Dental Caries Part 1 Dental Caries Part 2 Dental Caries Part 3 Dental Caries Part 4
One of the manifestations of irradiation injury in patients undergoing radiation therapy in the oral region is the rapid development of rampant dental caries.
At present the explanation for a decrease in dental caries frequency with advancing age is "maturation of enamel". According to this concept,mature enamel is less soluble in a caries-conductive environment than enamel which is not mature. Since most patients who receive radiation therapy are middle-aged or older, it is surprising that carious lesions should occur in these people with such rapidity and with so much devastation. This would seem to be an indication, that solubility of enamel is not the only mechanism in caries development.
According to Frank and also Baden three types of dental defects are observed as a consequence of irradiation (Frank,et.al,1965) (Baden,1970). The first type is a characteristic caries-like lesion usually completely encircling the neck of the tooth. Amputations of the crowns may and do occur due to this type of lesions. Sometimes extension to labial, buccal, or lingual surfaces are also observed. The second type of lesion begins with brown to black discoloration of the crown. The occlusion surface of posterior teeth and incisal edges of anterior teeth wear away. The third type of lesion begins as a spot depression which spreads from incisal or occlusal edges on labial or buccal and lingual surfaces. In time the enamel shell is destroyed and coronal dentine becomes partially disintegrated leaving the crown reduced to an irregular discolored stump projecting over the gingiva.
Del Regato in 1939 observed that xerostomia was a complication of radiation therapy and postulated that caries development may be due to a modification of saliva secretion. Besides xerostomia, an increase in viscosity and low pH of saliva after irradiation were also observed (Del Regato,1939). Frank and his group found a more direct relationship between irradiation-type caries and salivary glands. They observed that dental defects developed only in persons whose salivary glands received ionizing radiation, and concluded that the salivary gland system and saliva secretion is of fundamental importance for the maintenance of healthy tooth surfaces (Frank et,al,1961).
No one denies the importance of salivary secretion for the maintenance of oral health. However there are other observations and facts which should be considered and which may play a role in the rapid destructive tooth disease in the presence of irradiation but which were never taken into an account by cariologists.
For example, Watanabe studied the effect of Roentgen rays upon the cellular elements in human saliva in experiments made on healthy male adults! The irradiated field was a circular area 6.5 cm in diameter which was limited in front by the angle of the mouth, above by the zygomatic process, and below by the angle of the jaw. Watanabe presented data which showed an increased threshold of leukopedesis of mature leukocytes into saliva. The longevity of this increased leukopedesis is dependent upon the amount of radiation, thus the irradiation effect of 200-R is longer and more intense than effects after 50 or 100 R (Watanabe,1951). Watanabe also stated in the introduction of his paper in 1951: "There can be found in the saliva so many white blood cells migrated by leukopedesis that the oral cavity is sometimes called the graveyard of the white cells. Comparatively little consideration, however, has been given to the cytology in dental literature, which may be due to the fact, as Orban has pointed out, that this subject seems to fit into no branch of dental research. In other words, the cytology of the saliva has been the stepchild of dental research". To this I may add that still today in 1997 the cytology of the saliva is indeed the stepchild of dental caries research.
That the host plays an important role in dental caries development is born out also by experiments of Selvaraj and Sbarra. They noted that lesser hydrogen peroxide production and impaired bactericidal activity was obtained in phagocytizing neutrophyl leukocytes isolated from irradiated animals. Furthermore, total acid and alkaline phosphatase and beta-glucuronidase, used as marker enzymes of lysosomes, increased up to 10 days of post-irradiation and lysosomal enzymes returned to almost normal by the seventeenth day of post-irradiation. Also noted was the fact that all three lysosomal enzymes were released from the granules at a much faster rate during phagocytosis after whole-body radiation (Selvaraj,et.al,1967) The association of irradiation caries with increased migration of neutrophyl leukocytes into the oral cavity and increased excretion of lysosomal enzymes into the oral environment is a fact. Therefore this fact should be considered in dental caries development research.
Changes of lysosomal enzymes activities following the whole-body ionizing radiation have been recognized for some time. Many aspects of radiation damage were reviewed by Watkins including lysosomal membrane damage and subsequent tissue injury and cell death (Watkins,1975) The phenomenon of other tissue injury in the oral cavity due to ionizing radiation which may have an effect on dental caries development has not been considered at all. The concept that radiation damage of salivary glands is the whole reason for dental caries development prevails still these days.
Anybody who is interested in the pathophysiology of dental caries should read the review "Lysosomes and Radiation Injury" by Watkins (Watkins,1975). The review should be interesting as a concept for cariologists even though the author does not discuss the development of dental caries. It is apparent that measurements of salivary enzyme activity in irradiated patients should also be compared to normal controls and studied for the purpose of further elucidation of dental caries development.
What concerns me is the fact that data which implicate the host in dental caries development, besides the saliva and tooth morphology, are excluded from text books. Most of the references I used in the previous four pamphlets cannot be found in text books either. I do not know the reason, but the consequences are an indoctrination of our young generation almost exclusively with environmental factors in dental caries development.
Baden.E.(1970) Environmental pathology of the teeth. In: Thoma's Oral Pathology.Gorlin,RJ,Goldman,HM.(eds.) The C.V.Mosby Co. Saint Louis 1:184.
Del Regato,JA.(1939) Dental lesions observed after roentgen therapy in cancer of the buccal cavity,pharyngs and laryngs. Amer.J.Roentgen 42,404-410.
Frank,RM,Herdly,J,Philippe,E.(1965) Acquired dental defects and salivary gland lesions after irradiation for carcinoma. J.Amer.Dent.Assn.70,868-883.
Selvaraj,RJ,Sbarra,AJ.(1967) Role of the phagocyte in host-parasite interactions. J.Bacteriol.94,149-156.
Watanabe,Y.(1951) The effect of roentgen irradiation upon the cellular elements in the human saliva. Oral Surg.4,89-107.
Watkins,DK.(1975) Lysosomes and radiation injury. In Lysosomes in Biology and Pathology. Dingle,JT,Dean,RT.(eds.) North Holland Publishing Co. Amsterdam Oxford, American Elsevier Publishing Co.Inc.New York p.147.
John Gabrovsek can
be contacted via email at: GABROVJ@cesmtp.ccf.org
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