvarado L. Pathogenic mechanisms of neuronal damage in multiple sclerosis. Invest Clin. 2015;56(2):201-214.

23. Røsjø E, Myhr KM, Løken-Amsrud KI, et al. Increasing serum levels of vitamin A, D and E are associated with alteration of different inflammation markers in patients with multiple sclerosis. J Neuroimmunol. 2014;271(1-2):60-65.

24. Speakman JR, Mitchell SE. Caloric restriction. Mol Aspects Med. 2011;32(3):159-221.

25. Gupta SC, Tyagi AK, Deshmukh-Taskar P, et al. Downregulation of tumor necrosis factor and other proinflammatory biomarkers by polyphenols. Arch Biochem Biophys. 2014;559:91-99.

26. Vieira SM, Pagovich OE, Kriegel MA. Diet, microbiota, and autoimmune disease. Lupus. 2014;23(6):518-526.

27. Sales-Campos H, et al. Classical and recent advances in the treatment of inflammatory bowel diseases. Brazilian J Med Biol Res. 2015;48(2):96-107. Available at: http://dx.doi. org/10.1590/1414-431X20143774. Accessed January 18, 2016.



1. List of rare diseases and synonyms: listed in alphabetical order. Orphanet Report Series. May 2015. Available at: Accessed January 28, 2016.

2. Kadiwala SA, Dixit MB. Gingival enlargement unveiling sarcoidosis: report of a rare case. Contemp Clin Dent. 2013;4(4):551-555.

3. American Thoracic Society. Statement on sarcoidosis. Am J Respir Crit Care Med. 1999;160(2):736.

4. Patil PM, Sharma A, Jain H, Mishra V. Sarcoidosis: an update for the oral health care provider. J Cranio-Max Dis. 2015;4(1):69.

5. Prevalence and incidence of rare diseases: bibliographic data. diseases listed by decreasing prevalence, incidence number of published cases. Orphanet Report Series. July 2015. Available at: Accessed January 28, 2016.

6. Orphanet. Sarcoidosis. Available at: Accessed January 28, 2016.

7. Erdal BS, Clymer BD, Yildiz VO, et al. Unexpectedly high prevalence of sarcoidosis in a representative U.S. metropolitan population. Respir Med. 2012;106(6):893-899.

8. King SC, Kelly W. Treatment of sarcoidosis. Dis Mon. 2009;55:704-718.

9. Ipek E, Demirelli S, Ermis E, Inci S. Sarcoidosis and the heart: a review of the literature. Intractable Rare Dis Res. 2015;4(4):170-180.

10. Folwaczny M, Sommer A, Sander CA, Kellner H. Parotid sarcoidosis mimicking Sjögren’s syndrome: report of a case. J Oral Maxillofac Surg. 2002;60(1):117-120.

11. Valeyre D, Prasse A, Nunes H, et al. Sarcoidosis. Lancet. 2014;383(9923):1155-1167. Print.

12. American Lung Association. Diagnosing and treating sarcoidosis. Available at: Accessed January 29, 2016.

13. van Enschot JW, van Balkom RH. Sarcoidosis following Mycobacterium tuberculosis infection: coincidence or consequence. Respir Med Case Rep. 2013;9:11-14.

14. American Thoracic Society. What is sarcoidosis? Patient Information Series. Accessed January 29, 2016.

15. Gupta S, Tripathi AK, Kumar V, Saimbi CS. Sarcoidosis: oral and extra-oral manifestation. J Indian Soc Periodontol. 2015;19:582-585.

16. Malathi N, Mythili S, Vasanthi HR. Salivary diagnostics: a brief review. ISRN Dent. January 29, 2014:1-8.

17. Fatahzadeh M, Rinaggio J. Diagnosis of systemic sarcoidosis prompted by orofacial manifestations: a review of the literature. J Am Dent Assoc. 2006;137(1):54-60.

18. Motswaledi MH, Khammissa RA, Jadwat Y, et al. Oral sarcoidosis: a case report and review of the literature. Australian Dent J. 2014;59(3):389-394.

19. Vourexakis Z, Dulguerov P, Bouayed S, et al. Sarcoidosis of the submandibular gland: a systematic review. Am J Otolaryngol. 2010;31(6):424-428.

20. Holmes J, Lazarus A. Sarcoidosis: extrathoracic manifestations. Dis Mon. 2009;55(11):675-692.

Take the Accredited CE Quiz:

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COST: $35.00
PROVIDER: American Dental Hygienists’ Association
SOURCE: American Dental Hygienists' Association | June 2016

Learning Objectives:

  • Discuss the link between aspiration pneumonia and poor oral hygiene, dental decay, periodontal disease, and dysphagia.
  • Describe the challenges patients with CD present for the dental hygienist, such as pain management of oral lesions and caries risk assessment to nutritional counseling.
  • List some of the common autoimmune diseases that dental hygienists may see in their patients.
  • Discuss the etiology, incidence, and prevalence of sarcoidosis and identify intervention strategies.