Review of the Complications Associated with Treatment of Oropharyngeal Cancer: A Guide to the Dental Practitioner

Abstract

Objectives

Oropharyngeal cancer (OPC) is the 6^th most common cancer worldwide. Focus on risk factors, improved diagnostic methods and effective management strategies have made it possible to successfully treat OPC. However, the 5-year survival rate has not improved for several years due to multiple treatment complications, tissue morbidity, loss of function and diminished quality of life. Survivors are faced with complications like oral mucositis, hyposalivation, osteoradionecrosis; tissue fibrosis, morbidity from jaw resection; disfigurement and loss of function that further diminish quality of life. The aim of this review is to highlight major complications associated with treatment of OPC via a literature search and review of available options for identification and management of these complications.

Data Sources

Relevant publications on oral complications of OPC therapy were thoroughly reviewed from the literature published between the years 1988 and 2012.

Material and Method

We evaluated reported incidence, prevalence and risk factors for oral complications of chemotherapy and radiotherapy for OPC. The authors conducted electronic search using English language databases namely PubMed Plus, Medline (Pre-Medline and Medline), Cochrane Database of systematic reviews (evidence-based medicine), Dentistry & Oral sciences source, AccessScience, Embase, Evidence-Based Medicine Reviews Multifile, Google Scholar, ISI Journal Citation Reports, Ovid Multi-Database.

Conclusion

We identified the most common complications associated with the treatment of oral cancers. Based on the information gathered, there is evidence that survival of OPC extends beyond eradication of the diseased tissue. Understanding the potential treatment complications and utilizing available resources to prevent and minimize them are important. Caring for OPC survivors should be a multidisciplinary team approach involving the dentist, oncologist, internist and social worker to improve the currently stagnant 5-year survival rate of OPC. More emphasis on improved quality of life after elimination of the cancer will ultimately improve OPC survivorship.

Introduction

Head and neck cancers, especial oropharyngeal cancers (OPC) continue to be major health concerns because oral cancer is the sixth most common cancer worldwide (1, 2). In the United States, about 30,000 new cases of OPC are diagnosed annually and they cause more than 8000 deaths per year. About 26% of new OPC patients do not survive the first year after diagnosis and the 5-year survival rate of 52% has not improved for several years (3). Major public health initiatives on early detection and diagnosis have been beneficial, but there continues to be a need to improve the quality of life of survivors by reducing morbidity and treatment complications.

Several extrinsic and intrinsic risk factors contribute to development of OPC including age, ethnicity, gender, habitual use of tobacco and alcohol and viral infections. Fifty potential carcinogens have been identified in tobacco, making smoking a significant risk factor for oral cancer (4). These carcinogens can alter cellular mechanisms through genetic mutations, cell cycle disruption and altered immune response making smokers 5 to 7 times more susceptible to oral carcinogenesis than non-smokers (5). Acetaldehyde, a metabolite of alcohol, interferes with DNA synthesis and repair (6), while alcohol itself acts as a solvent on the oral mucosa exposing it to potential carcinogens. Habitual use of tobacco and alcohol simultaneously has a synergistic effect resulting in 13-fold increased risk for developing oral cancer compared to either tobacco or alcohol use alone (7).

Majority of OPCs are diagnosed in individuals over 65 years (8) and males are 2 to 4 times more likely to develop oral cancer than women (4). With advancing age, there is a tendency for prolonged exposure of oral tissues to potential carcinogens, and aging cells may be more susceptible to DNA damage (4). There is currently an unusual rise in oral cancer in younger individuals and women without obvious risk factors (9) yet the underlying reasons for this has not been fully clarified. Human papilloma virus (HPV), implicated in the development of oral squamous cell carcinoma, is associated with 30–40% of oral epithelial dysplasia and cancerous lesions (10). The roles played by viruses and exact mechanisms are still not completely clear, but viruses are known to affect host-processing mechanisms such as cell proliferation, invade surrounding host tissues and induce apoptosis (4).

Treatment of OPC is a multifaceted approach. It involves surgery, radiotherapy, chemotherapy or a combination of these, depending on type of cancer, location, and stage of the disease. However, the potential for long-term complications and impact on survivorship like loss of oral function, disfigurement, diminished quality of life and psychosocial outcomes continue to redefine oral cancer management strategies (11). Concomitant treatment complications have a major impact on the currently low 5-year OPC survival rate because survivorship of oral cancer extends beyond eradication of the diseased tissue. In spite of treatment advances, there is still a high rate of acute and chronic oral complications that significantly affect survivorship (12). Caring for OPC survivors during this precarious time is a multidisciplinary approach involving dental professionals, oncologists, internist and social workers. This review highlights the major complications associated with treatment of OPC and the interrelationships between healthcare professionals necessary for optimum care of oral cancer survivors. More emphasis on improved quality of life after elimination of the cancer will ultimately improve oral cancer survivorship.

Data Sources

The search strategies used a combination of controlled vocabulary and free text terms. Electronic search was performed in the following databases: ClinicalTrials.gov, PubMed, Ovid Old Medline, Ovid Medline, Ovid Medline in process, Medline Plus, LILACS, MEDCARIB, BBO + other non-index citations, CINAHL, EBM Reviews, NIH-CRI on Scientific Projects, Index of dissertations and abstracts, EBM Reviews (ACP Journal club, Cochrane Central Register of Controlled Trials, Cochrane Database of Systematic Reviews and Database of Abstracts of Reviews of Effects), ISI WEB, OSTMED and Google Scholar. The words and phrases used were: oral cancer, radiation therapy, oral cavity, chemotherapy, complications, radiation caries, xerostomia, mandible, maxilla, tongue and osteoradionecrosis. The search strategies used a combination of controlled vocabulary and free text terms. Electronic search was performed in the following databases: ClinicalTrials.gov, PubMed, Ovid Old Medline, Ovid Medline, Ovid Medline in process, Medline Plus, LILACS, MEDCARIB, BBO + other non-index citations, CINAHL, EBM Reviews, NIH-CRI on Scientific Projects, Index of dissertations and abstracts, EBM Reviews (ACP Journal club, Cochrane Central Register of Controlled Trials, Cochrane Database of Systematic Reviews and Database of Abstracts of Reviews of Effects), ISI WEB, OSTMED and Google Scholar. The words and phrases used were: oral cancer, radiation therapy, oral cavity, chemotherapy, complications, radiation caries, xerostomia, mandible, maxilla, tongue and osteoradionecrosis.

Study selection

The authors independently reviewed and extracted the data using a checklist. Any disagreement between the authors was discussed and where necessary, a third reviewer was consulted. The types of articles collected fell into the following categories: 1) Case series, 2) Review articles and 3) Randomized controlled trials. After eliminating case reports and editorial, 69 articles were reviewed for data extraction.

Complications Associated with Treatment of Oropharyngeal Cancers

Radiation and chemotherapeutic agents induce significant cellular changes on oral tissues with consequent loss of function (13, 14). These changes may be transient or permanent but often result in long-term repercussions (Table 1). Acute reactions from direct toxicity of treatment persist throughout the duration of treatment but gradually resolve within the first few weeks after completing treatment (15). Chronic complications, however, may be protracted for a significant period resulting in lifelong morbidity. Successful management of these complications often improves the patients’ quality of life.

Table 1.

Complications of Oral Cancer treatment

Organs affected	Chemotherapy	Radiation therapy
Oral mucosa	Infections: fungal, viral, bacterial	Mucositis
Skin		Dermatitis
Teeth	Caries: secondary to hyposalivation	Radiation caries
Jaws/bone	Chemotoxicity Secondary infections Mastication difficulties	Osteoradionecrosis Mastication difficulties
Muscles and soft tissues	Mastication and speech difficulties	Fibrosis, mastication and speech difficulties
TMJ		Fibrosis and trismus
Tongue and taste buds	Taste dysfunction	Taste dysfunction
Salivary glands	Hyposalivation/xerostomia	Hyposalivation/xerostomia (if glands are not-spared)
Others	Pain	Pain Dentofacial abnormalites

Oral complications after chemotherapy, in general, are of shorter duration, usually from a few weeks to a couple of months. After cessation of the radiation therapy, the oral complications tend to be more severe and quite often lead to permanent tissue changes that might lead to more serious chronic complications.

Types of Radiation therapy

The modes of radiation therapy include external beam radiotherapy (Linear accelerators/Betatrons), gamma ray therapy (radium, uranium, cobalt-60), brachytherapy (interstitial irradiation, internal radiotherapy), intraoperative radiotherapy, particle beam radiotherapy (high linear energy transfer radiation) using neutrons, pions and heavy ions and radioimmunotherapy using radiolabeled antibodies.

Chemotherapy

Includes palliative chemotherapy, use of alkylating agents, plant alkaloids, antitumor antibiotics and toposiomerase inhibitors. Chemotherapy can be used to treat cancers that are too large or have spread too far to be treated by surgery alone. The objective in such instances is to slow the growth of the cancer as long as possible and also relieve any symptoms. The drugs that are commonly used for the treatment of cancers are: Cisplatin, 5-fluorouracil (5-FU), carboplatin, paclitaxel, docetaxel, methotrexate, ifisfamide and beomycin. If chemotherapy is given at the same time as radiation, it is referred to as chemoradiation (16).

Oral mucositis

Oral mucositis is an acute reaction associated with radiotherapy, chemotherapy or a combination of both treatments. It is characterized by erythema, mucosal ulceration, oropharyngeal pain, and speech difficulties (Figures 1A and B). Etiologically, it is a direct result of injury to the oral epithelium by several free radicals released by the therapeutic agents; hence limiting the dose and rate of administration can control it (15, 17). Oral mucositis usually develops within 2 weeks of starting either radiotherapy or chemotherapy. A radiation dose of 10–20 Gy can cause mucositis, but significant oral changes beyond the radiation field gradually develops when cumulative doses rise above 30Gy. Additionally, chemotherapeutic agents further cause myelosuppression and inability to resist local factors that often exacerbate the oral lesions (18, 19). While direct contact of radiation with oral epithelium usually results in oral mucositis chemotherapy-induced mucositis depends on patient’s age, degree of stomatotoxicity of the chemotherapeutic agent and preexisting oral conditions (19, 20). Oral mucosa of younger patients have higher mitotic index that increases susceptibility to mucositis, but they also have higher amounts of epithelial-related growth factors that favor a more rapid recovery. Upon completion of therapy, oral mucositis gradually resolves within 3–6 weeks while scarring may develop after healing of radiation-induced lesions (20–22).

Figure 1.

Oral mucositis. Severe generalized oral mucositis (A) and moderate mucositis on lateral border and tongue (B).

Several agents have been used to manage oral mucositis. Cryotherapy by sucking on ice chips before therapy has been used to reduce blood flow and stomatotoxic effects of chemotherapy (23). The use of granulocyte-macrophage colony stimulating factor and granulocyte colony stimulating factor to improve local immune response and use of keratinocyte growth factor to accelerate wound healing have also produced some beneficial effects (24, 25). The goal of management is to minimize pain, reduce secondary infections and improve oral function. Poor oral hygiene, irritation from ill-fitting prosthesis and defective restorations can exacerbate oral ulcerations. Consequently, pre-therapy dental consultation to eliminate these potential risk factors will reduce oral morbidity (19). The use of chlorhexidine gluconate as an antimicrobial rinse may be beneficial by reducing oral microbial load and secondary infection. Topical application of lidocaine, benzocaine, or rinsing the mouth with a solution consisting of diphenhydramine, milk of magnesia, and a local anesthetic have beneficial palliative effects in oral mucositis patients. Benzydamine hydrochloride, a non-steroidal anti-inflammatory rinse with anesthetic and analgesic properties has been used successfully to reduce pain, duration and severity of oral mucositis. However, this product is not yet available in the United States (26). In severe cases, it may be necessary to administer systemic anti-inflammatory agents and opioid analgesics (21).

Infections

The risk for oral infections increases during and after OPC therapy because the oral microbial flora is altered by myelosuppression and the oral cleansing property of saliva is diminished by reduced salivary flow. In addition dormant viral, odontogenic and periodontal infections usually become reactivated to further complicate OPC therapy (27, 28).

Fungal Infections

Candida is a normal oral commensal in 34–68% of healthy individuals; hence, candidiasis is one of the most frequent oral infections during OPC therapy (15, 29). Oral candidiasis presents as a removable white pseudomembrane or erythematous patch on the tongue, palate and labial commissures (Figures 2A – C). It causes taste alterations, mucosal soreness and oral burning sensations. Heavy accumulations of candida may dislodge causing esophagitis, fungemia and pose aspiration risk to the patient. In rare circumstances, more invasive fungal organisms like mucormycosis and aspergillosis may affect myelosuppressed individuals and spread to the underlying bone. Topical antifungal therapy is very effective in reducing oral candidiasis (30). Persistent or systemic spread of fungal infections can be controlled with systemic antifungal treatment. Systemic fungal infections accounts for one third of deaths in immunocompromised patients (30) so it is often necessary to administer prophylactic antifungals to reduce morbidity and mortality during OPC therapy.

Figure 2.

Candidiasis. Heavy accumulation of pseudomembranous candidiasis on the oropharynx and buccal mucosa while another patient developed erythematous candidiasis on the dorsum of the tongue

Viral Infections

Reactivation of latent herpes simplex virus type-1 (HSV) is one of the most common causes of viral infection in OPC patients receiving radiotherapy and chemotherapy (Figures 3A and B) (21, 31). Most individuals before the age of 70 years have been exposed to HSV. The virus remains dormant in the trigeminal ganglion and can become reactivated by exposure to ultra-violet light, trauma, stress, illness, or immune suppression associated with OPC therapy (32). Small vesicles appear extra-orally and intra-orally along the affected branch of the trigeminal nerve. These eventually rupture to become shallow, painful ulcerations (32). In healthy individuals, herpetic lesions are self-limiting, usually resolving within 2 weeks. However, in OPC patients receiving therapy, HSV infections have atypical appearance, disseminate throughout the oral cavity and may become life threatening. While oral mucositis caused by direct drug stomatotoxicity occurs early, HSV lesions have a temporal relationship that helps with diagnosis because they generally appear about 18 days after initiation of OPC therapy. However viral cultures are the most useful diagnostic tools for HSV infections. Seropositive OPC patients usually receive prophylactic treatment with acyclovir, an inhibitor of viral thymidine kinase (28, 33). Valacyclovir and famciclovir are alternative drugs with better bioavailability than acyclovir. In cases of acyclovir-resistant HSV infections, other therapeutic options like foscarnet or cidofovir should be considered (28).

Figure 3.

Herpes simplex virus (HSV) infection. Chemotherapy caused reactivation of HSV infection on the labial and buccal mucosa (A) and hard palate (B) of these patients.

Bacterial Infections, Dental Caries and Periodontal Diseases

Bacterial infections often arise from mucosal, gingival or odontogenic sources. Poor oral hygiene and hyposalivation increase the oral microbial load thereby disrupting balance of the oral flora. Gram-positive organisms predominantly colonize the oral cavity; but during OPC therapy, the inability to mount appropriate inflammatory response allows other pathogenic organisms to flourish leading to various opportunistic infections (21, 34). Radiation-induced hyposalivation makes enamel surface more susceptible to demineralization and multiple dental caries (Figures 4A – C) (35). Smooth surface enamel in the cervical region of teeth that is usually less susceptible to caries becomes discolored, friable and progressively compromises the integrity of the tooth structure (36). Advanced radiation-induced dental caries may lead to tooth fracture, dental abscess, tooth loss and osteoradionecrosis (ORN).

Figure 4.

Radiation dental caries. Generalized advanced dental caries developed following head and neck radiotherapy on the incisal edges of anterior teeth (A) as well as cervical surfaces of posterior teeth. Bitewing (B) and periapical (C) radiographs demonstrate the rapidly advancing root caries.

Conventional signs and symptoms of bacterial infections such as swelling, suppuration, and erythema may be muted or absent due to immune suppression. Therefore, it is important to eliminate potential sources of dental infection prior to OPC therapy (21, 34). The teeth should be protected by judicious use of topical fluorides. The use of fluoride rinses, gels and construction of custom-made trays for fluoride application should be established during and following radiotherapy until normal salivary functions return (35). Teeth with periodontitis and bone loss may become exacerbated during OPC therapy resulting in local and systemic complications (33). Direct radiation injury to periodontal structures will compromise vascular supply, cause destruction of more periodontal tissues and promote bacterial invasion (37, 38). Chemotherapy causes neutropenia, neutrophil dysfunction and impaired inflammatory response, which further delay tissue healing and consequent loss of more periodontal tissues (39, 40). Due to significant long-term effects of periodontal disease, it is important to assess the periodontal status of teeth and tissues within the field of radiation prior to therapy (33). Teeth with advanced periodontal bone loss should be extracted before treatment to reduce the risk of ORN that often develops if the extraction is performed after radiotherapy (41).

Hyposalivation

Decreased salivary flow or hyposalivation is a common complication of OPC therapy. It is caused by damage to the salivary glands and presents as progressive xerostomia (dry mouth) (Figures 5) because salivary flow can decrease by about 50–60% in patients undergoing chemotherapy and those receiving up to 20 Gy radiotherapy (42, 43). Reduction in salivary flow is usually reversible depending on the dose of radiation received. But irreversible damage often occurs when the total dose is greater than 50 Gy and the salivary gland is in the field of radiation. Hyposalivation makes it difficult for patients to speak, smell, taste, chew or swallow (15). Glandular damage affects the composition and physiological functions of saliva thereby reducing saliva buffering capacity, antimicrobial activity and ability to re-mineralize damaged tooth enamel (19). Patients become more susceptible to oral infections, dental caries and periodontal diseases (Figure 4). A dry oral mucosa is friable and susceptible to trauma, inflammation, and irritation (15). Controlling hyposalivation involves minimizing salivary gland damage. Intensity modulated radiation therapy (IMRT) that involves direct tumor radiation in a narrow field has been effective in reducing salivary gland damage and xerostomia (44). Fractionated radiation allows delivery of radiation to the tumor region at doses that allow normal tissue to repair sub-lethal DNA damage before the next dose is administered (42). The introduction of Amifostine, a radioprotective drug administered prior to radiotherapy has been very effective in minimizing hyposalivation during OPC therapy. Amifostine protects the salivary glands by scavenging free radicals in normal cells without hindering tumor cell death (45–47).

Figure 5.

Hyposalivation. Radiotherapy-related hyposalivation caused xerostomia (dry mouth) and fissured atrophic tongue in this patient.

Stimulation of the salivary gland during treatment has the potential to preserve salivary function by reducing glandular damage. Sucrose-free lemon drops or sugarless gum are non-pharmacologic agents used to stimulate salivary flow during and after radiation therapy. The use of cholinergic agonists like pilocarpine and cevimeline are also beneficial in stimulating salivary flow from residual glandular tissue (38, 48). In cases of minimal residual salivary function, saliva substitutes can also be prescribed. These products contain carboxycellulose, a viscous substance that lubricates the mucosa to provide transient symptomatic relief from oral dryness (49). Reduced salivary flow secondary to radiation is dose dependent as the salivary gland parenchyma is very sensitive to irradiation. The parotid glands in particular, are much more sensitive than submandibular and sublingual glands. . Severity of radiation-induced xerostomia varies from patient-to-patient but complete inhibition of salivary flow can occur at a radiation dose of 60 Gy. In addition, the oral microbial population shifts to acidogenic microflora and increased concentrations of streptococcus mutans, lactobacillus and candida. Consequently, the patients become more susceptible to dental caries and opportunistic infections. It is common for salivary function to return to normal within 6–12 months. Recently, acupuncture has been shown to promote recovery from xerostomia in head and neck cancer patients treated with radiation. (50).

Osteoradionecrosis

Osteoradionecrosis (ORN), the most significant oral complication of OPC radiotherapy presenting as prolong soft tissue dehiscence with exposure of underlying necrotic bone (Figure 6). It was originally associated with the triad of trauma, infection, and radiation (14), but its etiology is linked more to radiation-induced hypoxic, hypocellular, hypovascular tissue and defective wound healing rather than infection (14). Clinically, ORN presents as painful or painless exposed bone that may become secondarily infected to cause development of a sinus tract or fistula. Extensive ORN may be associated with anesthesia or paresthesia (41, 51). ORN occurs in 15% of patients receiving radiotherapy, but this can rise as high as 44% when radiation doses exceed 50 Gy and the irradiated site is subsequently traumatized (13, 14, 51, 52). There is a higher incidence of ORN in the mandible than the maxilla purportedly due to lower vascular network and more cortical bone in the mandible. ORN can develop within 2 weeks of radiotherapy but it is usually a late complication occurring within the first year of treatment. Dentate patients are at higher risks of ORN than edentulous patients; so dental evaluation before OPC therapy is a standard protocol to eliminate potential sources of infections (15, 41, 51).

Figure 6.

Osteoradionecrosis. Panoramic radiograph shows osteoradionecrosis that developed in the left mandible (white arrow) within the first year of oral cancer radiotherapy.

In most cases of ORN, healing occurs after conservative therapy consisting of local debridement, antibiotic therapy, and saline irrigation. In severe cases, healing may be prolonged for up to 6 months and more aggressive use of surgical debridement and hyperbaric oxygen (HBO) therapy are warranted (15, 53, 54). Different protocols combining surgery and HBO therapy have shown variable success rates ranging from 15–90% recovery (55, 56). Recent advances have also demonstrated successful mobilization of stem cells to the damaged bone to promote healing (57).

Pain and loss of function

Neuropathic pain and neurosensory abnormalities can also complicate OPC therapy. Neuropathic pain occurs in 25% of OPC cases due to tumor invasion of peripheral or central nervous system or as a sequela of treatment (58). Chemotherapeutic agents derived from vinca alkaloids, taxanes and platinum are commonly associated with peripheral neuropathy (59). Surgical tumor resection can also stretch or transect adjacent nerves causing neuropathic pain (60). A wide range of pharmacologic agents such as anticonvulsants, antidepressants, local anesthetics, and N-methyl-D-aspartate receptor blockers are usually used to manage peripheral neuropathy and neuropathic pain (61).

Post-surgical tissue fibrosis, orofacial muscle contracture and trismus significantly affect jaw function. Patients have difficulty speaking, swallowing and chewing which ultimately affect long-term quality of life after OPC treatment (62). Judicious use of stretching exercises to maintain maximum jaw opening and mobility will prevent long-term disability. Passive stretching with tongue depressors or extra-oral devices will help prevent muscle contracture and gradually increase mandibular opening. Spastic reactions that cause abnormal jaw muscle closure can be controlled with botulinum toxin injections (63, 64). As the oral and pharyngeal mucosa are exposed to radiation, taste perception and taste discrimination will become progressively compromised (65). Decreased sensory discrimination contributes to altered taste perception that may affect diet and nutrition (18, 21). Extensive degeneration of the taste buds might occur following radiation therapy. Taste acuity decreases by a factor of 1000–10000 (65). Alteration and loss of taste may begin with the first 2–4 Gy. After three weeks of therapy, it takes 500–8,000 times normal concentrations of taste stimulant to elicit a normal taste response. If there is enough salivary flow to dissolve the tastants, the taste sensation returns within 60–120 days after completion of radiotherapy. While zinc sulfate has been used to improve taste alterations, its effectiveness after OPC radiotherapy is still inconclusive (66, 67)

Radiation caries

The developing tooth buds are destroyed if irradiated prior to mineralization. Also radiation therapy can increase the severity of dental developmental disturbances induced by chemotherapy (68). Therefore, tooth agenesis and retarded root development often occur in younger patients (Figure 7). In adults, the teeth are resistant to direct effects. Radiation caries has been categorized based on clinical and radiographic features. Type 1 radiation caries is widespread superficial caries, type 2 is caries of the cementum and dentin at the cervical region and type 3 is dark pigmentation of the entire crown; however, any combinations of these features may occur (69). The risk of radiation caries is mainly secondary to a number of factors that include a shift to a more cariogenic oral microbial flora, xerostomia and a reduction in the antimicrobial and mineralization properties of saliva.

Figure 7.

Delayed dental development. This 13-yr-old patient received radiation therapy before development of the permanent teeth. This has been complicated by delayed shedding of the deciduous molars, stunted development of the premolars and permanent molars as a result of radiation damage to the developing tooth buds.

Despite the multifactorial etiology of dental caries, radiation-related dental caries occurs as a consequence of hyposalivation. Therefore, radiation caries can be ideally prevented by sparing the salivary glands from the “line of fire” (direct path of the radiation beam). If this is not practicable in some patients, prevention can be achieved with comprehensive dental care before, during and after radiotherapy (54). Treatment strategies must be directed at each component of the caries process. Resistance to caries can be enhanced with application of topical fluorides and other mineralizing agents. The use of topical fluorides and chlorhexidine mouth rinses may help reduce the levels of Streptococcus mutans but not Lactobacilli. The dental care provider should motivate the patient to follow stringent plaque control. In addition, prescribing medications that stimulate salivary flow and nutritional counseling to limit cariogenic diet are essential aspects of reducing radiation caries to improve quality of life of OPC survivors.

Dental Management strategies for the general dental practitioner

The general dental practitioner can readily manage most oral complications of OPC radiotherapy. In addition to the management issues discussed under each complication, the National Cancer Institute (NCI) at the National Institutes of Health, Bethesda MD (www.cancer.gov) recommends the following specific dental health guidelines.

Tooth brushing and Dentifrice

Although the NCI recommends the use of soft nylon-bristled toothbrushes with two or three rows, the use of electric and ultrasonic toothbrushes are also acceptable if the patients can use them without causing trauma to the oral mucosa. The general dental practitioner should emphasize that the patient should perform the correct tooth brushing technique (bass sulcular scrub method) at least 2 or 3 times daily with frequent rinsing. Any fluoride-containing dentifrice can be used by most patients that received radiotherapy. However, non-mint flavored dentifrices are better tolerated than the mint-flavored dentifrices when there is co-existing graft versus-host disease (GVHD). The patients should be also be instructed to air-dry brushes between uses.

Mouth rinsing and Flossing

Post mucositis dental management should include frequent mouth rinses with 0.9% saline, sodium bicarbonate solution or a combination of both solutions. The patient should rinse with at least 8–12 fluid ounces in mouthful portions with expectoration until finished.

Fluoride supplementation

Typically, the dental practitioner should recommend to the patients the use of a 1.1% neutral sodium fluoride gel or a 0.4% stannous fluoride gel. The gel should be used to brush gently on the teeth followed by expectoration and rinsing the mouth gently. The fluoride should be applied at least once a day.

Topical antimicrobial rinses

The practitioner should recommend either 0.12 – 0.2% Chlorhexidine or providence iodine oral rinse for management of acute gingival lesions. The patient can be advised to hold the rinse in the mouth for 1 to 2 minutes before expectoration. This can be repeated up to four times a day depending on severity of the gingival and periodontal inflammation.

Care of dentures during and after radiation therapy

Wearing dentures should be discontinued during radiotherapy and for a few weeks after completion of radiotherapy to promote healing of radiation mucositis. The patient should be instructed to wear the dentures only when eating and discontinue their use at other times. When the dentures are not being used, they should be soaked in antimicrobial solutions. If necessary, a denture can be used a carrier to keep medications such as antifungals needed for oral care in close contact with the oral mucosa.

Care of lips and mouth

Preventing lip dryness will reduce risks of tissue injury. Patients should be advised to use lip care products containing petroleum based oils and waxes. Lanolin-based creams and ointments may be more effective in moisturizing and lubricating the lips and thereby protect the lips from trauma.

These recommendation indicate that the general dental practitioner can be the caregiver immediately after radiotherapy and during the follow up months or years of routine maintenance. Since dental caries secondary to xerostomia is a big complication, appropriate instructions to prevent the radiation caries along with methods to increase salivation will ensure the highest quality of patient lifestyle during the post-radiotherapy period. The dental practitioner plays a vital role in the overall management of the dental patient after radiotherapy and an even more significant role during the extended follow-up period (70).

Conclusion

More advanced knowledge about OPC and improved screening methods have undoubtedly improved survival. OPC therapy is aimed at complete elimination of the tumor, reduction of morbidity and preservation of tissue functions. Similarly, the goal of rehabilitation should be to improve quality of life OPC survivors and resumption of normal day-to-day activities. These can be better achieved by seamless multidisciplinary interactions and teamwork. It is important to understand potential complications of OPC therapy and harness the resources necessary to prevent or minimize them. Oral care is an integral component of both OPC chemotherapy and radiotherapy. A well-informed dental practitioner can become an effective caregiver for a debilitated patient during the recovery phase and later when the patient resumes normal day-to-day activities.