Radiation-induced oral mucositis is a frequent and potentially dose-limiting acute adverse event that afflicts most radiation patients. Severe oral mucositis of grade 3 or 4 according to the Common Terminology Criteria for Adverse Events (CTCAE) v3.0 occurs in 35 % and 45 % of head and neck cancer patients undergoing radiotherapy alone and concurrent chemoradiotherapy, respectively. Radiation-induced oral mucositis directly affects patient prognosis given that half of the patients with such severe mucositis require a change in treatment regimen and/or a decrease in the total radiation dose. In addition, radiation-induced mucositis of the head and neck region may not only lead to pain but also to aspiration pneumonia and malnutrition due to oral and pharyngeal dysfunction. The common sites where oral mucositis occurs are the buccal mucosa, tongue margin, and soft palate, although mucositis occurs on all mucosa included within the radiation field. The pathway of radiation- and chemotherapy-induced mucositis is described by Sonis [1]. Clinically, it occurs from day 7 of irradiation and becomes worse in a dose-dependent manner; it heals promptly within 2–3 weeks after the end of radiotherapy provided that there are no accompanying bacterial infections [1, 2].

The risk factors of radiation-induced oral mucositis are shown in Table 15.2. Accelerated hyperfractionation and concurrent chemotherapy are the most important treatment factors for oral mucositis. Since most of the patient-related factors of mucositis can be avoided by oral and dental management, such management before and during radiotherapy is of paramount importance. Recently, various clinical trials using sucralfate, chlorhexidine, or antimicrobial lozenges have been performed to prevent and treat radiation-induced oral mucositis; however, the Multinational Association of Supportive Care in Cancer (MASCC) clinical practice guidelines recommend oral care, midline radiation blocks, three-dimensional radiation, and benzydamine [3].

Radiation-induced salivary gland dysfunction and taste disturbance are highly frequent acute or late adverse events that afflict most radiation patients similarly to oral mucositis. Salivary gland dysfunction is caused by ischemia following vascular occlusion and atrophy of the acinous cells [4, 5]. The degree of dysfunction depends on the radiation dose and the irradiated volume of the parotid gland; the dysfunction is nonreversible when the irradiated volume exceeds 75 % and the radiation dose is between 30 Gy and 45 Gy. Therefore, most external irradiation patients with oral cancer cannot recover after treatment [6]. Salivary dysfunction leads to oral adverse events, such as dental caries, periodontitis, and oral infections, which decrease the buffering capacity and antibacterial effect of saliva. Clinically, most patients complain about the viscosity of their saliva from day 3 and dry mouth from day 14 of radiotherapy; treatment with pilocarpine hydrochloride, a salivation accelerant, is prescribed. If the effects of pilocarpine hydrochloride are insufficient, a moisturizer is co-prescribed. Finally, if symptoms do not improve, herbal medicines such as byakkokaninjinto or bakumondoto may be prescribed. In recent years, mitigation of radiation-induced salivary gland dysfunction by a dose reduction to the parotid gland using intensity-modulated radiation therapy (IMRT) has been studied [7].

Radiation-induced taste disturbance is caused by atrophy of the taste buds by radiation [8] and is also affected by tongue coating and hyposalivation. Clinically, most patients complain of hypogeusia from day 7 of radiotherapy and some patients progress to ageusia from approximately day 14; near-normal taste levels are recovered 90–180 days after the end of irradiation [9] and only a few patients continue to have dysgeusia for over a year. Taste disturbance during radiotherapy does not only impair the patients’ quality of life but also their nutritional status and motivation for cancer treatment; appropriate supportive care, such as oral care instructions including tongue brushing and moisture retention of the oral cavity, is therefore required. Dietary modifications following the counseling of a nutritionist are also important. Finally, zinc sulfate, which aids taste bud cell regeneration, has been reported to accelerate the recovery from taste disturbance [10].

Radiation caries and periodontal disease are highly frequent late adverse events and are a major risk factor for osteoradionecrosis. Therefore, periodic oral and dental management after radiotherapy for their prevention is essential. Radiation causes the following changes in tooth and periodontal tissues: (i) a decrease in the microhardness of the dentin; (ii) gap formation at the enamel–dentin junction; (iii) derangement of periodontal ligament fiber; and (iv) cytopenia, hypovascularization, and fibrosis of periodontal tissues [11–13]. However, the main factor influencing radiation caries and periodontitis is thought to be radiation-induced salivary dysfunction given that the above radiogenic damages are mild [14].

The preferred sites for radiation caries are the occlusal surface and cervical region of the tooth, indicating that they occur on the exposed dentin. Cervical caries, in particular, must be carefully monitored since an attachment loss of approximately 1–2 mm develops after radiotherapy [15]. Radiation caries progress rapidly; DMFT has been reported to increase to 7.7 within 4 years after radiotherapy [16]. Following strong hypersensitivity symptoms on a tooth, the radiation caries turns into pulpitis. In addition, oral radiotherapy patients often present with trismus.

The use of topical fluoride applications is recommended to prevent radiation caries following head and neck radiotherapy. However, Spak et al. described that 80 % of patients with an unstimulated salivary flow rate of <0.1 mL/min may develop at least 1 carious lesion per year, despite daily applications of a fluoride gel [17]. Topical fluoride applications may not be able to completely control dental caries in irradiated patients with severe hyposalivation for the following reasons: (i) extended meal times due to dysphagia caused by hyposalivation, causing demineralization of the root surface to progress more during meals, and (ii) the calcium and phosphate required for remineralization are insufficiently supplied due to the considerable decrease in saliva. Remineralizing agents have been added to topical fluoride applications with an aim to improve caries control in hyposalivation patients [18, 19].

Radiation periodontal disease progresses as rapidly as radiation caries and causes tooth loss by resorption of the alveolar bone; poor oral hygiene caused by hyposalivation and periodontal tissue atrophy caused by radiation are its main causes. Radiation periodontal disease can be stabilized through good oral hygiene. However, inflammatory symptoms such as the swelling and redness of the gingiva may often be unclear due to hypovascularization of periodontal tissue caused by radiation. Therefore, periodical evaluation of periodontal tissue through dental and/or panoramic radiography is necessary.

Trismus, or limited jaw mobility, has been reported in 6–86 % patients who received radiation to the temporomandibular joint and/or the masseter/pterygoid muscles. The different incidence rates are attributed to a difference in the observation period and evaluation methods. The prevalence of trismus after conventional radiation, IMRT, and chemoradiotherapy has been reported to be approximately 25 %, 5 %, and 30 %, respectively. In addition, the prevalence increases following a higher radiation dose (over 60 Gy). The main cause of trismus is fibrosis of the soft tissue included within the radiation field. The early treatment of trismus aims to minimize the limitation of jaw mobility after radiotherapy; treatment should begin upon the first presentation of clinical signs of impaired jaw mobility. Treatment consists of a forced jaw opening exercise using various appliances. The US National Cancer Institute recommends opening of the jaw as wide as possible without causing pain 20 times, 3 times a day.

Osteoradionecrosis of the jaws is a rare late adverse event. However, patients suffering from osteoradionecrosis of the jaws experience a substantial deterioration in their quality of life due to serious clinical symptoms such as chronic spontaneous pain, dysphagia, and facial deformation.

The risk factors for osteoradionecrosis of the jaws are the location of the primary tumor relative to the jaws, the radiation dose received by the jaws, and oral conditions such as dental caries with periapical lesion, periodontal disease, and poor oral hygiene [20–23]; predominant risk factors are shown in Table 15.3. In addition, osteoradionecrosis of the jaws is classified into spontaneous and traumatic osteoradionecrosis. Endarteritis, hyperemia, hyalinization, cellular loss, hypovascularization, thrombosis, and fibrosis are the most common histological findings in spontaneous osteoradionecrosis [24]; the pathogenesis is described as hypovascular, hypocellular, and hypoxic tissue formation [25]. These changes are the direct, dose-dependent, and irreversible effects of radiation. Traumatic osteoradionecrosis of the jaws occurs for a long period after radiotherapy and is caused by dental caries with periapical lesion, periodontal disease (Fig. 15.5a), teeth extraction (Fig. 15.5b), poor oral hygiene, and inadequate denture irritation (Fig. 15.6); tooth extraction is the greatest risk factor. The most common reasons for tooth extraction are untreatable dental caries and periodontitis. Therefore, periodical oral management is essential to decrease the risk of dental caries and periodontitis. In fact, the incidence rate of osteoradionecrosis of the jaws is decreased to less than 10 % by systematic oral management before and after radiotherapy [26].

There is no established cure for osteoradionecrosis of the jaws, although conservative treatments such as local irrigation and antimicrobial administration are considered to be the safest. Segmental or marginal mandibulectomy combined with hyperbaric oxygen therapy can be performed if conservative treatment is difficult to perform. In this case, the patient’s quality of life is seriously impaired by dysfunction and deformity of the jaws.

Hypoplasia of the jaws and dental development abnormalities caused by radiation are limited to the radiation area. When patients receiving radiotherapy are younger, these abnormalities become more severe; the effects of radiation are stronger in patients aged 12 years or younger due to jaw growth and the formation of permanent teeth. Representative dental abnormalities caused by radiation are dental agenesis, microdontia, enamel hypoplasia, and shortened or tapering root. These adverse events do not only cause oral dysfunction and facial dysmorphic disorders but also mental distress in patients. Therefore, the long-term follow-up by a pediatrician, a psychiatrist, a plastic surgeon, and a dentist is required.

Oral and dental management for head and neck radiotherapy patients aims to prevent and alleviate acute and late oral adverse events in order to improve the patient’s overall survival rate and quality of life. Given that the treatments available for teeth included in the radiation field are limited, dentists and dental hygienists have to confirm or speculate the radiation field before dental treatment or management. Dental management for radiotherapy patients can be performed in three stages, namely before, during, and after radiotherapy. These stages aim to prepare the base for alleviation and prevention of acute and late oral adverse effects and improve the patient’s quality of life. If the pre-radiotherapy stage is not conducted appropriately, subsequent stages cannot proceed smoothly. For reference, Table 15.4 shows the summary of our oral management protocol for radiotherapy patients. Considering the increasing number of cancer survivors, it is expected that dental management after radiotherapy will soon be provided in general dental clinics.