Late salivary tissue changes induced by radiation therapy include loss of acinar cells, alteration in duct epithelium, fibrosis, and fatty degeneration. The early response to irradiation resulting in markedly decreased salivary flow rates within the first week of treatment is followed by a further decline in saliva secretion and worsening of xerostomia after radiation therapy (1–3 months posttreatment), whereafter salivary secretion and xerostomia gradually recover over time (maximum recovery, 1–2 years posttherapy), depending on the total radiation dose to the gland tissue. Recovery of salivary gland function is usually incomplete, and the overall degree of dryness can range from mild to severe.
It should be noted that salivary gland hypofunction and xerostomia may also be sequelae of other radiation regimens, e.g., radioactive iodine treatment of thyroid cancer and preconditioning total body irradiation in hematopoietic stem cell transplantation for the treatment of hematologic malignancies—although to a much lesser severity.[7,8]
Symptoms and signs of salivary gland hypofunction include the following:
- Lip dryness/crusting.
- Fissures at lip commissures.
- Atrophy of dorsal tongue surface.
- Atrophic and fragile oral mucosa.
- Difficulties in speech, chewing, and swallowing.
- Difficulty in wearing dentures (edentulous patients).
- Oral burning sensation.
- Taste disturbances.
- Increased thirst.
- Sensitivity/pain in response to spicy foods and strong flavorings.
Salivary gland tissues that have been excluded from the radiation portal may become hyperplastic, partially compensating for the nonfunctional glands at other oral sites.
Salivary gland hypofunction also alters the mechanical cleansing ability and the buffer capacity of the mouth, thereby contributing to a high risk of accelerated dental caries (cavities) and periodontal disease. Also, the progression of dental caries is accelerated by the reduction in antimicrobial proteins normally contained in saliva.
In summary, salivary gland hypofunction produces the following changes in the mouth that collectively cause patient discomfort and increased risk of oral lesions:
- Increase in salivary viscosity, with resultant impaired lubrication of oral tissues.
- Decrease in flushing/clearance of acid production after sugar exposure, resulting in demineralization of the teeth and leading to dental decay.
- Compromise of buffering capacity and salivary pH, with increased risk for dental caries and erosion.
- Increase in pathogenicity of oral flora.
- Accumulated bacterial plaque levels caused by patient difficulty in maintaining oral hygiene (caused by soreness of oral mucosa and/or muscular fibrosis/trismus).