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This educational activity was developed by PennWell’s Dental Group with no commercial support.This course was written for dentists, dental hygienists and assistants, from novice to skilled. Educational Methods: This course is a self-instructional journal and web activity. Provider Disclosure: PennWell does not have a leadership position or a commercial interest in any products or services discussed or shared in this educational activity nor with the commercial supporter. No manufacturer or third party has had any input into the development of course content.Requirements for Successful Completion: To obtain 2 CE credits for this educational activity you must pay the required fee, review the material, complete the course evaluation and obtain a score of at least 70%.CE Planner Disclosure: Heather Hodges, CE Coordinator does not have a leadership or commercial interest with products or services discussed in this educational activity. Heather can be reached at hhodges@pennwell.comEducational Disclaimer: Completing a single continuing education course does not provide enough information to result in the participant being an expert in the field related to the course topic. It is a combination of many educational courses and clinical experience that allows the participant to develop skills and expertise.Scientific Integrity Statement: Information shared in this CE course is developed from clinical research and represents the most current information available from evidence based dentistry. Registration: The cost of this CE course is $49.00 for 2 CE credits. Cancellation/Refund Policy: Any participant who is not 100% satisfied with this course can request a full refund by contacting PennWell in writing.

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Dental Board of California: Provider 4527, course registration number CA# 02-4527-13079“This course meets the Dental Board of California’s requirements for 2 unit of continuing education.”

The PennWell Corporation is designated as an Approved PACE Program Provider by the Academy of General Dentistry. The formal continuing dental education programs of this program provider are accepted by the AGD for Fellowship, Mastership and membership maintenance credit. Approval does not imply acceptance by a state or provincial board of dentistry or AGD endorsement. The current term of approval extends from (11/1/2011) to (10/31/2015) Provider ID# 320452.

Publication date: July 2013 Expiration date: June 2016

AbstractMucosal ulceration, dental disease and other tooth abnormalities, oral soft tissue tumors, periodontal disease, bone pathology, and orofacial pain may be directly related to or confounded by underlying systemic disease. An understanding of the relationship between systemic disease and oral pathology is important with respect to establishing the diagnosis and determining the complexity of subsequent management. For example, dental caries that is confounded by nutritional deficiency or psychological problems such as bulimia or anorexia, or a medical problem that directly or indirectly (via medication use) causes xerostomia or dry mouth, or a medical condition that alters the patient’s ability to maintain appropriate oral hygiene may need to be managed using a comprehensive strategy that takes into account the underlying medical issue as well as the dental issues. This course reviews such problems and their impact on oral conditions.

Educational Objectives:At the end of this educational activity, participants will be able to: 1. Discuss the complexity of the relationship

between systemic disease and various oral conditions.

2. Identify the different oral manifestations associated with specific systemic diseases.

3. Differentiate between potential systemic diseases associated with some specific oral conditions such as ulceration.

4. Have improved diagnostic skills in relation to the connection between systemic disease and oral pathology.

Author ProfileJeff Burgess, DDS, MSD, (Retired) Clinical Assistant Professor, Department of Oral Medicine, University of Washington School of Dental Medicine; (Retired) Attending in Pain Center, University of Washington Medical Center; (Retired) Private Practice in Hawaii and Washington; Director, Oral Care Research Associates. He can be reached at jeffreyaburgess@hotmail.com .

Author DisclosureJeff Burgess, DDS, MSD, has no commercial ties with the sponsors or providers of the unrestricted educational grant for this course.

Oral Manifestations of Systemic Disease A Peer-Reviewed Publication Written by Jeff Burgess, DDS, MSD

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Educational ObjectivesAt the end of this educational activity, participants will be able to: 1. Discuss the complexity of the relationship between

systemic disease and various oral conditions.2. Identify the different oral manifestations associated

with specific systemic diseases.3. Differentiate between potential systemic diseases

associated with some specific oral conditions such as ulceration.

4. Have improved diagnostic skills in relation to the con-nection between systemic disease and oral pathology.

AbstractMucosal ulceration, dental disease and other tooth ab-normalities, oral soft tissue tumors, periodontal disease, bone pathology, and orofacial pain may be directly related to or confounded by underlying systemic disease. An un-derstanding of the relationship between systemic disease and oral pathology is important with respect to estab-lishing the diagnosis and determining the complexity of subsequent management. For example, dental caries that is confounded by nutritional deficiency or psychological problems such as bulimia or anorexia, or a medical prob-lem that directly or indirectly (via medication use) causes xerostomia, or a medical condition that alters the patient’s ability to maintain appropriate oral hygiene may need to be managed using a comprehensive strategy that takes into account the underlying medical issue as well as the dental issues. This course reviews such problems and their impact on oral conditions.

IntroductionNumerous orofacial conditions are associated with system-ic disease. The most serious problems of concern to dental professionals include caries, oral ulcers, mucosal erythema and sloughing, gingival bleeding and hypertrophy, soft tis-sue exophytic masses, dry mouth, facial pain, movement disorders, tooth abnormalities, abnormal dental wear, tooth/mucosal discoloration, developmental and bone pathology. This review focuses on the systemic conditions that may cause or contribute to the above oral problems.

CariesDental caries may be caused or aggravated by a number of systemic diseases via their impact on the three primary factors that are thought to contribute to dental caries: the presence of bacteria and biofilm known to cause caries, the availability of a consistent food source (e.g. sugar) for these bacteria, and oral hygiene. Other factors such as genetics (e.g. tooth development, matrix metalloproteinases) and the use of medications in the treatment of systemic disease (e.g. affect on salivation) may also play a role in the devel-opment of caries.

A very complex relationship exists between these factors with respect to caries initiation in both primary and adult teeth. It is known that any perturbation of the oral environ-ment can increase the potential for the development of dental caries. For example, in a study on the relationship between dental caries and nutritional status, snack foods, and the consumption of sugar-sweetened beverages in schoolchil-dren in Thailand, it was found that malnutrition as well as food intake habits at bedtime were significantly related to the development of dental caries in the primary dentition.1

In addition to malnutrition, other conditions impacting diet are also cited in the literature as associated with the development of caries. These include medical (e.g. diabetes) and psychological (e.g. drug abuse, bulimia, etc.) problems. The following subsections detail some of the specific sys-temic problems that are suspected of impacting the develop-ment of caries.

Diabetes In animal models, a number of studies suggest that rapid progressive caries is associated with chemically induced hyperglycemia.2,3 In contrast to the animal studies, at least one systematic review of the literature questions the scientific validity of a causative link between caries and diabetes in humans.4 The authors of this review suggest that because multiple studies report variable caries experiences between subjects with and without diabetes (e.g. increased, decreased, and similar experiences), that the evidence is, at present, insufficient to determine if a true risk-relationship actually exists in humans.

Drug AbuseMultiple studies have linked the abuse of drugs to the devel-opment of dental caries.5-8 The problem has been identified in many countries throughout the world.9-12

One of the drugs that has been most recently studied in relation to caries is methamphetamine.13 The street descrip-tion of ‘meth mouth’ is not without merit as this particular drug and its abuse appears to be associated with considerable tooth decay as well as other oral problems such as periodon-tal disease. Some evidence suggests that salivary pH may be the reason the drug contributes to dental caries.14

The abuse of narcotics and alcohol has also been associ-ated with an increased risk of caries. However, in at least one comparative study, alcohol abuse was less likely than ‘drug’ abuse to lead to the development of caries. The combination of alcohol and drug abuse (which included self-reported use of not only heroin and methadone but also cannabis, benzo-diazepines, and cocaine) led to the greatest caries risk (38% increased risk).15

The authors of this study speculate that the lower rate in persons abusing alcohol, and particularly those that drink beer may be related to the effect of increased fluoride con-sumption which is an ingredient in beer.

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The caries risk from narcotics is not just related to street use. A recent case report describes the development of rampant caries from the abuse of oral transmucosal fen-tanyl citrate lozenges which are used for the oral manage-ment of breakthrough cancer pain.16 Presumably caries risk associated with drug use is behavioral in nature and relates to neglect of oral hygiene.

Smokeless tobacco use has also been linked to dental caries, specifically root caries.17 With respect to cannabis use, one study found that subjects using this drug exces-sively had significantly greater smooth surface caries than controls. The authors speculate that this was related to the drugs effect on salivation (hyposalivation during use) and on subsequent post-smoking sugar intake (from the ‘munchies’).18

In addition, as noted previously, any medication that reduces salivation has the potential to increase the risk of caries, particularly if it is used over a prolonged period of time.19 However, other than anecdotes, there is little docu-mented research assessing the link between the commonly used drugs that cause xerostomia and caries progression. In one animal study chronic administration of clonidine20 and propranolol21 was found to increase caries in rats. Other drugs causing dry mouth that are utilized by patients that could cause caries include antihistamines, anti-depressants such as Elavil® (amitriptyline), Asendin® (amoxapine), Anafranil® (clomipramine), Remeron® (mirtazapine) and Aventyl® or Pamelor® (nortriptline), and Detrol® which is commonly used to treat incontinence.

Bulimia and AnorexiaBulimia, a condition associated with repeated vomiting, has been connected to the development of dental caries in both men and women.22 This is presumed to be related to the fact that patients who chronically vomit, bathe their teeth in stomach acid during this purging behavior. In addition to bulimia, anorexia is another psychological condition that may include vomiting and has also been associated with an increase in dental caries.

However in a recent systematic review of the literature assessing the orofacial manifestations of these conditions, including caries, the authors suggest that the development of caries in patients with eating disorders may not be an automatic sequalae of these abnormalities.23

Nonetheless, in otherwise healthy patients with good oral hygiene but with unusual smooth surface lesions or rampant caries, eating disorders should be considered as a potential cause of the disease. Caries activity in this group of patients may also be confounded by general diet and oral hygiene as well as salivary gland disturbance.

Medical Conditions Reducing Hygiene BehaviorAny medical condition that contributes to a reduction in oral hygiene can increase the potential for the development

of dental caries. Diseases which reduce coordination, limit cognitive activity, or involve significant physical or mental disability have the potential to facilitate dental disease, including caries, and subsequent tooth loss.24 Finally, there is limited evidence that genetic factors such as a mutant allele for MMP13 (one of the genes that is responsible for producing a matrix metalloproteinase) may contribute in some manner to the etiology of dental caries.25

Oral UlcersThe systemic conditions that can cause oral ulceration include infection (e.g. syphilis,26, 27 tuberculosis,28 HIV/AIDS,29,30 viral infection including herpangina and primary herpetic stomatitis including herpes simplex virus causal-ity (HSV-1 or 2),31 candida and other fungal organisms (e.g. mucormycosis or histoplasmosis,32-35 autoimmune disease (e.g. lupus,36,37 pemphigus and paraneoplastic pem-phigus,38,39 lichen planus,40 inflammatory bowel disease,41

thyroid disease,44 malignancy/haematologic disease,45,46 cyclic neutropenia,47 allergy and other drug reactions,48-50 and vascular inflammatory disease.51 Oral ulceration may also be associated with organ transplants and the medica-tions used to manage rejection or treat other diseases (e.g. thyroid disease),52 liver transplant,53 or renal transplant.54 Nutritional deficiencies are also associated with intraoral ulceration.55,56 Oral ulceration has also been reported with hypogammaglobulinemia.57

Generally the clinical presentation of oral ulcers is not specific enough to allow identification of the underlying pa-thology in cases involving systemic disease. There are, how-ever, several clinical features that may be helpful in guiding the clinician with respect to the differential diagnosis in these cases. These include ulcer location, duration, reoccurrence, depth, number, size, scarring, and non-healing.

Lesion LocationLesions associated with primary herpetic stomatits occur not only on the intraoral mucosa of the cheek, tongue, pal-ate, and posterior pharynx, but also on the attached gingiva. This is not a typical presentation that is associated with most other oral ulcerative diseases and thus can be used to help differentiate between non-viral and viral etiology.

Lesion DurationViral lesions and aphthous ulcers typically persist for 10-14 days and heal with complete resolution. In contrast, lesions associated with Behcet’s disease may persist for up to four to six weeks. Ulcers related to underlying neoplasm, a compro-mised immune system, or nutritional deficiency persist for a much longer period of time.

Lesion ReoccurrenceUlceration reoccurring on the attached gingiva is likely to represent secondary (or reoccurring) HSV-1 or HSV-2.

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Lesion DepthDeep cratering of the oral mucosa is typical of the ulcers associated with Behcet’s disease and HIV/AIDS. However, lesions associated with major aphthous, tuberculosis and syphilis may also be relatively deep. Deep tongue lesions may also be associated with amyloidosis58 and malignancy.

Number of LesionsMultiple ulcers clustered throughout the mouth suggest vi-ral etiology (e.g. herpes zoster, primary herpetic stomatitis, or herpangina).

The Size of the LesionLarge (>1cm or greater) oral ulcers are most typically seen with erythema multiforma, allergy, benign mucous mem-brane pemphigoid (BMMP) disease, pemphigus vulgaris, erosive lichen planus, radiation mucositis or mucositis associated with chemotherapy and lesions associated with severe immunosuppression or uremic stomatits. Large lesions are not typically observed with viral infection al-though sometimes small lesions will coalesce to form larger ulcers.59

Post lesion scarringUlceration occurring with Bechet’s disease occurs with post-healing scarring. Typically patients with this condition will have areas of mucosa that are scarred from past episodes.

Non-healing ulcersThese are most commonly found with malignancy.

Gingival Bleeding, Hyperplasia, Discoloration

Gingival BleedingSystemic conditions that can cause gingival bleeding include some of those that also cause ulceration such as benign mucous membrane pemphigoid (BMMP), pem-phigus, lupus erythematosis, leukemia, and erythema mul-tiforme. Other conditions such as uncontrolled diabetes,60 Crohn’s disease (which can cause gingival hyperplasia as well as erythema and bleeding),61 and idiopathic thrombo-cytopenia62,63 have also been linked to gingival bleeding.

In addition to the above, what is termed hormonal gingivitis, a condition that can occur with pregnancy or disease associated with pregnancy, can also cause general-ized gingival erythema and bleeding.64-66

Several medications utilized in the management of a number of systemic conditions can cause gingival erythema and bleeding. These include: Trileptal®,68 anticoagulant drugs such as Coumadin®, warfarin or heparin and chemo-therapeutic agents such as methotrexate and 5-fluorouracil. A complete list of the chemotherapy agents that can cause mucositis and gingival as well as mucosal bleeding can be found at: http://www.webmd.com/oral-health/guide/

oral-side-effects-of-medications?page=2. Non-steroidal anti-inflammatory drugs, including aspirin may also cause gingival bleeding if used over a prolonged period of time. A number of herbal medicines may interact with non-herbal medications (e.g. the anticoagulants) to increase the po-tential for gingival bleeding including ginkgo biloba, dong quai, and danshen.69 Other herbal preparations associated with gingival bleeding include ginger, ginseng, garlic, and papaya.70

Gingival HyperplasiaSpecific classes of drugs including the immunosuppressants, calcium channel blockers, and anticonvulsants that are used in the treatment of a variety of medical conditions can induce gingival hyperplasia.71, 72 The medications most frequently cited as problematic for abnormal gingival growth include;73 immunosuppressants, calcium channel blockers, and anti-epileptic drugs.

Gingival DiscolorationGingival discoloration (other than erythema) may be a sign of Addison’s disease (primary hypoadrenocorticism), silver poisoning, primary or metastatic malignancy (melanoma), Kaposi’s sarcoma (with or without associated AIDS), hereditary hemorrhagic telangiectasia, and Peutz-Jeghers syndrome (lip lesions).

Intraoral Soft Tissue TumorsGeneral medical conditions that can cause intraoral soft tissue tumors include parathyroid disease (e.g. primary hyperparathyroidism or hyperparathyroidism secondary to an adenoma or carcinoma of a parathyroid gland - Brown’s tumor), malignant acanthosis nigricans (hyperplastic, peb-bly lesions on the lips), immunosuppression (squamous papillomas), metastatic neoplasms (typically from the breast, prostate, thyroid, lung), amyloidosis secondary to multiple myeloma (pebbly lesions of the lip and cheek).

Some of the other systemic conditions that can cause single or multiple exophytic papules, tissue enlargement, or other growths include; chronic granulomatous disease (Crohn’s disease) (which results in granulomatous gingival enlargement, cobblestone or corrugated labial mucosa), lymphoma, syphilis (ulcer plus atypical clinical presenta-tions in AIDS), end stage kidney disease with dialysis (causes furred tongue); lymphangioma (results in a pebbly mucosal surface).74-88

Dry MouthAny systemic disease that affects the major or minor sali-vary glands via direct disease involvement or secondarily as a consequence of medication use, radiation, or surgical trauma can cause dry mouth or xerostomia. Those systemic conditions capable of impacting the salivary glands in-clude:89-93 Sjogren’s disease, chronic renal failure (CRF),

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other autoimmune diseases (rheumatoid arthritis, seronega-tive spondyloarthritis, connective tissue disease, systemic lupus erythematosis), non-Hodgkin lymphoma, diabetes, Parkinson’s disease, HIV/AIDS, psychological problems (anxiety disorders and depression), stroke and Alzheimer’s disease, anemia, cystic fibrosis, and other conditions such as head trauma with nerve damage and chemo or radiation therapy for head and neck cancer.

Classes of medications used to treat systemic diseases capable of causing dry mouth include:94 antihistamines, an-tipsychotics, diuretics, chemotherapeutic agents, migraine medications, anticholinergic/antispasmodic agents, antidi-arrhetics, analgesics – antinflammatory type, narcotic anal-gesics, anti-acne, anti-anxiety medications, anticonvulsants, antihypertensives, anti-nausea and anti-emetic medications, anti-parkinsonian drugs, bronchodilators, muscle relaxants, and other drugs such as cannabis.

Dry mouth can occur as a secondary effect of treatment in patients using C-pap for sleep apnea and consequent to the use of COPD inhalers.95

Orofacial PainPain in the region of the mouth and face may be caused by a number of systemic problems. It is not within the purview of this course to extensively review the clinical pain characteristics of the following conditions. How-ever several references are listed for additional review.96,

97 Below are several systemic conditions that can cause orofacial pain:

Cardiac disease (e.g. myocardial infarction, angina)

Thyroid disease (e.g. thyroiditis)

Sinus disease (e.g. acute and chronic sinusitis)

Autoimmune disease (e.g. rheumatoid arthritis, lupus, sclero-derma)

Secondary trigeminal neuralgia (e.g. from tumors such as me-ningioma, epidermoid tumor, acoustic neurinoma, metastatic tumor, brain stem glioma; vascular lesions such as basilar artery or cavernous sinus aneurysm; connective disease such as scleroderma; Paget’s disease; syphilis; or toxins; MS)

Craniofacial pain of musculoskeletal origin (e.g. TMD, TMJ osteoarthritis, bone infection or primary or metastatic tumor)

Infection (e.g. otitis media, infection secondary to immuno-suppression)

Sickle cell disease (sickle cell arthropathy)

Vascular inflammatory conditions (e.g. giant cell arteritis, temporal arteritis, Systemic Lupus Erythematosus)

Psychological abnormality (e.g. somatoform disorder, pain of psychological origin in the head or face)

Medication neurotoxicity (e.g. vincristine)

Suboccipital or cervical nerve or muscle problems

Diabetes

Jaw movement disordersJaw movement can be altered by several medical conditions affecting the musculature, nervous system, vascular system, or the bones of the cranium or mandible. Movement disor-ders include opening stiffness, opening difficulty, painful movement, and unintentional movement. The conditions that should be considered in the differential diagnosis relat-ed to systemic disease for the above jaw movement problems are listed below.98-102

Jaw opening stiffness Jaw opening stiffness can be caused by scleroderma, fibro-myalgia, muscular dystrophy, and multiple sclerosis (MS).

Opening difficultyDifficulty in opening the jaw may result from infection (in-cluding the cephalic form of tetanus), poisoning, neurologic disease, psychogenic abnormality, tumor, substance abuse, dystonia, radiation induced trismus, ‘locked-in’ syndrome, brain stem lesions, idiopathic inflammatory myopathies.

Painful jaw movementMovement of the jaw may be limited by fibromyalgia, teta-nus, tumor, and dystonia associated with Behcet’s disease.

Intermittent unintentional movementAdditional jaw movement abnormality including intermit-tent unintentional movement can result from Parkinson’s disease, epilepsy, dystonia, nocturnal paroxysmal dysto-nia, serotonin syndrome, and substance abuse.

Tooth Morphologic AbnormalityDental problems associated with systemic disease include excessive tooth wear (from bulimia, anorexia, neurologic disease, psychological problems, genetic disorders),114-120 de-velopmental (genetic) abnormalities causing malformed or excessive or impacted teeth, discoloration (from medication use), and tooth root resorption (bulimia, gastroesophageal reflux disease, excessive soft drink consumption associated with obesity, diabetes, drug abuse, salivary gland agenesis, and high blood pressure).103-113

Tooth and Mucosal Discoloration

Dental discolorationDental discoloration can arise from the treatment of sys-temic infection with tetracycline and tetracycline-derived broad spectrum antibiotics. The result is permanent if the drugs are used during development of the teeth and bone as they are incorporated into the dental and enamel structure. Tissues affected include the teeth, bone, and car-tilage. Both primary and permanent teeth are susceptible to discoloration which can range from grey to brown or be yellow. Minocycline hydrochloride application during

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growth and development of bone leads to black or green tooth roots and a blue-gray darkening of the crowns of the permanent teeth. Staining may also occur in erupted per-manent teeth from minocycline and within the mucosa of the palate.121-124

Environmental exposure to a number of elements has also been associated with discoloration of teeth. These include silver, iron, and manganese which stain black; mercury and lead dust which stains the teeth blue-green; copper and nickel stain blue to blue/green, and chromic acid which can stain the teeth deep orange.125, 126 Excessive fluoride during development tends to mottle the color of enamel.127 In addition to the above causes of tooth dis-coloration, neonatal sepsis has also been associated with emergence of ‘green teeth’.128

Mucosal discolorationMucosal discoloration can be indicative of systemic disease. A large number of conditions can cause varying types of mucosal discoloration. The following are systemic problems that are known to cause mucosal discoloration and the specific type of discoloration that has been de-scribed for each condition.129-131 Minocycline is associated with a palatal ring. Kaposi sarcoma (KS) is associated with multiple red lesions within the mucosa, Addison’s disease results in hyperpigmentation of the mucosa, melanoma re-sults in a diffuse or more discrete solitary blue black tissue, thrombocytopenic purpura/leukemia and hemophilia are characterized by mucosal petechiae, pernicious anemia causes tongue discoloration, infection (such as infectious mononucleosis) is associated with petechiae on the palate.

Generalized redness of the oral mucosa is associated with a number of systemic diseases including: pemphigus, erosive lichen planus, radiation necrosis, mucositis, candi-dosis secondary to immunosuppression, allergy, erythema multiforme, polycythemia, Crohn’s disease, epidermoly-sis bullosa, viral infection, leukemia, uremic stomatitis, and vitamin B deficiency

Bone PathologyRadiolucencies associated with the pericoronal or follicular spaces adjacent to the teeth are not uncommon. However systemic disease that can cause this type of bone loss is rare. Those conditions that have been linked to lesions associated with unerupted teeth include Ewing’s sarcoma, histiocytosis X, pseudotumor of hemophilia, and salivary gland tumors. The diseases that can cause unilocular or multilocular radiolucency or radiolucency in the maxilla or mandible not linked to the dentition include metastatic carcinoma, giant cell tumor resulting from hyperparathy-roid disease or neurofibromatosis type 1, Burkitt’s lym-phoma, chondrosarcoma, eosinophilic granuloma, fibrous dysplasia, cherubism, Ewing’s sarcoma, Langerhan’s cell disease (idiopathic histiocytosis), malignant lymphoma of

bone, multiple myeloma, neuroblastoma, neurosarcoma, sarcoidosis, tuberculosis, and scleroderma.

For a complete review of disease that can cause bone pathology the reader is referred to the authoritarian texts that are provided as references.

The differential diagnosis is refined clinically by the patient’s gender, age, predominant jaw and region of the jaw where the lesion is located, the type of lesion (unilocu-lar or multilocular) and the configuration of the lesion’s borders (e.g. well defined or diffuse/ill-defined), the pa-tient’s symptom history (e.g. presence or absence of pain, dyesthesia/paresthesia,), and examination findings (e.g. localized swelling, gingival involvement, tooth mobility, tooth vitality). Other important considerations include serum chemistries, general symptoms, and bone biopsy.

Another condition involving the jaw bones is osteone-crosis caused by the use of bisphosphonates as treatment for advanced forms of cancer.133 Bone resorption of the mandibular angle has been associated with progressive systemic sclerosis. A generalized rarefaction of the jaw bones may also result from nutritional abnormality such as calcium deficiency (causing osteomalacia or ‘rickets’) or vi-tamin C deficiency as well as the hereditary hemolytic ane-mias such as thalassemia and sickle cell anemia. Leukemia can also cause rarefaction of the skull and jaw ramus. In the early stages of Paget’s disease (osteitis deformans) rarefac-tion and bone resorption are associated with radiographic radiolucency and in the later stage when there is fibrous deposition the bones take on a ‘cotton-wool’ appearance when viewed radiographically.

The temporomandibular joints may be affected by con-nective tissue diseases such as rheumatoid arthritis, juvenile idiopathic arthritis, psoriatic arthritis, and arthritis associ-ated with lupus as well as systemic cancer with metastasis. Gout may also affect the TMJ. Dermatomyositis has been reported to be associated with condylar resorption.141-146

ConclusionThe effect of systemic health on oral disease is well docu-mented and includes soft and hard tissue abnormality and pathology. The diagnosis of oral pathology by dental professionals may contribute towards the discovery of sys-temic disease. Regardless of which way the arrow points, the complexity of management of oral disease associated with systemic disease is likely to be confounded by the connec-tion between the two and successful management warrants an understanding of both problems.

Further ReadingSection on Pain:1. Surgical management of pain. Editor Kim J Burchiel, Thieme,

New York, 2002. Chapter 20, Jeffrey A Burgess, p 276-287.2. Neurosurgical management of pain. Editors Richard B North,

Robert M. Levy, Springer, New York, 1996, Chapter 7: Facial and Cranial Pain; Kim J Burchiel and Jeffrey A Burgess.

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Sections on Bone, Tooth, and Mucosal Pathology:1. Differential Diagnosis of Oral Lesions. Editors Norman K

Wood and Paul W Goaz. C.V. Mosby Company, St Louis, Second edition. 1980.

2. Tumors of the Head and Neck; Clinical and Pathological Considerations. 2nd Ed. John G Batsakis, Williams and Wilkins, Baltimore, 1982.

3. Oral and Maxillofacial Pathology. Editors Brad W Neville, Douglas D Damm, Carl M Allen, Jerry E Bouquot, W.B. Saunders Company, Philadelphia, 1995.

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3. Sano T, Matsuura T, Ozaki K, Narama I. Dental caries and caries-related periodontitis in type 2 diabetic mice. Vet Pathol. 2011/03;48(2):506-12.

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8. Turkyilmaz I. Oral manifestations of “meth mouth” a case report. J Contemp Dent Pract. 2010/01;11(1):E073-80.

9. Carter EF. Dental implications of narcotic addiction. Aust Dent J. Aug 1978;23(4):308-10. [PMID: 282833].

10. Sakki TK, Knuuttila ML, Vimpari SS, Kivelä SL. Lifestyle, dental caries and number of teeth. Community Dent Oral Epidemiol. Oct 1994;22(5 Pt 1):298-302. [PMID: 7813180].

11. Scheutz F. Dental health in a group of drug addicts attending an addiction-clinic. Community Dent Oral Epidemiol. 1984/02;12(1):23-8.

12. Reece AS. Dentition of addiction in Queensland: poor dental status and major contributing drugs. Aust Dent J. Jun 2007;52(2):144-9. [PMID: 17687962].

13. Morio KA, Marshall TA, Qian F, Morgan TA. Comparing diet, oral hygiene and caries status of adult methamphetamine users and nonusers: a pilot study. J Am Dent Assoc. Feb 2008;139(2):171-6. [PMID: 18245685].

14. Ravenel MC, Salinas CF, Marlow NM, Slate EH, Evans ZP, Miller PM. Methamphetamine abuse and oral health: a pilot study of “meth mouth”. Quintessence Int. Mar 2012;43(3):229-37. [PMID: 22299123].

15. Dasanayake AP, Warnakulasuriya S, Harris CK, Cooper DJ, Peters TJ, Gelbier S. Tooth decay in alcohol abusers compared to alcohol and drug abusers. Int J Dent. 2010;2010:786503. [PMID: 20379366].

16. Mandel L, Carunchio MJ. Rampant caries from oral transmucosal fentanyl citrate lozenge abuse. J Am Dent Assoc. Apr 2011;142(4):406-9. [PMID: 21454846].

17. Winn DM. Tobacco use and oral disease. J Dent Educ. Apr 2001;65(4):306-12. [PMID: 11336115].

18. Schulz-Katterbach M, Imfeld T, Imfeld C. Cannabis and caries--does regular cannabis use increase the risk of caries in cigarette smokers?. Schweiz Monatsschr Zahnmed. 2009;119(6):576-83.

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Author ProfileJeff Burgess, DDS, MSD, (Retired) Clinical Assistant Professor, Department of Oral Medicine, University of Washington School of Dental Medicine; (Retired) Attend-ing in Pain Center, University of Washington Medical Cen-ter; (Retired) Private Practice in Hawaii and Washington; Director, Oral Care Research Associates. He can be reached at jeffreyaburgess@hotmail.com .

DisclaimerJeff Burgess, DDS, MSD, has no commercial ties with the sponsors or the providers of the unrestricted educational grant for this course.

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Questions

Online CompletionUse this page to review the questions and answers. Return to www.ineedce.com and sign in. If you have not previously purchased the program select it from the “Online Courses” listing and complete the online purchase. Once purchased the exam will be added to your Archives page where a Take Exam link will be provided. Click on the “Take Exam” link, complete all the program ques-tions and submit your answers. An immediate grade report will be provided and upon receiving a passing grade your “Verification Form” will be provided immediately for viewing and/or printing. Verification Forms can be viewed and/or printed anytime in the future by returning to the site, sign in and return to your Archives Page.

Questions

Online CompletionUse this page to review the questions and answers. Return to www.ineedce.com and sign in. If you have not previously purchased the program select it from the “Online Courses” listing and complete the online purchase. Once purchased the exam will be added to your Archives page where a Take Exam link will be provided. Click on the “Take Exam” link, complete all the program questions and submit your answers. An immediate grade report will be provided and upon receiving a passing grade your “Verification Form” will be provided immediately for viewing and/or printing. Verification Forms can be viewed and/or printed anytime in the future by returning to the site, sign in and return to your Archives Page.

1. Systemic conditions that may result in tooth discoloration include:a. Neonatal sepsisb. Hemophiliac. Thyroid diseased. Sinus disease

2. Which systemic disease may be associated with x-ray follicular space and pericoronal radiolucency:a. Tuberculosisb. Progressive systemic sclerosisc. Paget’s disease d. Pseudotumor of hemophilia

3. Name the one systemic condition that is not likely to be associated with temporo-mandibular joint pathology:a. Juvenile idiopathic arthritisb. Goutc. Dermatomyositisd. Cherubism

4. Which systemic condition has NOT been associated with tooth erosion:a. High blood pressureb. Obesityc. Diabetesd. Liver disease

5. Which systemic condition is NOT associ-ated with mucosal discoloration:a. Peutz-Jegher b. Kaposi sarcoma (KS) c. Pancreatic cancerd. Laugier’s disease

6. When a patient presents with jaw muscle stiffness which of the following systemic conditions should be considered in the differential diagnosis:a. Sclerodermab. Thyroid diseasec. Kidney diseased. Rheumatoid arthritis

7. Which of these systemic diseases does NOT cause unintentional jaw movement:a. Serotonin syndromeb. Substance abusec. Epilepsyd. Jaw metastatic neoplasm

8. In a study on the relationship between dental caries and nutritional status, snack foods, and sugar-sweetened beverage consumption in schoolchildren in Thailand it was found that the following factor was strongly associated with caries development:a. Malnutritionb. Weightc. A diet of meatd. Soft drinks

9. Which one of these conditions is not associated with jaw pain:a. Tetanusb. Fibromyalgiac. Tumord. Pancreatic disease

10. The term ‘hormonal’ gingivitis is associated with:a. Thyroid abnormalityb. Adrenal insufficiencyc. Pregnancyd. Pituitary disease

11. Sarcoidosis is manifested in the mouth by:a. Fibroepithelial hyperplasiab. Non-caseating granulomasc. Deep ulcersd. Blue stained gingiva

12. Which of these clinical features of oral ulcers is not helpful in defining a possible underlying systemic disease:a. Ulcer depthb. The number of ulcersc. Scaringd. Reoccurrence frequency

13. Oral ulcers that persist for a long time may be most likely to be indicative of which systemic disease:a. Kidney diseaseb. Thyroid diseasec. Immune deficiencyd. Dermatomyositis

14. Which of the following systemic condi-tions has not been associated with the development of dental caries:a. Diabetesb. Bulimiac. Drug abused. Dermatologic disease

15. Multiple painful punctuate oral ulcers occurring on the attached gingiva sug-gests which systemic condition:a. Behcet’s diseaseb. Lymphoepithelial diseasec. Viral infectiond. Lichen planus

16. Which of these conditions does not cause oral ulceration:a. Viral infectionb. Thyroid diseasec. Pulmonary diseased. Inflammatory bowel disease

17. Smokeless tobacco has been linked to what type of caries:a. Mesial interproximal cariesb. Occlusal cariesc. Cervical (root) cariesd. Distal interproximal caries

18. A brain tumor such as a meningioma can cause:a. (Secondary) trigeminal neuralgiab. Burning tonguec. TMJ paind. Ear pain

19. Hypogammaglobulinemia has been associated with what type of oral problem:a. Periodontal diseaseb. Cariesc. Oral tumorsd. Oral ulceration

20. In healthy patients with good oral hygiene but unusual smooth surface lesions or rampant caries what problem should be considered as a potential cause of the oral disease:a. Thyroid diseaseb. Pancreatic diseasec. Bulimiad. Sarcoidosis

21. Heck’s disease is most likely to result in what type of oral problem:a. Periodontal Diseaseb. Impacted third molarsc. Epithelial hyperplasiad. Gingival discoloration

22. Which class of medication is not likely to cause gingival hyperplasia:a. Corticosteroidsb. Immunosuppressantsc. Calcium channel blockersd. Antiepileptic drugs

23. Which systemic disease is most likely to result in post-oral ulceration scaring:a. Tuberculosisb. Syphilisc. Kidney failured. Behcet’s disease

24. Sjogren’s disease causes what oral problem:a. Periodontal diseaseb. Tooth developmental abnormalityc. Dry mouthd. Jaw movement abnormality

25. Large oral ulcers are most likely to be observed with which systemic disease:a. Erythema multiformab. Herpes c. Uremic poisoningd. Aphthous stomatitis

26. Intermittent unintentional jaw move-ment is not likely to be associated with which one of these systemic problems:a. Dystoniab. Anorexiac. Parkinson’s diseased. Serotonin syndrome

27. Which of these intraoral problems is NOT caused by Crohn’s disease:a. Gingival hyperplasiab. Gingival bleedingc. Gingival erythemad. Gingival blackening

28. Gardner’s syndrome results in what oral problem:a. Periodontal bleedingb. Gum hyperplasiac. Dental malformationsd. Mandibular osteomas

29. Multiple ulcers clustered throughout the mouth suggest what type of etiology:a. Kidney diseaseb. Pulmonary diseasec. Viral infectiond. Cardiac disease

30. In the study of caries activity of school children in Thailand, what condition besides malnutrition was found to contribute to the development of dental caries in primary teeth?a. The type of food eaten during the dayb. Food intake habits at bedtimec. The number of meals eaten in a dayd. The amount of food intake

Educational Objectives1. Discuss the complexity of the relationship between systemic disease and various oral conditions.

2. Identify the different oral manifestations associated with specific systemic diseases.

3. Differentiate between potential systemic diseases associated with some specific oral conditions such as ulceration.

4. Have improved diagnostic skills in relation to the connection between systemic disease and oral pathology.

Course Evaluation1. Were the individual course objectives met? Objective #1: Yes No Objective #3: Yes No

Objective #2: Yes No Objective #4: Yes No

Please evaluate this course by responding to the following statements, using a scale of Excellent = 5 to Poor = 0.

2. To what extent were the course objectives accomplished overall? 5 4 3 2 1 0

3. Please rate your personal mastery of the course objectives. 5 4 3 2 1 0

4. How would you rate the objectives and educational methods? 5 4 3 2 1 0

5. How do you rate the author’s grasp of the topic? 5 4 3 2 1 0

6. Please rate the instructor’s effectiveness. 5 4 3 2 1 0

7. Was the overall administration of the course effective? 5 4 3 2 1 0

8. Please rate the usefulness and clinical applicability of this course. 5 4 3 2 1 0

9. Please rate the usefulness of the supplemental webliography. 5 4 3 2 1 0

10. Do you feel that the references were adequate? Yes No

11. Would you participate in a similar program on a different topic? Yes No

12. If any of the continuing education questions were unclear or ambiguous, please list them. ___________________________________________________________________

13. Was there any subject matter you found confusing? Please describe. ___________________________________________________________________ ___________________________________________________________________

14. How long did it take you to complete this course? ___________________________________________________________________ ___________________________________________________________________

15. What additional continuing dental education topics would you like to see? ___________________________________________________________________ ___________________________________________________________________

For IMMEDIATE results, go to www.ineedce.com and click on the button “Take Tests Online.” Answer sheets can be faxed with credit card payment to (440) 845-3447, (216) 398-7922, or (216) 255-6619.

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PLEASE PHOTOCOPY ANSWER SHEET FOR ADDITIONAL PARTICIPANTS.

OMSD713DIG

COURSE EVALUATION and PARTICIPANT FEEDBACKWe encourage participant feedback pertaining to all courses. Please be sure to complete the survey included with the course. Please e-mail all questions to: hhodges@pennwell.com.

INSTRUCTIONSAll questions should have only one answer. Grading of this examination is done manually. Participants will receive confirmation of passing by receipt of a verification form. Verification of Participation forms will be mailed within two weeks after taking an examination.

COURSE CREDITS/COSTAll participants scoring at least 70% on the examination will receive a verification form verifying 2 CE credits. The formal continuing education program of this sponsor is accepted by the AGD for Fellowship/Mastership credit. Please contact PennWell for current term of acceptance. Participants are urged to contact their state dental boards for continuing education requirements. PennWell is a California Provider. The California Provider number is 4527. The cost for courses ranges from $20.00 to $110.00.

PROVIDER INFORMATIONPennWell is an ADA CERP Recognized Provider. ADA CERP is a service of the American Dental association to assist dental professionals in identifying quality providers of continuing dental education. ADA CERP does not approve or endorse individual courses or instructors, not does it imply acceptance of credit hours by boards of dentistry.

Concerns or complaints about a CE Provider may be directed to the provider or to ADA CERP ar www.ada.org/cotocerp/

The PennWell Corporation is designated as an Approved PACE Program Provider by the Academy of General Dentistry. The formal continuing dental education programs of this program provider are accepted by the AGD for Fellowship, Mastership and membership maintenance credit. Approval does not imply acceptance by a state or provincial board of dentistry or AGD endorsement. The current term of approval extends from (11/1/2011) to (10/31/2015) Provider ID# 320452

RECORD KEEPINGPennWell maintains records of your successful completion of any exam for a minimum of six years. Please contact our offices for a copy of your continuing education credits report. This report, which will list all credits earned to date, will be generated and mailed to you within five business days of receipt.

Completing a single continuing education course does not provide enough information to give the participant the feeling that s/he is an expert in the field related to the course topic. It is a combination of many educational courses and clinical experience that allows the participant to develop skills and expertise.

CANCELLATION/REFUND POLICYAny participant who is not 100% satisfied with this course can request a full refund by contacting PennWell in writing.

IMAGE AUTHENTICITYThe images provided and included in this course have not been altered.

© 2013 by the Academy of Dental Therapeutics and Stomatology, a division of PennWell

ANSWER SHEET

Oral Manifestations of Systemic Disease

Name: Title: Specialty:

Address: E-mail:

City: State: ZIP: Country:

Telephone: Home ( ) Office ( )

Lic. Renewal Date: AGD Member ID:

Requirements for successful completion of the course and to obtain dental continuing education credits: 1) Read the entire course. 2) Complete all information above. 3) Complete answer sheets in either pen or pencil. 4) Mark only one answer for each question. 5) A score of 70% on this test will earn you 2 CE credits. 6) Complete the Course Evaluation below. 7) Make check payable to PennWell Corp. For Questions Call 216.398.7822

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AGD Code 739