Oral manifestations of diseases of the gastrointestinal, cardiovascular, endocrine systems
Dental health care workers are expected to recognize, diagnose, and treat oral conditions associated with gastrointestinal diseases, as well as provide dental care for afflicted individuals. To provide safe and appropriate dental care, dentists are typically concerned with the proper diagnosis of oral manifestations of gastrointestinal disorders, homeostasis, risk of infection, drug actions and interactions, the patient’s ability to withstand the stress and trauma of dental procedures, and proper medical referral (wheecessary). These dental management issues are therefore discussed, where appropriate, for each gastrointestinal disorder.
Gastroesophageal Reflux Disease
ORAL HEALTH CONSIDERATIONS
Patients who experience gastric reflux disease complain of dysgeusia (foul taste), dental sensitivity, erosion and/or pulpitis. Dental sensitivity is generally due to the erosion of enamel by gastric acid. Erosion leads to dentin sensitivity and, at times, irreversible pulpal involvement. Patients who exhibit signs of reflux disease must be medically evaluated and referred appropriately. Patients who have a diagnosis of GERD may need to be treated in a semisupine position and premedicated with H2 receptor antagonists or antacids. Any medications that may cause nausea (such as narcotic analgesics) should be prescribed judiciously because of the increased likelihood of regurgitation and possible aspiration. Mild baking soda mouth rinses (one half teaspoon of sodium bicarbonate in 8 ounces of water) may be rinsed and expectorated to minimize dysgeusia due to acid reflux. Topical fluoride applications via a custom-made occlusive tray will ensure optimal dental mineralization. H2 receptor antagonists may cause central nervous system (CNS) effects in a continuum from fatigue and lethargy to confusion, delirium, and seizures. These effects are dose dependent; thus, they may be seen more commonly in elderly persons or in those with impaired kidney or liver function. Patients who are taking cimetidine may experience a toxic reaction to lidocaine if injected intravascularly. Cimetidine also has been shown to inhibit the absorption (and therefore, the blood concentration) of the systemic antifungal drug ketaconazole. Soft-tissue changes such as esophageal fibrosis and stricture may complicate intubation if the patient requires general anesthesia. Oral mucosal changes are minimal; however, erythema and mucosal atrophy may be present as a result of the exposure of tissues to acid.
DUODENAL ULCER DISEASE, PEPTIC ULCER DISEASE
Oral Health Considerations.
If a patient presents with symptoms of epigastric pain, as described previously, the dentist should refer this person to the primary care physician for diagnostic work-up. Oral manifestations of peptic ulcer disease are rare unless there is anemia from gastrointestinal bleeding or persistent regurgitation of gastric acid as a pyloric stenosis leading to dental erosion, typically of the palatal aspect of the maxillary teeth. Vascular malformations of the lip have been reported and range from a very small maculae to a large venous pool. The dentist will often see patients with a history of peptic ulcer disease. To prevent the aggravation of the disease in these patients, the avoidance of actions that increase the production of acid is essential. Thus, lengthy dental procedures should be avoided or spread out over shorter appointments to minimize stress. Also, dentists should avoid administering drugs that exacerbate ulceration and cause gastrointestinal distress, such as aspirin and other NSAIDs; acetaminophen products are preferable and are recommended. A patient who reacts to dental procedures in a particularly stressful way may be a candidate for sedation. Dentists should be aware that patients who are taking anticholinergic drugs often present with dry mouth. This may be particularly problematic for denture wearers.
Denture adhesives and artificial saliva may aid in the retention of these prostheses. There is an increased risk of dental caries if hyposalivation is prolonged and if the patient places sugarcontaining items into the mouth in an effort to stimulate saliva flow or uses sugar-ladened antacid lozenges. Therefore, artificial saliva and/or chewing sugarless gum to stimulate salivary flow may help prevent dental caries. Informing the patient of this side effect of anticholinergic drugs and stressing proper diet and oral hygiene are critical for these patients. Additionally, because many antacids contain calcium, magnesium, and aluminum salts that bind antibiotics such as erythromycin and tetracycline, the dentist should be aware that administration of one of these drugs within an hour of antacid therapy may decrease the absorption of the antibiotic by 75 to 85%.Consequently, antibiotics should be taken 2 hours before or 2 hours after ingestion of antacids. Exogenous steroid administration is likely to exacerbate the ulcer because of the increased production of acid caused by the steroid and should be avoided. Although it is generally good policy to prescribe penicillin V instead of penicillin G (because of the destruction of penicillin G by gastric acid), it is essential with patients who have peptic ulcers. Before extensive oral surgical or periodontal procedures are undertaken, it may be prudent to determine the patient’s red blood cell count, hemoglobin, hematocrit, and platelet count. If the patient has a history of ulcer perforation and subsequent hemorrhage, blood loss can result in anemia. Consequently, the associated risks of performing surgery on an anemic patient will be encountered. Delayed healing, risk of bacterial infection (particularly with anaerobic bacteria, due to tissue hypoxia), and grave side effects of respiratory depression by narcotic analgesics enhanced by a state of anemia are examples of such associated risks. Lastly, cimetidine and rantidine, drugs commonly prescribed for duodenal ulcer patients, have occasionally been associated with thrombocytopenia.
ULCERATIVE COLITIS
Oral Health Considerations.
Due to the symptoms of severe frequent diarrhea and abdominal pain or cramping, it is unlikely that a patient will be seeking routine dental care with undiagnosed ulcerative colitis. Nonetheless, should an undiagnosed patient attend a dental office for care, then the risks associated with anemia (such as delayed healing, an increased risk of infection, the side effects of narcotic analgesics, and depression of respiration) collectively contraindicate surgical treatment until the disease is under control. Obviously, following a history and a thorough examination, signs and symptoms of ulcerative colitis and/or anemia would warrant a referral to the patient’s primary care physician. More likely is the situation of a diagnosed and medically managed patient attending a dental office for routine or episodic oral health care. The following section addresses those issues a dentist must be knowledgeable about when treating patients who have ulcerative colitis. The oral changes that occur in ulcerative colitis cases are nonspecific and uncommon, with an incidence of less than 8%. Aphthous stomatitis of the major and minor variety has been reported in patients with active ulcerative colitis. There is nothing unique about these lesions, and it has been suggested that their appearance is coincidental. However, they may result from nutritional deficiencies of iron, folic acid, and vitamin B12 due to poor absorption in the gut and/or blood loss directly related to the ulcerative colitis. In addition, anti-inflammatory medications such as the 5-aminosalicylates which often represent the mainstay of therapy for IBD( inflammatory bowel disease) patients and which are excreted in saliva, are known to cause aphthous ulcers and RAU in some patients. In patients who are prone to develop aphthous ulcers, the appearance of a new crop of oral ulcers often heralds a flare-up of the bowel disease. Other nonspecific forms of ulceration associated with skin lesions have been reported. Pyoderma gangrenosum may occur in the form of deep ulcers that sometimes ulcerate through the tonsillar pillar. Pyostomatitis vegetans, a purulent inflammation of the mouth, may also occur. These oral lesions are characterized by deep-tissue vegetating or proliferative lesions that undergo ulceration and then suppuration. As the lesions disappear with a total colectomy, it is speculated that these manifestations are due to the effects of circulating immunocomplexes induced by antigens that are derived from the gut lumen or the damaged colonic mucosa. Lastly, ulcerative colitis patients also can develop hairy leukoplakia, a lesion more commonly associated with acquired immunodeficiency syndrome (AIDS). This lesion probably serves as a marker of severe immunosuppresion and may result from the use of corticosteroids or other immunosuppressive agents. Medical management for ulcerative colitis may necessitate alterations of dental therapy or special precautions. Sulfasalazine interferes with folate metabolism, and supplemental folic acid may be needed, especially if a macrocytic anemia is revealed in a complete blood count.
Many side effects are associated with the use of corticosteroids and ACTH. The development of hypertension and diabetes are serious side effects for patients who are taking these two drugs and the dentist must be aware of this. Obtaining a blood pressure reading and obtaining a blood glucose measurement by finger prick in the office and/or consultation with the treating physician to understand the patient’s current medical status is critical. Long-term corticosteroid therapy may cause osteoporosis and vertebral compression fractures; thus, carefully positioning the patient in the dental chair and encouraging the patient to take dietary calcium supplements may help prevent fractures. Long-term use of steroids can also result in adrenal suppression. Major operative procedures can precipitate adrenal insufficiency if the steroid doses are not adjusted properly. Patients undergoing surgery require increased doses of steroids before and after the procedure because their own adrenal response to stress is blunted. Patients who were formerly on steroid therapy may also experience adrenal suppression. For example, 20 mg of prednisone daily for 7 to 10 days can cause adrenal suppression, and adrenal activity may not return to normal for 9 to 12 months. Clearly, consultation with the patient’s physician is warranted prior to surgical procedures. Chronic bleeding can be associated with ulcerative colitis. Prior to dental procedures, blood studies that include hemoglobin, hematocrit, and a red blood cell count should be undertaken to rule out the presence of anemia. Further, patients on immunosuppressive agents such as azathioprine might be expected to have changes in white and red blood cell counts, and total and differential white blood cell counts should be ascertained before embarking on surgical procedures. Patients who have extensive bowel surgery may suffer from malabsorption of vitamin K, vitamin B12 , and folic acid. Again, before any surgical procedures are completed, these patients should be evaluated for both macrocytic and microcytic anemia and bleeding disorders from insufficient levels of vitamin K (fibrin clot formation). Clotting factors II, VII, IX, and X are all dependent on Vitamin K. Thus, a prothrombin time and a partial thromboplastin time should be obtained. Alternatively, an international normalized ratio (INR) will also provide critical information about the patient’s ability to form a blood clot. Finally, patients taking the immunosuppressive agent azathioprine may suffer from additional side effects that impact dental management. Suppression of the liver can be expected, and liver function tests should be completed in those patients who will receive dentist-prescribed medications that aremetabolized in the liver. Typically, patients taking an immunosuppressive agent like azathioprine are monitored by their primarycare physician with liver function tests. Consequently, consultation with the patient’s physician will help the dentist determine the patient’s liver function. Obviously, toxic doses of the same drugs may be reached if reduced drug metabolism is not taken into consideration.
CROHN’S DISEASE
Oral Health Considerations
Oral lesions, both symptomatic and asymptomatic, affect 6 to 20% of Crohn’s disease patients. Most oral manifestations of Crohn’s disease occur in patients with active intestinal disease, and their presence frequently correlates with disease activity. Recurrent aphthous ulcers are the most common oral manifestation of Crohn’s disease. It is not clear whether these oral manifestations are true expressions of Crohn’s disease, pre-existing and/or co-incidental findings, direct results of medical treatment, or manifestations of an associated problem such as anemia. Certainly, pyostomatitis vegetans, cobblestone mucosal architecture, and minor salivary gland duct pathology represent granulomatous changes that constitute the hallmark of Crohn’s disease. Biopsy specimens of these multiple small nonhealing aphthous ulcers reveal granulomatous inflammation. Less often, Crohn’s disease patients develop diffuse swelling of the lips and face, inflammatory hyperplasias of the oral mucosa with a cobblestone pattern, indurated polypoid taglike lesions in the vestibule and retromolar pad area, and persistent deep linear ulcerations with hyperplastic margins. Granulomatous lesions have also been observed in the salivary glands, where they may cause rupture of the ducts and localized mucocele formation. Numerous medications, including anti-inflammatory and sulfa-containing preparations that are commonly used to manage IBD patients, have been reported to cause oral lichenoid drug reactions. Superinfection with Candida albicans is often associated with IBD and may represent a primary manifestation of the disorder, a reaction to the bacteriostatic effect of sulfasalazine, or an impaired ability of neutrophils to kill this granuloma-provoking organism. Of interest is the possibility that oral lesions may precede the radiologic changes of the disease by up to 1 year. This underscores the sometimes subtle signs and symptoms of Crohn’s disease and the possibility that a dentist may encounter a patient with undiagnosed Crohn’s disease. Frequently, patients will complain of pain associated with ulcerative lesions in the oral cavity. Palliative rinses, ointment, and topical steroids may be helpful. There appears to be an increased risk of dental caries that is probably related to dietary changes in patients with IBD. The causes of the dental caries and increased incidence of bacterial and fungal infections are multifactorial but appear to be related to either the patient’s altered immune status or diet. Oral effects of malabsorption may also be seen. Pallor angular cheilitis, and glossitis, all oral manifestations of anemia, may occur, particularly in undiagnosed or poorly controlled disease. Nutritional deficiencies that are directly related to the section of the bowel affected by the disease can occur. Malnutrition is often a problem, and monitoring the patient’s compliance with dietary supplementation is essential. As with ulcerative colitis, the medical management of a patient with Crohn’s disease may alter his or her dental management. The following description of dental management is applicable to patients with a diagnosis of IBD. The underlying assumption of this management is that patients with IBD are at increased risk for the development of oral infections, including dental caries. Consequently, dental management of patients with IBD should include the following:
1. Frequent preventive and routine dental care to monitor oral health and to prevent the destruction of hard and soft tissue. If the patient is taking a systemic corticosteroid, monitoring of blood pressure and evaluation of blood glucose is necessary.
2. Evaluation of hypothalamic-pituitary-adrenocortical function, to determine the patient’s ability to undergo extensive dental procedures.
3. Diagnosis of oral inflammatory, infectious, or granulomatous lesions (including performance of a biopsy if necessary).
4. Treatment of oral manifestations of IBD, particularly symptomatic lesions. Palliative rinses and topical steroid therapy ( fluocinonide 0.05%) may be helpful. Topical steroid therapy should be short-term and monitored because of the side effect of mucosal atrophy and systemic absorption.
5. Consultation with the patient’s physician to completely comprehend the medical management of the patient. In particular, knowledge of the effects, side effects, and drug interactions of any medications the patient is taking is essential.
▼DISEASES OF THE HEPATOBILIARY
SYSTEM
Drug-Induced Hepatotoxicity
ORAL HEALTHCONSIDERATIONS
As stated previously, drug-induced liver disease can present as any acute or chronic disorder. Also, since idiosyncratic reactions often have an immunoallergic basis, the patient can present not only with jaundice and other features of chronic liver disease but also with fever, dermatitis, arthralgias, and eosinophilia. Regardless of clinical presentation, referral to the patient’s primary care physician is necessary should the dentist suspect drug-induced hepatotoxicity. It is simplistic to recommend that, since any drug may produce hepatotoxicity, the drug in question should be stopped. Rather, consultation with the physician is necessary to weigh the relative risks of stopping or changing therapy. Fortunately, most of the drugs that dentists might use or prescribe that are known to be hepatotoxic have safe and effective alternatives, and stopping the most likely offending drug is a prudent course of action. Nonetheless, coordination of dental therapy and medical therapy is critical. For example, the alternative agent in the case of NSAID toxicity would be a drug from a different subclass. However, after starting the alternative agent, the patient should be followed for at least 4 to 8 weeks with biochemical tests in order to ensure that the original drug reaction has resolved. Since many drugs produce idiosyncratic drug toxicity, there is no way to predict or prevent such reactions. A patient who experiences an abrupt episode of hepatocellular injury should be considered to have an idiosyncratic drug reaction and should not be challenged again. For patients who take drugs associated with dose-dependent drug reactions, the obvious precaution is to keep the dose to a minimum. Since it is possible to take a toxic dose of acetaminophen without greatly exceeding the recommended doses, patients with chronic pain should be warned of the potential toxicity of acetaminophen. Also, patients who are taking large doses of acetaminophen should be advised to avoid alcohol and to ensure adequate nutrition. Because most drug reactions are hepatocellular and may lead to hepatocyte failure and death, patients with a history of drug-induced hepatotoxicity should be evaluated with serial liver function tests. There may be cell death to the extent that drug metabolism and homeostasis are affected and that the patient’s ability to undergo dental care is significantly affected.
Liver Cirrhosis
MEDICAL ASPECTS
Cirrhosis is neither a single process nor a single disease; rather, it is the end result of a variety of conditions that produce chronic inflammatory change and liver cell injury. The progressive scarring leads to abnormal fibrosis and nodular regeneration. Cirrhosis is a leading cause of death in the
ORAL HEALTH CONSIDERATIONS
Oral findings may be associated with vitamin deficiencies and anemia; these findings include angular cheilitis, glossitis, and mucosal pallor. Yellow pigmentation may be observed on the oral mucosa and may be accompanied by scleral and cutaneous jaundice. Salivary gland dysfunction secondary to Sjögren’s syndrome may be associated with primary biliary cirrhosis. Pigmentation of the oral mucosa is only rarely observed in cases of hemochromatosis. The dental patient who presents with a history of liver cirrhosis deserves special attention. First, patients with cirrhosis may have significant hemostatic defects, both because of an inability to synthesize clotting factors and because of secondary thrombocytopenia. These deficits can be overcome with replacement with fresh frozen plasma and platelets. Therefore, laboratory evaluation prior to any surgical or periodontal procedures should be directed at bleeding parameters; specifically, complete blood count, prothrombin time or INR, partial thromboplastin time, platelet count, and bleeding time values should be obtained. Second, the ability to detoxify substances is also compromised in patients with hepatic insufficiency, and drugs and toxins may accumulate. Patients may become encephalopathic due to an ammonia buildup from the incomplete detoxification of nitrogenous wastes. Patients with encephalopathy are likely to be taking neomycin or lactulose. The use of sedatives and tranquilizers should be avoided in patients with a history of taking encephalopathy narcotics. Additionally, there may be an induction of liver enzymes, leading to a need for increased dosages of certain medications. Consequently, consultation with the patient’s physician is essential to the proper management of the dental patient with liver cirrhosis. The patient with ascites may not be able to fully recline in the dental chair because of increased pressure on abdominal vessels. Lastly, liver transplantation patients who are on immunosuppressive therapy should be monitored for systemic infection of oropharyngeal origin, oral viral infection (herpes simplex virus, Cytomegalovirus), and oral ulcers of unknown origin.
▼GASTROINTESTINAL SYNDROMES
Eating Disorders: Anorexia and Bulimia
ORAL HEALTH CONSIDERATIONS
The cardinal oral manifestation of eating disorders is severe erosion of the enamel on the lingual surfaces of the maxillary teeth. Acids from chronic vomiting are the cause. Examination of the patient’s fingernails may disclose abnormalities related to the use of fingers to initiate purging. Mandibular teeth may be affected but not as severely as the maxillary teeth. Parotid enlargement may develop as a sequela of starvation. Rarely does one observe soft-tissue changes of the oral mucosa because of trauma from gastric acids. The dentist should be aware of a possible eating disorder when these symptoms are encountered and should take steps to arrange for referral to other practitioners. Support of the patient both physically, by treatment of tooth desensitization and esthetics, and psychologically, by demonstrating a caring and compassionate attitude, is a part of the dental practitioner’s treatment responsibility to these patients.
Gardner’s Syndrome
Plummer-Vinson Syndrome
Plummer-Vinson syndrome, originally described as “hysterical dysphagia,” is noted primarily in women in the fourth and fifth decades of life. The hallmark of this disorder is dysphagia resulting from esophageal stricture, causing many patients to have a fear of choking. Patients may present with a lemontinted pallor and with dryness of the skin, spoon-shaped fingernails, koilonychia, and splenomegaly. The oral manifestations are the result of an iron deficiency anemia. Oral findingsinclude atrophic glossitis with erythema or fissuring, angular cheilitis, thinning of the vermilion borders of the lips, and leukoplakia of the tongue. Inspection of the oral mucous membranes will disclose atrophy and hyperkeratinization. These oral changes are similar to those encountered in the pharynx and esophagus. Carcinoma of the upper alimentary tract has been reported in 10 to 30% of patients. Thorough oral, pharyngeal, and esophageal examinations are mandatory to ensure that carcinoma is not present. Artificial saliva may reduce the sensation (and thereby, the fear) of choking.
Peutz-Jeghers Syndrome
Peutz-Jeghers syndrome is characterized by multiple intestinal polyps throughout the gastrointestinal tract but primarily in the small intestine. Malignancies in the gastrointestinal tract and elsewhere in the body have been reported in approximately 10% of patients with this syndrome. Pigmentation (present from birth) of the face, lips, and oral cavity is a hallmark of this syndrome. Interestingly, the facial pigmentation fades later in life although the intraoral mucosal pigmentation persists. No specific oral treatment is necessary.
Cowden’s Syndrome
Cowden’s syndrome (multiple hamartoma and neoplasia syndrome) is an autosomal dominant disease characterized chiefly by facial trichilemmomas, gastrointestinal polyps, breast and thyroid neoplasms, and oral abnormalities. Cowden’s syndrome is considered to be a cutaneous marker of internal malignancies. Pebbly papilloma-like lesions and multiple fibromas may be found widely distributed throughout the oral cavity.
▼DISEASES OF THE
CARDIOVASCULAR SYSTEM
HYPERTENSION
Oral Health Considerations
It is clear that patients with high BP are at increased risk for adverse advents in a dental setting when target organ disease is present. However, the absence of target organ disease does not mitigate a careful evaluation and treatment of patients within safe and appropriate parameters of care. Based on the medical model for assessment, risk stratification, and treatment of patients with hypertension, dental guidelines can be proposed (Table 1).
TABLE 1 Blood Pressure Measurement in the Dental Setting
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Routine BP measurements: |
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-Measure and record at initial visit |
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-Recheck: |
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Every 2 years for patients with BP < 130/85 |
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Every year for patients with BP of 130–139/85–89 |
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Every visit for patients with BP ≥140/90 |
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Every visit for patients with diagnosed hypertension |
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Before initiating dental care: |
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Assess presence of hypertension |
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Determine presence of target organ disease |
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After checking BP, determine treatment modifications |
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Dental treatment for patients with elevated BP: |
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–Asymptomatic, BP < 159/99, no target organ disease |
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No dental modifications needed |
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Can safely be treated in a dental outpatient setting |
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–Asymptomatic, BP = 160–179/100–109, no history of target organ disease |
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Assessment on individual basis with regard to type of dental procedure |
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–BP ≥180/110, no history of target organ disease |
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No elective dental care |
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–Target organ disease or poorly controlled DM |
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Elective dental care only when BP is controlled, preferably < 140/90 |
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BP = blood pressure; DM = diabetes mellitus |
These guidelines do not release the dental practitioner from good clinical judgment, and they should be used in accordance with the dental provider’s knowledge, training, and experience. Oral health care providers also need to be aware of medications that (1) may have systemic side effects that are of importance to the provision of care, (2) interact with medications used during dental care, and (3) cause intraoral changes (see Table 2).
TABLE 2 Common Oral Hypertensive Medications
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Drug Trade Name Side Effects |
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Diuretics ———Increased cholesterol and glucose levels; oral dryness: · Chlorthalidone— Hygroton · Hydrochlorothiazide (HCTZ)— Hydrodiuril, Microzide, Esidrix · Indapamide— Lozol · Metolazone— Mykrox, Zaroxolyn Potassium-sparing agents · Amiloride and HCTZ— Moduretic · Spironolactone— Aldactone · Spironolactone and HCTZ— Aldactizide · Triamterene— Dyrenium · Triamterene and HCTZ— Dyazide · Bumetanide— Bumex · Ethacrynic acid— Edecrin · Furosemide— Lasix · Torsemide— Demadrex |
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Adrenergic inhibitors—— Postural hypertension; nasal congestion; sedation; bradycardia; oral dryness; oral ulcerations |
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Peripheral agents · Guanadrel— Hylorel · Guanethedine monosulfate— Ismelin · Reserpine— Serpasil Central alpha-agonists · Clonidine Catapres · Guanfacine Tenex · Methyldopa Aldomet alpha−Blockers · Doxazosin mesylate— Cardura · Prazosin—- Minipress · Terazosin— Hytrin beta-Blockers · Acebutolol— Sectral · Betaxolol— Kerlone · Bisoprolol fumarate— Zebeta · Carteolol hydrochloride— Cartrol · Metoprolol tartrate— Lopressor · Metoprolol succinate— Torpol-XL · Penbutolol sulfate— Levatol · Propranolol hydrochloride—- Inderal, Inderal LA Combined alpha- and beta-blockers · Carvedilol —Coreg · Labetalol hydrochloride— Normodyne, Trandate Direct vasodilators— Headaches; tachycardia · Hydralazine hydrochloride— Apresoline · Minoxiil |
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Calcium antagonists—- Gingival overgrowth |
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Nondihydropyridines · Diltiazem hydrochloride— Cardizem SR, Cardizem CD, Dilactor XR, Tiazac · Mibefradil dihydrochloride— Posicor Dihydropyridines · Amlodipine besylate— Norvasc · Felodipine— Plendil · Isradipine— DynaCirc, DynaCirc CR · Nifedipine— Procardia XL, Adalat CC · Nisoldipine—- Sular |
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ACE inhibitors——- Cough; loss of taste; lichenoid reactions of the oral mucosa |
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· Benazepril— Lotensin · Captopril— Capoten · Enalapril— Vasotec · Fosinopril— Monopril · Lisinopril— Prinivil, Zestril · Moexipril— Univasc · Perindopril— Aceon · Quinapril— Accupril · Ramipril— Altace · Trandolapril— Mavik |
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Angiotensin II receptor blockers |
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· Candesartan— Atacand · Losartan potassium— Cozaar · Valsartan— Diovan · Irbesartan— Avapro |
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ACE = angiotensin-converting enzyme. |
Oral Health Considerations
Antibiotic prophylaxis should be considered for all patients with valvular heart disease. Oral and dental procedures for which antibiotic prophylaxis is recommended are listed in Table 3.
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TABLE 3 Oral Procedures and Need for Antibiotic Prophylaxis to Minimize Risk of Bacterial Endocarditis |
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Oral Procedures Requiring Antibiotic Prophylaxis |
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*Clinical judgment may indicate antibiotic prophylaxis with any procedure that may result in significant bleeding. |
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· Extractions |
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· Periodontal procedures including surgery, subgingival placements of antibiotic fibers or strips, scaling, and root planning |
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· Placement of subgingival antibiotic fibers or strips |
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· Implant placement |
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· Tooth reimplantation |
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· Placement of orthodontic bands (not brackets) |
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· Endodontic instrumentation (beyond the apex) or surgery |
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· Intraligamentary injections |
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· Prophylactic cleaning of teeth where bleeding is anticipated |
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· Other procedures in which significant bleeding is anticipated |
These guidelines serve as an aid to practitioners but are not intended as a standard of care or a substitute for clinical judgment. According to AHA (American Heart Association) guidelines, antibiotic prophylaxis should be administered to patients who have undergone mitral or aortic valve repair or replacement, patients with a prior history of infective endocarditis, and patients with mitral or aortic regurgitation or stenosis. Patients with MVP(mitral valve prolapse) should receive prophylaxis only if there is valvular regurgitation or thickening of the mitral leaflets. Patients with MVP who do not have valvular regurgitation or thickening of the leaflets do not require antibiotic prophylaxis as the incidence of endocarditis among them is identical to that in the general population. The risk for thromboembolism increases for patients with prosthetic heart valves if anticoagulation therapy is discontinued. It is therefore prudent to continue anticoagulation therapy in patients who require intensive high INR levels.
▼ORAL DISEASES AND DIABETES
Oral conditions that are seen in individuals with diabetes may include burning mouth, altered wound healing, and an increased incidence of infection. Enlargement of the parotid glands and xerostomia can occur; both are conditions that may be related to the metabolic control of the diabetic state. Medications that diabetic patients often take for related or unrelated systemic conditions may have significant xerostomic effects. Thus, the xerostomia seen in individuals with diabetes may result more from medications than from the diabetic condition itself. Neuropathy of the autonomic system can also cause changes in salivary secretion since salivary flow is controlled by the sympathetic and parasympathetic pathways. Dry mucosal surfaces are easily irritated and are associated with“burning mouth” syndrome; they also provide a favorable environment for the growth of fungal organisms. Some studies have shown an increased incidence of oral candidiasis in patients with diabetes whereas other studies have not. The effect of diabetes on the dental caries rate is unclear. Some studies have demonstrated increased caries in people with diabetes, which has been associated with xerostomia or increased gingival crevicular fluid glucose levels. Other studies have shown similar or decreased caries rates in people with diabetes. Since most diabetic individuals limit their intake of fermentable carbohydrates, the less cariogenic diet may limit caries incidence. In recent studies of type 2 diabetic patients and nondiabetic control subjects, no differences were seen in salivary flow rates, organic constituents of saliva, salivary counts of acidogenic bacteria, salivary counts of fungal organisms, or coronal and root caries rates. These findings suggest that diabetic individuals as a group are similar to nondiabetic people in regard to these oral conditions. Periodontal Health and Diabetes Strong evidence suggests that, unlike the conditions discussed above, diabetes is a risk factor for the prevalence and severity of gingivitis and periodontitis. Diabetes is associated with increased gingival inflammation in response to bacterial plaque, but the degree of glycemic control is an important variable in this relationship. In general, well-controlled diabetic individuals and nondiabetic people have similar degrees of gingivitis, with the same level of plaque. Conversely, poorly controlled diabetic subjects have significantly increased gingivitis, compared to either well-controlled diabetic or nondiabetic individuals. In large epidemiologic studies, diabetes has been shown to significantly increase the risk of attachment loss and alveolar bone loss approximately threefold when compared to nondiabetic control subjects. These findings have been confirmed in meta-analyses of multiple studies in various diabetic populations. Diabetes increases not only the prevalence and severity of periodontitis but also the progression of bone loss and attachment loss over time. Periodontitis is similar to the classic complications of diabetes in its variation among individuals. Just as retinopathy, nephropathy, and neuropathy are more likely to be seen in diabetic patients with poor glycemic control, progressive destructive periodontitis is also more common in those with poor control. However, some poorly controlled diabetic patients do not develop significant periodontal destruction, just as some do not develop the classic diabetic complications. Conversely, well-controlled diabetes places the person at a lower risk for periodontal disease, similar to the risk of nondiabetic individuals; yet,well-controlled diabetic patients may still develop periodontitis, just as nondiabetic individuals do. Other risk factors for periodontitis, such as poor oral hygiene and smoking, play a similar deleterious role in both diabetic and nondiabetic individuals. Hyperglycemia results in increased gingival crevicular fluid glucose levels, which may significantly alter periodontal wound-healing events by changing the interaction between cells and their extracellular matrix within the periodontium. Vascular changes seen in the retina, glomerulus, and perineural areas also occur in the periodontium. Theformation of AGEs results in collagen accumulation in the periodontal capillary basement membranes, causing membrane thickening. AGE-stimulated smooth-muscle proliferation increases the thickness of vessel walls. These changes decrease tissue perfusion and oxygenation. AGE-modified collagen in gingival blood vessel walls binds circulating LDL, which is frequently elevated in diabetes, resulting in atheroma formation and further narrowing of the vessel lumen. These changes in the periodontium may dramatically alter the tissue response to periodontal pathogens, resulting in increased tissue destruction and diminished repair potential. Diabetes results in changes in the function of host defense cells such as polymorphonuclear leukocytes (PMNs), monocytes, and macrophages. PMN adherence, chemotaxis, and hagocytosis are impaired. Defects in this first line of defense against periodontopathic microorganisms may significantly increase periodontal destruction. Monocytes and macrophages in diabetic individuals are often hyper-responsive to bacterial antigens. This up-regulation results in a significantly increased production of proinflammatory cytokines and mediators. The net effect of these host defense alterations is an increase in periodontal inflammation, attachment loss, and bone loss. Collagen is the primary structural protein in the periodontium. Changes in collagen metabolism in diabetic individuals contribute to wound-healing alterations and periodontal destruction. The production of matrix metalloproteinases (MMPs) such as collagenase is increased in many diabetic patients. Increased collagenase production readily degrades newly formed collagen. Conversely, AGE modification of existing collagen decreases its solubility. The result of these changes in collagen metabolism is a rapid dissolution of recently synthesized collagen by host collagenase and a preponderance of older AGE-modified collagen. Thus, diabetes induces a shift in the normal homeostatic mechanism by which collagen is formed, stabilized, and eventually turned over; this shift alters healing responses to physical or microbial wounding of the periodontium. Tetracycline antibiotics and chemically modified tetracycline agents reduce host collagenase production and collagen degradation through mechanisms that are independent of their antimicrobial activity. These drugs may have benefits in managing conditions such a periodontitis, arthritis, diabetes, osteoporosis, and others in which collagen metabolism is altered.
DENTAL MANAGEMENT OF THE DIABETIC PATIENT
General Dental Treatment
Overall, diabetic patients respond to most dental treatments similarly to the way nondiabetic patients respond. Responses to therapy depend on many factors that are specific to each individual, including oral hygiene, diet, habits such as tobacco use, proper dental care and follow-up, overall oral health, and metabolic control of diabetes. For example, the diabetic patient with poor oral hygiene, a history of smoking, infrequent dental visits, and a high fermentable-carbohydrate intake is more likely to experience oral diseases such as caries and periodontitis and to respond poorly to dental treatment than a diabetic patient without these factors. Glycemic control appears to play an important role in the response to periodontal therapy. Well-controlled diabetic patients with periodontitis have positive responses to nonsurgical therapy, periodontal surgery, and maintenance that are similar to those of people without diabetes. However, poorly controlled diabetic patients respond much less favorably, and short-term improvements in periodontal health are frequently followed by regression and by recurrence of disease. It is imperative that the dental practitioner have a clear understanding of each diabetic patient’s level of glycemic control prior to initiating treatment. Patients may present to the dental office with oral conditions that suggest an undiagnosed diabetic state. An example is severe rapidly progressing periodontitis that exceeds what would be expected given the patient’s age, habit history, oral hygiene, and level of local factors (plaque, calculus) (Figures 1 and 2).
FIGURE 1
Radiograph of area 18-19 in a 35-year-old male with a 4-year history of type 1 diabetes. The patient had generalized moderate plaque levels but minimal alveolar bone loss. He rarely used dental floss. Widening of the periodontal ligament (space 18) was due to occlusal trauma, which was treated by occlusal adjustment.
FIGURE 2
Radiograph of area 18-19 in the same patient shown in
Figure 21-1 at 39 years of age and with an 8-year history of poorly controlled
type 1 diabetes (HbA1c values were 10.2 to 11.3%). There is a rapid progression
of bone loss, the severity of which exceeds that expected from
plaque and calculus levels.
Other findings seen in some undiagnosed diabetic patients include enlarged gingival tissues that bleed easily upon manipulation and the presence of multiple periodontal abscesses (Figures 3, 4, and 5).
FIGURE 4
Palatal view of the maxillary right sextant in the same
patient shown in Figure 3. An abscess can be noted on the palatal aspect
of tooth 2.
FIGURE 3
Lingual view of mandibular incisors of a 60-year-old
female with poorly controlled type 2 diabetes. The HbA1c value at initial
examination was 13.9%. Multiple periodontal abscesses (teeth 22, 23, 25,
26, and 27) with severe inflammation and bone loss can be seen
.
FIGURE-5
Radiograph of the same sextant shown in Figure 4.
Severe bone loss can be noted on tooth 2.
If the clinician suspects an undiagnosed diabetic state, the patient should be questioned to elicit a history of polydipsia, polyuria, polyphagia, or unexplained weight loss (see Table 4).
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TABLE 4 Signs and Symptoms of Undiagnosed Diabetes |
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Polydipsia (excessive thirst) |
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Polyuria (excessive urination) |
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Polyphagia (excessive hunger) |
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Unexplained weight loss |
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Changes in vision |
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Weakness, malaise |
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Irritability |
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Nausea |
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Dry mouth |
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Ketoacidosis* |
*Ketoacidosis is usually associated with severe hyperglycemia and occurs primarily
in type 1 diabetes.
The patient should be questioned about a family history of diabetes. If diabetes is suspected, laboratory evaluation
and physician referral are indicated (see Table 5).
TABLE 5 Laboratory Diagnostic Criteria for Diabetes
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Diagnosis is by any of the following three methods and must be confirmed on a subsequent day by any one of the same three methods. |
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1. Presence of diabetes symptoms plus casual (nonfasting) plasma glucose ≥200 mg/dL (casual glucose may be drawn at any time of day without regard to time since last meal) |
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2. Fasting plasma glucose* ≥126 mg/dL (fasting is defined as no caloric intake for at least 8 hours) |
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3. Two-hour postprandial glucose† ≥200 mg/dL during an oral glucose tolerance test using a glucose load containing the equivalent of 75 g of anhydrous glucose dissolved in water‡ |
*Categories of fasting plasma glucose are as follows: < 110 mg/dL = normal; ≥110 mg/dL and < 126 mg/dL = impaired; ≥126 mg/dL = provisional diagnosis of diabetes (must be confirmed on a subsequent day, as described above).
†Categories of 2-hour postprandial glucose are as follows: < 140 mg/dL = normal glucose tolerance; ≥140 mg/dL and < 200 mg/dL = impaired glucose tolerance; ≥200 mg/dL = provisional diagnosis of diabetes (must be confirmed on subsequent day, as described above).
‡This method is not recommended for routine use.
A patient with previously diagnosed but poorly controlled diabetes may present with oral findings similar to those of the undiagnosed diabetic individual. The dental practitioner must establish the level of glycemic control early in the treatment process; this can be done by physician referral or by a review of the patient’s medical records. Patients who perform SBGM may be asked to bring their glucose log to the dental office for review by the dental team. The clinician should determine the patient’s recent glycated hemoglobin values since this test provides a measure of glycemic control over the preceding 2 to 3 months. HbA1c values of less than 8% indicate relatively good glycemic control; values greater than 10% indicate poor control.
Physician referral is appropriate any time glycemic control is in question. The issue of glycemic control should be addressed often by the dental team since dental treatment outcomes may be dependent partly on good metabolic control of the underlying diabetic state. Other key dental treatment considerations for diabetic patients include stress reduction, treatment setting, and the use of antibiotics, diet modification, appointment timing, changes in medication regimens, and the management of emergencies. Endogenous production of epinephrine and cortisol increase during stressful situations. These hormones elevate blood glucose levels and interfere with glycemic control.
Adequate pain control and stress reduction are therefore important in treating diabetic patients. Profound anesthesia reduces pain and minimizes endogenous epinephrine release. The small amounts of epinephrine in dental local anesthetics at 1/100,000 concentration have no significant effect on blood glucose. Conscious sedation should be considered for extremely anxious patients. Most practitioners who use intravenous sedation elect to use fluids without dextrose, such as normal saline. However, fluids such as D5W (a 5% solution of dextrose in water) in small amounts should not produce wide fluctuations in glycemia in most patients. Most diabetic patients can easily be managed on an outpatient basis in the dental office. Patients with very poor glycemic control, severe head and neck infections, other systemic diseases or complications, and dental-treatment needs that will require long-term alteration of medication regimens or diet may be considered for treatment in a more controlled medical environment. The use of systemic antibiotics for routine dental treatment is not necessary for most diabetic patients. Antibiotics may be considered in the presence of acute infection. Some clinicians prefer to prescribe prophylactic antibiotic coverage prior to surgical therapy if the diabetic patient’s glycemic control is poor. This usually applies to emergency situations since elective procedures are generally deferred until glycemic control improves. In patients with severe periodontitis, adjunctive use of tetracycline antibiotics in conjunction with mechanical periodontal therapy may have beneficial effects on glycemic control as well as on periodontal status. Dental treatment can result in postoperative discomfort. This may necessitate changes in the diet, especially in cases of extensive dental therapy. Because diet is a major component of diabetes management, diet alterations that are made because of dental treatment may have a major impact on the patient. Whereas some patients are very knowledgeable about their diabetic condition and can adjust for changes in diet, this may not be the case with others. The clinician may need to consult the patient’s physician prior to therapy, to discuss diet modifications and required changes in medication regimens. Another diet change occurs when patients are placed on orders to take nothing by mouth (NPO) before dental treatment, a common recommendation before conscious sedation. Consultation with the patient’s physician may be needed to adjust the dose of insulin or oral agents in this situation; however, some patients are able to make these adjustments themselves. Physicians often recommend reducing the insulin dose that immediately precedes lengthy or extensive dental procedures. Appointment timing for the diabetic patient is often determined by the individual’s medication regimen. Conventional wisdom holds that diabetic patients, like other medically compromised individuals, should receive dental treatment in the morning. While this may be true for some patients, it is not true for others. It is generally best to plan dental treatment to occur either before or after periods of peak insulin activity. This reduces the risk of perioperative hypoglycemic reactions, which occur most often during peak insulin activity. For those who take insulin, the greatest risk of hypoglycemia will thus occur about 30 to 90 minutes after injecting lispro insulin, 2 to 3 hours after regular insulin, and 4 to 10 hours after NPH or Lente insulin. For those who are taking oral sulfonylureas, peak insulin activity depends on the individual drug taken. Metformin and the thiazolidinediones rarely cause hypoglycemia. The main factor to consider in determining appointment times is the peak action of insulin and the amount of glucose being absorbed from the gut following the last food intake The greatest risk would occur in a patient who has taken the usual amount of insulin or oral agent but has reduced or eliminated a meal prior to dental treatment. For example, if the patient takes the usual dose of regular insulin before breakfast but then fails to eat or eats less than the usual amount, the patient will be at increased risk for hypoglycemia during a morning dental appointment. Patients with good long-term glycemic control and patients with a previous history of severe hypoglycemic episodes are at greater risk for future hypoglycemia. Often, it is not possible to plan dental treatment so as to avoid peak insulin activity. This is particularly true for patients who take frequent insulin injections. In these instances, the clinician must be aware that the patient is at risk for perioperative hypoglycemia. It is helpful to check the pretreatment blood glucose level (using the patient’s glucometer) and to have a source of carbohydrates readily available. When treating patients with a history of asthma or angina, dentists usually have the patients bring their inhaler or nitroglycerine with them to dental appointments. In the same way, diabetic patients should be encouraged to bring their glucometer with them to the dental office. Before dental treatment begins, the patient may check his or her blood glucose. If the level is near the lower end of the normal range, a small amount of pretreatment carbohydrate may prevent hypoglycemia during the appointment. Having the glucometer available also allows rapid determination of blood glucose levels should the patient experience signs and symptoms of hypoglycemia.
CONCLUSION
Diabetes mellitus is a metabolic condition affecting multiple organ systems. The oral cavity frequently undergoes changes that are related to the diabetic condition, and oral infections may adversely affect metabolic control of the diabetic state. The mechanisms underlie the oral effects of diabetes share many similarities with the mechanisms that are responsible for the classic diabetic complications. The intimate relationship between oral health and systemic health in individuals with diabetes suggests a need for increased interaction between the dental and medical professionals who are charged with the management of these patients. Oral health assessment and treatment should become as common as the eye, foot, and kidney evaluations that are routinely performed as part of preventive medical therapies. Dental professionals with a thorough understanding of current medical treatment regimens and the implications of diabetes on dental care are able to help their diabetic patients achieve and maintain the best possibleoral health.
Diabetes mellitus presented with an ulcerating rash
A 63-year-old woman with a 4 1/2-year history of diabetes mellitus presented with an ulcerating rash, primarily on the shins, groin, and face (Panel A); cheilitis (Panel B); and glossitis. Her symptoms had been worsening for 4 years despite specialized wound care. In addition, she noted concurrent weight loss, depression, abdominal pain, and intractable nausea. She was taking 500 mg of metformin daily. Given her history of diabetes mellitus and the skin findings, abdominal computed tomography was performed, and glucagon levels were measured. An enhancing, lobulated mass measuring 7 cm in diameter was found in the tail of the pancreas, and the patient’s fasting glucagon level was elevated, at 890 pg per milliliter (normal range, 0 to 80). The mass was resected, and pathological examination of the specimen confirmed a diagnosis of glucagonoma. Glucagonomas are rare neuroendocrine tumors that can cause diabetes and a rash known as necrolytic migratory erythema, which has a characteristic annular pattern of erythema with central crusting and bullae. The prognosis correlates with the stage of tumor development and the potential for resection. In this patient, 1 day after resection, the rash had faded significantly. Four weeks after discharge, the patient had normal glucose levels (while taking no medication), and the necrolytic migratory erythemahad completely resolved
ENDOCRINE DISEASE
▼ADRENAL DISEASES AND CONDITIONS
Patients with ACTH (adrenocorticotrophic hormone)-secreting pituitary tumors have Cushing’s disease whereas those with similar symptoms (central obesity, cutaneous atrophy, easy bruising,muscle wasting, osteoporosis, hypertension, diabetes mellitus, immunosuppression, and psychiatric symptoms) from iatrogenic glucocorticoids, from adrenal tumors, or from ectopic secretion of ACTH have Cushing’s syndrome. Cushing’s disease is rare and occurs five times more often in women than in men, with a peak incidence between 20 to 50 years of age. Rarely, ectopic production of ACTH occurs, usually in a malignant tumor of pulmonary origin, leading to the classic symptoms of Cushing’s syndrome.
Oral Health Considerations
HEMOSTASIS
Patients who are on chronic glucocorticoid therapy have decreases in subcutaneous collagen and the production of other extracellular proteins by fibroblasts. This lack of collagen fibrils and other proteins has been postulated to explain the tendency of patients with Cushing’s syndrome to bleed and to bruise easily. There may also be related defects in the walls of small blood vessels, resulting in defective constriction of these vessels during bleeding. Wound healing is also impaired, and scar formation is less timely and less vigorous than in a normal subject.
SUSCEPTIBILITY TO INFECTION
Patients who are on chronic glucocorticoid therapy are considered to be immunocompromised and more thaormally susceptible to infection. Antibiotic prophylaxis is decided on the basis of the underlying disease, however, and not on the basis of glucocorticoid therapy. Patients with Cushing’s syndrome are also more likely to have Candida and fungal infections, possibly due to abnormal flora on the skin and mucosa.
DRUG ACTIONS AND INTERACTIONS
Drug actions and interactions have been described in the above section that deals with the iatrogenic origin of most cases of Cushing’s syndrome seen by the oral health care practitioner. The severe effects of adrenal insufficiency, which can be caused by previous or coexistent glucocorticoid therapy in the pres-ence of stress, infection, or an invasive surgical procedure, are the likely consequence of not recognizing this syndrome.
ABILITY TO WITHSTAND DENTAL CARE
The stable patient with chronic inflammatory disease who is receiving low-dose glucocorticoid therapy will withstand
dental care well as long as the potential consequences of adrenal insufficiency are avoided. Those patients on higher doses of glucocorticoids often exhibit the signs and symptoms of Cushing’s syndrome and are thus subject to difficulties with wound healing and to minor difficulties with hemostasis and immunosuppression that may complicate oral health care delivery.
▼THYROID DISEASE
After diabetes mellitus, thyroid disease is the most common endocrine problem in the general population. Many signs and symptoms of thyroid disease are observable during examination of the orofacial complex. Furthermore, under- or overactivity of the thyroid gland can cause life-threatening cardiac events. Consequently, the dental practitioner must be knowledgeable about thyroid pathophysiology and the treatment of thyroid conditions. Thyroid diseases often require long-term treatment, are frequently intermittent diseases, and worsen during life stresses such as childbirth or depression. Thyroid diseases occur more often in women and most often in women older than 50 years of age. It has been estimated that the lifetime risk of thyrotoxicosis (eg, clinically significant hyperfunction of the thyroid gland) is 5% for women and 1% for men. Routine screening for thyroid disease in an older (> 50 years of age) population of women will detect an unsuspected symptomatic thyroid dysfunction in 1 in 71 women. For adults, the most common signs and symptoms of hyperthyroidism and hypothyroidism are shown in Table 6. The signs and symptoms of hyperthyroidism are the result of increased secretion of T4 by the thyroid gland, but many are identical to the signs and symptoms of anxiety. In the dental patient in pain, signs of hyperthyroidism may coexist with and exacerbate the patient’s normal response to pain and anxiety. In addition, routine examination of the head and neck may disclose signs of thyroid disease, including changes in oculomotor function, protrusion of the eyes, excess sweating, enlargement of the thyroid or the tongue, lingual thyroid tissue, and difficulty in swallowing. Treatment of thyroid disease can accelerate the protrusion of the eyes and can cause agranulocytosis. Atrial fibrillation, increasing thyroid size, and swings in thyroid hormone levels to symptomatic hypothyroid or hyperthyroid status are also possible during medical therapy for underlying thyroid disease.
TABLE 6 Signs and Symptoms of Hyperthyroidism and Hypothyroidism
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Hyperthyroidism Hypothyroidism |
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Anxious appearance Lethargic appearance |
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Tachycardia Low hoarse voice |
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Excess sweating Slow pulse rate |
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Warm moist skin Dry skin |
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Heat intolerance Cold intolerance |
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Atrial fibrillation Elevated blood cholesterol levels |
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Muscle wasting Increase of subcutaneous tissue |
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Goiter Goiter |
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Fine tremor of outstretched hands Decreased hearing |
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Some weight loss Some weight gain |
Oral Health Considerations
In hyperthyroidism, exophthalmoses, goiter, lid lag, and oculomotor defects are seen. Facial myxedema, an enlarged tongue, and a hoarse voice are observed in the hypothyroid state.
HEMOSTASIS
Patients with hyperthyroidism may have elevated blood pressure and heart rates on the basis of the effects of thyroid hormone on sympathetic nervous system activity. Patients with high arteriolar pressures may require increased attention and a longer duration of local pressure to stop bleeding. Hyperthyroidism patients who are on warfarin (Coumadin) may have an increased metabolism of this drug, leading to decreases in previously therapeutic coagulation indices. Patients with long-standing hypothyroidism may have increased subcutaneous mucopolysaccharides due to decreases in the degradation of these substances. The presence of excess subcutaneous mucopolysaccharides may decrease the ability of small vessels to constrict when cut and may result in increased bleeding from the infiltrated tissues, including mucosa and skin. Local pressure for an extended time will probably adequately control the small-vessel bleeding.
SUSCEPTIBILITY TO INFECTIONS
Patients with hypothyroidism may have delayed wound healing due to decreased metabolic activity in fibroblasts. Delayed wound healing may be associated with an increased risk for infection because of the longer exposure of the unhealed tissue to pathogenic organisms. Hypothyroid patients are not considered to be immunocompromised.
DRUG ACTIONS AND INTERACTIONS
Drug interactions may result from the increased metabolic rate associated with hyperthyroidism or the decreased metabolic rate associated with hypothyroidism. Well-controlled hyperthyroidism and hypothyroidism should not present an excess risk to the patient undergoing dental care. A complete history and physical examination of the patient with thyroid disease is necessary to define the particular thyroid disease and determine the stability of the individual patient. Consultation with the physician of the patient at risk is advised when history and physical examination indicate undiagnosed, untreated, or unstable disease.
Information was prepared by Matsko N.V.
