#39564: Dental Considerations for Older Adult Patients

The goals for the management of hypertension are to lower the blood pressure to a range in which the cardiovascular risks are decreased and to minimize the side effects of any medications utilized. Lifestyle modifications are the cornerstone to management of hypertension, and pharmacotherapeutic regimens may supplement these changes. Risk factors such as smoking, a high-sodium diet, excessive weight, and a lack of physical activity are all modifiable items that patients can change to lower their blood pressure and their overall risk for cardiovascular disease. Some studies found interventions for periodontitis could help in controlling hypertension [24].

Some patients become noncompliant with antihypertensive therapy as a result of problematic side effects. Further, patients who do not have symptoms of high blood pressure may consider such therapy of minimal benefit.

Numerous medications are used in the treatment of hypertension. The degree of blood pressure elevation will dictate the type of medication used, either individually or in combination with other agents, to achieve therapeutic goals.

Most dental treatment and many medical procedures are performed with the patient in a reclined position. Upon the conclusion of an appointment and the resumption of a sitting or standing position, orthostatic hypotension can occur with any patient, but especially those taking blood pressure medications. Fainting and potential injury can occur. The incidence of orthostatic hypotension can be minimized by raising the chair gradually and allowing the patient to remain in an upright seated position for some time before attempting to stand. A staff member should be ready to assist the patient if necessary.

Diuretics

Diuretics are one of the primary agents available to treat hypertension [20]. Diuretics are a group of drugs that decrease blood pressure by decreasing the resorption of sodium, chloride, or both, within the kidneys. Along with the decrease in resorption of these elements is a decrease of the resorption of water. This leads to decreased extracellular volume and cardiac output, with a resultant decrease in blood pressure.

There are several different types of diuretics. Hydrochlorothiazide, a thiazide diuretic, acts to increase sodium and water excretion in the distal tubules of the kidneys. This medication and other thiazides can also decrease the plasma concentration of potassium, which can lead to arrhythmias. A potassium supplement may be needed.

Loop diuretics, such as furosemide, inhibit resorption of sodium and chloride in the ascending loop of Henle and distal renal tubule within the kidneys. The increased excretion of water will achieve the same therapeutic goal as hydrochlorothiazide. Medications within this category have been used in the management of treatment-resistant hypertension. Potassium-sparing diuretics, such as spironolactone, work at the kidney's distal tubules to increase sodium excretion and minimize the excretion of potassium.

Nonsteroidal anti-inflammatory drugs (NSAIDs) are a group of medications frequently used as an analgesic for dental problems. Ibuprofen and naproxen are commonly used analgesic agents within this category. These medications can decrease the efficacy of any of the thiazide diuretics and should be avoided as dental analgesics for such patients.

Because the principle mechanism by which diuretics work is a decrease in water volume, xerostomia (dry mouth) can develop. This can be a problem for those who wear prostheses, such as dentures or partial dentures, as oral tissues that are less lubricated are more prone to sore spots and ulcerations.

The increase in the frequency of urination (polyuria) that accompanies the use of thiazide diuretics will usually require that the patient be given restroom breaks during longer appointments.

Beta-Adrenergic Blockers (Beta Blockers)

Another group of medications utilized to treat hypertension are beta-adrenergic blockers, more commonly referred to as beta blockers. These medications compete with endogenous epinephrine for available receptor sites, thus diminishing the stimulatory effect. The goal is to prevent the heart from an excessive response to physical strain and emotional stress by decreasing the heart rate and causing dilation of the arterioles in the skeletal muscle and the liver.

Beta blockers such as atenolol and metoprolol are cardioselective in that they selectively bind with beta-1 receptor sites in the cardiac tissue. Propranolol is a non-selective beta blocker and can interact with beta-1 receptors in cardiac tissue and beta-2 receptors within the arterioles of skeletal muscle and the bronchiolar smooth muscle. The cardiac effect is to reduce the rate of firing of the sinoatrial node, which slows conduction through the atrioventricular node. The contractile strength of the heart is reduced as is the pressure with which the blood is pumped. The arterioles are dilated, which causes a decrease in diastolic blood pressure [25].

NSAIDs can decrease the efficacy of these medications. Patients who take propranolol may be more sensitive to the epinephrine used in local anesthetics, resulting in a pronounced increase in blood pressure followed by reflex bradycardia. Anesthetic preparations without vasoconstrictors, such as epinephrine or levonordefrin, are preferable for these patients.

Similar to thiazide diuretics, beta blockers can also cause xerostomia. Use of beta blockers can also result in side effects involving the central nervous system, such as insomnia, depression, and nightmares, which can discourage patients from continuing their use [26]. Healthcare professionals should verify compliance with prescribed medication regimes. Measuring blood pressure for all patients with hypertension before the initiation of any treatment is mandatory.

Angiotensin-Converting Enzyme (ACE) Inhibitors

Angiotensin-converting enzyme (ACE) inhibitors, such as lisinopril and enalapril, prevent the conversion of angiotensin I to angiotensin II, a potent vasoconstrictor. A decrease in vasoconstriction leads to a decrease in blood pressure via decreased peripheral vascular resistance [27]. These medications can be given alone or in combination with other antihypertensive drugs.

As a group, ACE inhibitors are generally well-tolerated by the patients for whom they are prescribed. However, some patients can develop a dry cough that can range from a minor irritation to severe spasms of coughing. Other potential side effects related to the oral tissues include xerostomia, taste alterations, oral ulcerations, and glossitis. These problems subside with discontinuation of the drug.

Calcium Channel Blockers

Calcium channel blockers (e.g., nifedipine) exert their effects by decreasing the entry of calcium into the smooth muscle within arteriolar walls. The ensuing muscular relaxation and vessel dilation causes a reduction in blood pressure. Calcium channel blockers can also cause a decrease in sodium, which decreases water resorption, blood volume, and blood pressure.

A unique oral side effect of nifedipine, seen in approximately 10% of patients, is gingival hyperplasia. This can occur within a few weeks to several months after nifedipine therapy is begun. Gingival tissues should begin to regress after the drug is discontinued, with full resolution in approximately 15 days [26]. However, resuming use of the drug generally results in recurrence of the disorder unless additional steps are taken.

If nifedipine cannot be discontinued, surgical removal of the excessive tissues may be necessary to restore optimal tissue contours. If excellent plaque control is maintained, the hyperplasia usually does not recur [26]. Oral hygiene instructions should be tailored to the degree and location of any area of nifedipine-induced hyperplasia.

The evaluation of a patient's overall health and of any medications being taken, either for hypertension or any other co-existing chronic illnesses, should be undertaken before any dental treatment is initiated. Consultation with the patient's physician may be necessary to establish a parameter in which dental treatment can be performed safely. Patients' stress during dental procedures can cause the release of endogenous epinephrine and norepinephrine, with a commensurate rise in blood pressure. This can be problematic for patients with hypertension, especially those for whom blood pressure is difficult to control. For these patients, profound anesthesia should be achieved, as a procedure perceived as being free of painful stimuli will decrease the amount of endogenous catecholamine release. Oral sedatives that do not interact with any of the patient's prescribed medications and nitrous oxide inhalation sedation can also be used to reduce stress. Extensive oral surgical procedures may need to be done in a hospital setting under general anesthesia. If the pre-procedural blood pressure measurement is high enough to be of concern to the staff, deferral of the procedure may be needed in the interest of patient safety.

Angina is classified according to the degree of cardiac stability with which the patient presents. Stable angina refers to chest pain that occurs infrequently, usually when physical exertion and/or emotional stress cause the metabolic demand of the myocardial tissues to exceed the available supply of oxygenated blood provided by the cardiac circulation. The pain is relieved by a sublingual spray or tablet of nitroglycerin. If the frequency and/or intensity of angina attacks increases when the patient is at rest, unstable angina has developed.

Patients with unstable angina are at increased risk for acute myocardial infarction and arrhythmias, including ventricular tachycardia and fibrillation. Patients with suspected unstable angina should have dental treatment deferred until their cardiac condition is stabilized. A patient with a known history of angina who presents with chest pain that is not relieved by nitroglycerin should be sent to the emergency department.

Another variant of angina pectoris is Prinzmetal angina. Spasms of the coronary artery caused by this type of angina usually occur when the patient is at rest. This type of angina is a manifestation of atherosclerosis, which is caused by atheromatous plaques developing on the inner wall of the coronary arteries. The vessel lumen narrowed in this fashion will result in a decreased flow of oxygenated blood for the cardiac myocardium.

Treatment

Angina pectoris is treated by one or more drugs that aim to decrease cardiac workload and facilitate vasodilation, the result of which is increased perfusion of the myocardium. Some medications used to treat hypertension, including nifedipine, can cause vasodilation of the coronary arteries. Furthermore, beta blockers can decrease the oxygen demand of the myocardium. Immediate-acting nitrates, such as nitroglycerin, are potent direct-acting vasodilators that decrease myocardial workload and commensurate demand for oxygen. Isosorbide dinitrate and isosorbide mononitrate are both extended-acting vasodilators with longer action as compared to the immediate vasodilation effects of nitroglycerin.

When undergoing any medical or dental procedures, patients who are afflicted with angina for whom nitroglycerin has been prescribed should have nitroglycerin with them. This medication should also be a staple of every medical emergency kit. Because the anxiety associated with a medical or dental appointment can precipitate an angina attack, stress reduction techniques may be utilized. Morning appointments are beneficial for cardiac patients as they allow the patient to arrive in a rested condition and preclude their ability to worry throughout the day about a late afternoon appointment.

Before any dental treatment is initiated, the dentist should record the vital signs and discuss any change in the frequency or duration of angina pectoris attacks. If there is a trend toward more frequent and intense angina pectoris attacks, dental treatment should be deferred and the patient should be referred to a cardiologist.

If ACE inhibitors and/or calcium channel blockers are utilized to treat angina, NSAIDs should not be utilized for pain management. Opioid-based analgesics can accentuate the hypotensive effect of nitroglycerin and should be prescribed cautiously or avoided. Epinephrine or levonordefrin, two vasoconstrictors utilized in local anesthetics, should be used sparingly. Dental surgical procedures may need to be done in an outpatient hospital setting.

Nitroglycerin and isosorbide dinitrate can diminish normal salivary flow and cause xerostomia. This problem will resolve when the medications are discontinued.

As noted, ischemic heart disease is common among patients older than 65 years of age, and myocardial infarction is a leading cause of death in this age group [29]. An infarction is defined as a localized area of necrotic tissue that develops when the oxygenation of that tissue is inadequate. Within the myocardium of the heart, this can occur rapidly and without any previous symptoms; the presence of angina does not always precede myocardial infarction. The substernal pain of an acute myocardial infarction can radiate to the left mandible, which may be a presenting symptom.

Because many myocardial infarctions occur without warning, initial treatment is often of an emergency nature. Within the dental office, all staff members should be trained in the current regimens of cardiopulmonary resuscitation. Requirements for offices that provide deeper levels of sedation can require training in advanced cardiac life support as well.

Many states require dental offices to have an automated external defibrillator and also require staff members to be trained in its use. A supply of oxygen, nitroglycerin, chewable aspirin (for a conscious patient), and an analgesic that can be administered intramuscularly are among the core items that should be available in the event of a cardiac emergency. All staff members should have designated assignments in the case of a medical emergency in order to ensure stabilization of the patient. One staff member should have the responsibility of contacting emergency medical services. Additionally, each office should have a protocol to practice simulated medical emergency situations, and all medications utilized for medical emergencies should be routinely inspected to ensure that they have not expired.

A myocardial infarction can have an acute onset, yet the underlying pathophysiologic causes of an infarction may be present for years before the event. The lumen of the coronary arteries can be gradually narrowed by the accumulation of atherosclerotic lesions within the walls, caused by the formation of small cholesterol-containing aggregates, or plaques, in the walls of blood vessels. This also causes the surface texture of the blood vessel to become rough and conducive to the adhesion of platelets. This process of clotting in an undamaged blood vessel is called thrombosis. The clot, or thrombus, impedes the supply of oxygenated blood to the myocardium, and when circulation is diminished enough to cause necrosis of the myocardial cells, a myocardial infarction occurs. Surgical procedures, such as the placement of stents or balloon angioplasty, may be undertaken to widen a lumen narrowed by atherosclerotic plaques and to re-establish circulation appropriate for the metabolic demands of the cardiac tissue.

Hypertension and/or angina may be precursor conditions to myocardial infarction. If a patient is taking medications for these conditions and experiences a myocardial infarction, the drugs are usually continued, although the amount, dose schedule, or agent may be modified. Many patients who experience myocardial infarction are placed on anticoagulant therapy in order to minimize platelet adhesion and blood clot formation within blood vessels.

Anticoagulant Therapy

Anticoagulant medications exert their effects either by modifying platelet function or by interfering with the synthesis of coagulation factors. Aspirin and clopidogrel are examples of medications used in antiplatelet therapy. By contrast, warfarin is an anticoagulant and minimizes coagulation by interfering with the synthesis of vitamin K-dependent clotting factors II, VII, IX, and X within the liver [30].

The most frequently utilized platelet-inhibiting medication for prophylaxis against ischemic heart disease or a cardiovascular or cerebrovascular incident is aspirin [31]. As a single agent or combined with clopidogrel, aspirin acts to prevent the aggregation of platelets and increases bleeding time. Aspirin ultimately interferes with the release of thromboxane A2, a substance that is responsible for platelet aggregation [31]. This effect lasts for the 10-day average life span of any platelet affected. Clopidogrel acts by blocking adenosine diphosphate (ADP) receptors on the platelet membrane, inhibiting platelet aggregation [31].

Prior to any dental treatment, especially oral surgery or periodontal treatment, the reason for which the patient has been placed on anticoagulant therapy should be discerned. If a dental procedure may affect hemostasis, the best route of action should be discussed with the patient's physician. The patient's prothrombin time should be noted. Prothrombin time is reported as an international normalized ratio (INR). The INR is a ratio of the prothrombin time for the patient and a control and is based on a scale of 1.0–5.0 [32]. An INR of 1.0 indicates a patient who clots normally. The target INR of patients who take anticoagulants depends upon the goals of treatment and underlying medical condition and can range from 2.0 to 3.5 [32]. If a surgical procedure is planned, an INR value should be obtained as close to the time of surgery as possible. Higher values are associated with more difficulty in obtaining hemostasis. It is important to determine if the patient's status allows for a temporary discontinuance of anticoagulant medication. In some cases, this is an option. However, the cardiovascular or cerebrovascular status of some patients may preclude the discontinuance of anticoagulant therapy due to the potential risks of a thromboembolic event. Those patients who cannot cease anticoagulant therapy may require that invasive treatment modalities, such as oral surgery, be performed in a hospital environment, especially when numerous teeth are involved. It is imperative that only a cardiologist or primary care physician with knowledge of the patient's condition direct the patient to stop anticoagulant or antiplatelet therapy. Patients should never stop taking anticoagulants on their own volition to expedite the completion of a surgical procedure.

Before any oral surgery or periodontal treatment is begun, compliance with the agreed upon regimen (e.g., discontinuance of anticoagulants) should be verified. Anticoagulant medications can interact with many medications. As noted, many medications prescribed for dental pain, including NSAIDs, can accentuate the anticoagulant effect of clopidogrel and warfarin. Additionally, macrolide antibiotics, such as erythromycin and clarithromycin, can attenuate the anticoagulant effect of clopidogrel but enhance this same activity for warfarin. It is essential that analgesics and/or antibiotics used for dental conditions do not enhance or detract from the intended effect of any anticoagulant medication.

The degree of recovery from a stroke depends upon the area(s) of the brain involved and the extent of neural cells lost. Many patients experience permanent motor, cognitive, and sensory impairment. When the dominant side is affected, the ability to maintain oral hygiene can become an arduous task. Patients may require toothbrushes mounted in special hand grips to facilitate proper cleansing techniques. Flossing devices may be needed to assist in flossing. The assistance of a caregiver may be necessary to maintain ideal oral hygiene. If plaque control becomes problematic, more frequent recall appointments should be considered.

The ability to comprehend and remember instructions related to oral hygiene may be difficult for patients who have suffered a stroke. Written instructions that can be relayed to a family member or caregiver may assist in the ability for stroke victims to maintain oral health. Patients who wear prostheses such as partial dentures or complete dentures may need assistance with their placement and maintenance. Dentists should consult with patients' physicians when oral surgery or periodontal therapy is necessary. Blood pressure levels should be recorded before the start of any dental procedure, and treatments should be deferred if these levels are elevated.

Because hypertension is a contributing factor to the development of cerebrovascular accidents, many patients who have had a stroke take medication for the condition. Anticoagulant medications may also be used if a thromboembolic event was the precipitating event. The impact of these medications on oral health and the delivery of oral care have been discussed in this course.

Varied formulations of insulin are used to treat type 1 diabetes; type 2 diabetes is often managed with oral hypoglycemic agents, which may or may not be supplemented with insulin.

As a hormone, insulin is the only compound that lowers blood glucose levels. Insulin acts by hastening the transport of glucose into the cells, particularly skeletal muscle cells, and stimulating the formation of glycogen, the storage form of glucose, in the cells of the liver and skeletal muscle. It also decreases the rate by which glycogen is converted into glucose. The dosage schedule of insulin will depend upon the degree of hyperglycemia experienced by the patient.

Insulin is compatible with most medications prescribed for dental problems. However, there are some medications that may result in untoward effects. Extended doses of NSAIDs and salicylates can enhance the hypoglycemic effect of insulin and should be used sparingly. Epinephrine can decrease the hypoglycemic effect of insulin, and the minimum possible dose should be used in conjunction with local anesthetics [37]. Extensive surgical cases, such as full-mouth extractions, may need to be completed in a hospital environment, especially for patients with type 1 diabetes with uncontrolled blood glucose levels.

Metformin, a biguanide oral hypoglycemic agent, may be used in patients with type 2 diabetes to decrease glucose release and production and to reduce insulin resistance of the liver cells [38]. Another agent used in the management of type 2 diabetes, rosiglitazone, improves the target cell response to insulin without increasing the beta-cell production of insulin [39]. Due to findings of an increased risk of stroke and heart attack, in 2010 the U.S. Food and Drug Administration (FDA) recommended rosiglitazone be used only if all other medications are ineffective in controlling diabetes [40]. However, following review of data from a large, long-term clinical trial and a re-evaluation of the elevated risk of heart attack, the FDA removed the prescribing and dispensing restrictions for rosiglitazone in 2013 [41]. Sulfonylurea oral hypoglycemic agents, such as glyburide, act by stimulating the release of insulin from the pancreatic beta cells and by reducing hepatic glucose production; the response of peripheral target cells to insulin is also heightened [26]. Metformin and rosiglitazone have no reported interactions with medications used for dental treatment. Due to the action of glyburide, an increase in hypoglycemic effect similar to the reaction with insulin may be noted with extended concomitant use of NSAIDs and salicylates. Similarly, the tablet form of the antifungal agent ketoconazole, which is used for some cases of oral candidiasis, can also enhance glyburide's hypoglycemic effect.

Diabetes is a treatable disease, but it is not curable. Patients who exhibit good glycemic control can usually tolerate dental treatment. Further, studies showed that periodontal therapy combined with good home oral health care was effective in improving glycemic control for patients with type 2 diabetes in 3 to 4 months [42]. However, one complication that may arise when treating patients with diabetes is hypoglycemia. This can occur when patients take the prescribed dose of insulin and/or oral hypoglycemic agent and eat either minimally or not at all prior to their dental appointment. Before dental treatment is initiated for patients with diabetes, it is important to verify that they have taken their prescribed dose of medication and have eaten appropriately. Even with these precautions, hypoglycemia may still develop. Initial signs of a hypoglycemic crisis can include hunger, sweating, pallor, tachycardia, and tremors. This can progress very rapidly to incoherence, disorientation, and unconsciousness. It is important to treat patients immediately at the onset of symptoms of insulin shock. Glucose (in paste form) or sugar-containing beverages can be given to conscious patients. Patients who have lapsed into unconsciousness may require intravenous glucose or an injection of glucagon; emergency medical services must be contacted. After the patient is stabilized, any remaining dental treatment should be deferred until after consultation with the patient's physician.

Patients with diabetes should be given specific instructions to avoid insulin shock. Patients who have extensive oral surgery or placement of prostheses may have difficulty eating for several days. A pureed or liquefied diet can be planned in order to maintain appropriate blood glucose levels. Adjustments in the dosage of insulin or hypoglycemic medications should only be made by a physician.

Patients with diabetes are vulnerable to the same odontogenic infections as those unaffected by the disease. However, the effects may be greater among patients with diabetes. Diabetes increases the incidence and progression of periodontitis by 86% [43]. The generalized systemic defense against infections causes an increased metabolic demand, with a commensurate increase in the need for glucose to provide the energy source. Therefore, patients with type 1 diabetes with infections may require increased insulin dosages. Patients with type 2 diabetes, alternatively, may require temporary supplementation with insulin until the infection is resolved.

Patients with chronic poor glycemic control may be immunocompromised as a result of problems with neutrophil dysfunction, T-lymphocyte dysfunction, and decreased bactericidal activity of immune system cells [44]. Problems related to immunosuppression can also increase the risk of developing oral candidiasis, aphthous ulcers (canker sores), and oral lichen planus [45]. Infections in all patients with diabetes should be treated aggressively, and some within this group may require intravenous antibiotics and even hospitalization.

Gingivitis, periodontal disease, and alveolar bone loss occur with increased frequency in patients with diabetes with poor glycemic control [46]. Variances in the host response to periodontal pathogens and the production of collagen along with diabetes-associated vascularity problems may contribute to the heightened prevalence of the spectrum of periodontal problems in this patient population [47].

It is important to stabilize patients with diabetes and chronic periodontal problems as mounting evidence demonstrates a correlation between poor glycemic control and periodontal pathology [48]. If periodontal problems cannot be rectified by nonsurgical and/or surgical periodontal therapy, extractions may be necessary. Patients with generalized periodontal problems who are not motivated to maintain optimal oral hygiene may require drastic interventions, including full-mouth extractions and the placement of dentures. Dental treatment for patients with diabetes should be done in a way that does not compromise their ability to maintain glycemic control.

Consultations with the interdisciplinary healthcare team should be made if there is doubt about the ability of a patient with diabetes to withstand any form of dental treatment. Referral to an oral surgeon with hospital privileges may be necessary for patients with poor control of their diabetes for whom oral surgery is planned. The goal of maintaining optimal oral health amidst proper diabetic control should be shared by the patient and by the allied healthcare professionals involved in his or her care.

Surgical excision of oral malignancies consists of removal of the lesion, the adjacent tissues, and any lymph nodes suspected of being involved in the metastasis of cancerous cells. As noted, most lesions are diagnosed in advanced stages, requiring extensive surgery to remove the tumor and the contiguous tissues damaged by direct growth of the malignancy.

Mucosal, muscular, osseous, and neural tissues can be destroyed by an infiltrating lesion and by the surgery that is used to remove lesions, especially those for which the boundaries are extensive and/or difficult to delineate. Functions as basic as speaking, eating, swallowing, and masticating can become arduous tasks when surgical intervention requires the removal of the muscles, nerves, bone, and supporting connective tissue. Reconstructive surgery may not be successful in restoring the patient to presurgical form and function. Physical therapy may be required to help patients adjust to an oral and maxillofacial environment that functions in a vastly different fashion. In some cases, specialized prostheses may be needed to replace lost teeth, gingival tissues, mucosa, and alveolar bone. Dentures and partial dentures can be difficult to wear by any patient, but the level of difficulty is often magnified for patients with oral cancer who have a substantial loss of supporting tissue. Again, the emphasis should be on the early identification of oral malignancies. This would allow the lesion(s) to be diagnosed and treated in an early stage of development, and the excision could be as conservative as possible.

Surgical excision of an oral malignancy, the affected adjacent tissue, and ipsilateral and contralateral lymph nodes, where applicable, is followed by several sessions of radiation therapy, or radiotherapy. Some malignant cells may remain in tissues in close proximity to the site from which the tumor was removed. Radiotherapy is designed to irradiate the affected area with tumoricidal doses of radiation to kill the remaining malignant cells. Doses of radiation are measured in gray (Gy) or centigray (cGy). The cumulative dose of radiation is dependent upon tumor size and location; doses are fractionated on a daily basis for several weeks. Despite improvements in shielding techniques, radiotherapy will kill healthy cells of any oral structure within the primary beam of radiation. These deleterious effects can be temporary or permanent and can have a profound influence upon the patient's quality of life.

Patients undergoing radiotherapy can experience a wide range of complications within and around the oral and maxillofacial complex. The associated morbidity can vary from annoying to life-threatening. The most common complications will be discussed in the following sections.

Mucositis

Most patients with oral cancer receive a cumulative dose of 66–72 Gy (6,600–7,200 cGy) during radiotherapy [75]. The cumulative radiation dose at which mucositis develops varies, but the majority develop with a dose of 10–30 Gy (1,000–3,000 cGy) [76]. Therefore, most patients with oral cancer will develop mucositis during treatment [77].

Radiation impairs the ability of the basal cell layer to provide new cells for the renewal of the outermost surface of the multi-layered oral epithelium. Because the external surface of the oral epithelium has a lifespan of two to three days, ulcerative mucositis generally develops during the second week of therapy. These ulcerative lesions can vary from singular areas of mild erythema to multiple areas of hemorrhage and necrosis in the deep layers of connective tissue.

Some cases may advance to such severity that the scheduled treatment regimen of radiotherapy should be interrupted until the initial epithelial healing has occurred. Patients with more severe forms of mucositis may be unable to eat, requiring hospitalization to provide intravenous therapy for nutrition, analgesia, and prophylactic antibiotic therapy. Patients who wear dentures or partial dentures may be unable to do so if the supporting tissues have been afflicted with any degree of mucositis. A pureed or liquid diet may be required in order for these patients to maintain adequate nutrition. Oral lesions of mucositis of any degree are potential areas of bacterial, fungal, or viral entry and systemic dissemination of infections.

Mucositis will resolve after radiotherapy is completed, with healing time proportionate to the extent of the lesions [77]. Only emergency dental treatment should be attempted while the patient is undergoing radiotherapy, and even this should be discussed with the patient's oncologist and surgeon.

Treatment for mucositis, as determined by the extent of the lesions, usually involves palliative care with non-narcotic or narcotic analgesics. Oral rinses such as benzydamine hydrochloride can provide limited temporary topical anesthesia for mucositis lesions. Oral rinses work best if they are initiated the day before radiotherapy begins. Patients should rinse, hold the analgesic against the afflicted areas for 30 seconds, then expectorate the excess. This protocol can be repeated three to four times daily, as needed [77]. Viscous lidocaine in a 2% solution may also be used three to four times daily. A dose of 5 cc of this solution is placed in contact with afflicted areas for 30 seconds to 1 minute, followed by the expectoration of any excess. Patients should be cautioned to avoid biting or traumatizing any tissue that is anesthetized; traumatic ulcers can develop and prolong the healing time. Patients with mucositis should be advised to remain on a cooler, softer diet that excludes foods with sharp edges. Hot, spicy, and acidic foods should not be consumed until the mucositis has resolved. Patients should be instructed to maintain optimal oral hygiene [77]. However, alcohol-based mouth rinses should be avoided due to the potential to irritate the lesions of mucositis. Established guidelines for oral care for patients in whom mucositis has developed include twice daily oral assessments (for hospitalized patients) and frequent oral care (i.e., minimum every four hours and at bedtime) that increases in frequency as the severity of mucositis increases [77].

Salivary Gland Problems

The major salivary glands, including the bilateral parotid, submandibular, and sublingual, are very sensitive to ionizing radiation. Damage can occur to these glands with a cumulative dose of 10 Gy (1,000 cGy) radiation. When the cumulative dose of 54 Gy (5,400 cGy) has been reached, the secretory elements of the major salivary glands will have sustained irreversible damage [77]. If the malignancy occurs in the area of the parotid gland, which is a pure serous (watery secretion) gland, shielding techniques may not be able to prevent its subsequent damage. A higher degree of damage to this gland, with a subsequent loss of the serous component of saliva, causes the remaining saliva to be increasingly viscous. Patients with oral malignancies in which the primary beam of radiation minimizes or avoids damage to any or all of these glands are rare.

Unlike mucositis, salivary gland dysfunction, which is associated with higher cumulative doses of radiation, will not resolve after the cessation of radiotherapy. Eating, swallowing, speaking, and enjoying a good quality of life become difficult when the quantity and quality of saliva is diminished.

Serous secretions are important in the lubrication of the tissues. Oral soft tissues become more prone to damage when long-term desiccation occurs. Patients may have difficulty or be unable to wear dental prostheses on tissue that has become inadequately lubricated.

Interventions for xerostomia (dry mouth) include artificial saliva substitutes, frequent sips of water, or cholinergic medications, such as pilocarpine [77]. Unfortunately, cholinergic medications have minimal or no effect on salivary flow when severe damage from higher cumulative doses of radiotherapy has occurred. Immunoglobulins and other compounds present in saliva that support immune functions will have a decreased output and can subject patients to recurring opportunistic infections, such as oral candidiasis. Impaired salivary flow will also cause a decrease in saliva's cleansing action upon the teeth. Further, the ability of salivary components to maintain the pH of saliva as a mild base is altered, which causes the oral environment to become more acidic. This combination of effects can have devastating effect on teeth, resulting in radiation caries [77].

Radiation caries are characterized by a pattern of aggressive progression of dental caries on surfaces of teeth that are usually considered to be at a low risk for caries, such as the buccal (outer) and lingual (inner) surfaces of posterior teeth and the labial (outer) and lingual (inner) surfaces of anterior teeth. The incisal edges of anterior teeth and the cusp tips of the posterior teeth are also at increased risk for these caries. Teeth that are affected in this manner need not have pre-existing decay or existing restorations. Unfortunately, teeth afflicted with radiation caries can be difficult to restore and may eventually need to be extracted.

Osteoradionecrosis

Among the deleterious effects of radiotherapy, the most severe is osteoradionecrosis (ORN). Ionizing radiation can cause deterioration of the vessels that supply oxygenated blood to the bones of the maxillary and mandibular arches. The resultant hypoxia can lead to the necrosis of osseous tissue unable to be protected from the primary beam of radiation. ORN occurs more frequently on the mandibular arch, which has less of a blood supply as compared to the maxillary arch [78].

Risk of ORN is directly related to radiation dose and the volume of tissue irradiated [78]. However, osteoradionecrosis can occur at any time after radiotherapy, and passage of time does not decrease the risk [78,79]. ORN is rare in patients who receive less than 60 Gy radiation therapy. The overall incidence of ORN has decreased from up to 11.8% in the last part of the 20th century to around 3.0% currently. However, the true frequency of ORN is impossible to determine because no mechanism exists for reporting the disease. More valuable than understanding the frequency is understanding the decrease in reparative capacity in tissue exposed to more than 60 Gy radiation [78]. Necrotic pieces of bone, which can have a considerable range in size, often break away from the affected bone and may emerge though the tissues. Small segments of bone can be removed with conservative surgical techniques, but large segments require extensive surgical resection. The development of osteoradionecrosis may be precipitated by trauma to the alveolar bone, as encountered with oral or periodontal surgery, odontogenic infections from periapical or periodontal pathology, or tissue irritation and subsequent ulceration that extends toward the bone. Patients who wear dentures or partial dentures may require the fabrication of new prostheses if this pathologic process dramatically alters the shape of the underlying supporting alveolar bone.