X-rays were discovered in 1895, and since then, these rays were applied in several fields such as physics, chemistry and biology. In the beginning, people using these rays were not aware of the biological effect of X-rays. X-ray tubes were calibrated based on the erythema produced on skin when the operator placed his hand in front of the X-ray beam. There were numerous episodes of injury to operators and patients. The first biological effects of X-rays were reported in 1896 and included skin burns, epilation and eye irritation. In 1906, two French radiobiologists, Bergonie and Tribondeau described a law which states that ‘the radiosensitivity of a cell is directly proportional to its reproductive activity and inversely proportional to its degree of differentiation’.
X-rays interact with atoms and molecules in the body within pico to femto second (10−13 to 10−15 s) of exposure. This reaction may occur directly on biological molecules or indirectly through the action on water molecules. This results in the formation of free radicals. Free radicals are fragments of molecules which have unpaired electrons, and hence high reactivity. They react with surrounding molecules and become stable by cross-linking or dissociation. Thus, there is an alteration of cellular molecules which further results in biological effects.
Living tissues may be affected by radiation in two ways—directly by the action on cellular molecules and indirectly by the action on water. While direct effects account for one-third of damages, indirect effects account for the remaining two-thirds.
where RH represents a biological molecule such as a carbohydrate and R* is a free radical formed after the loss of an electron e−. Both R* and H+ immediately react with other biological molecules either by dissociation:
Water is the most abundant molecule in living tissues and hence X-rays passing through the body readily encounter water molecules. A series of complex chemical reactions then occur in water and finally result in the formation of highly reactive molecules. This is termed radiolysis of water.
Exposure of proteins to radiation leads to changes in their secondary and tertiary structures although the primary structure remains unaffected. Exposure of enzymes, however, has a cascading effect, since altered enzymes may not perform their physiological actions, resulting in intracellular molecular alterations. These changes occur at radiation doses much higher than that which causes cell death.
The nucleus is more often affected due to radiation, but changes can occur in mitochondria on exposure to higher doses of radiation. Mitochondria become swollen with disorganization of internal cisternae.
Most base damages, protein–DNA crosslinks and protein-protein crosslinks are usually minor damages which can be repaired and probably play a minor role in carcinogenesis. Single strand breaks are characterized by damage to a single strand of the helix of DNA and are repaired easily using the intact strand as a template. However, double strand breaks, characterized by damage to both strands at the same site or in close proximity, are more difficult to repair. Thus, they frequently result in cell death. Fortunately, these are less common in occurrence. An exposure of 1–2 Gy to a cell produces approximately more than 1,000 base damages, about 1,000 single strand breaks and only about 40 double strand breaks.
Cells not undergoing division remain in G0 phase. Typical cell division times are 10–40 hours with the G1 phase taking about 30%, S phase 50%, G2 phase 15% and M phase 5% of the cell cycle time. There are checkpoints at the G1/S and G2/M boundaries that monitor the accuracy of cell division.
Radiosensitivity differs throughout the cell cycle with late S phase being most radioresistant, G2/M being most radiosensitive and G1 phase taking an intermediate position. In G2/M phase, chromatin is tightly compacted and a poor repair capacity. This explains the high radiosensitivity of this period. DNA synthesis is almost complete by late S phase. Damage by X-rays at this phase can be repaired, and thus the cell is radioresistant at this phase. DNA has an open structure in G1 phase having a better repair capacity; this makes G1 phase radioresistant.
Cells close to irradiated cells but not themselves exposed to radiation may also exhibit DNA damage and reduced survival. This phenomenon is termed bystander effect. This may occur due to the damaging signals communicated by irradiated cells through gap junctions, or through damaging molecules released into the surrounding medium.
Radiation exposure can lead to many harmful health effects. Such effects were classified by International Commission on Radiological Protection (ICRP) in 1990 into deterministic and stochastic effects.
Deterministic effects also called ‘tissue reactions’, refer to those effects in which the severity of response is proportional to the dose. These effects, usually cell killing, occur in all people when the dose is large enough. Deterministic effects have a dose threshold below which the response is not seen. Examples of deterministic effects include oral changes after radiation therapy.
Stochastic effects also called ‘cancer/ heritable effects’, refer to those effects for which the probability of the occurrence of a change, rather than its severity, is dose dependent. Stochastic effects are all-or-none, i.e. a person either has or does not have the condition. For example, radiation-induced cancer is a stochastic effect because greater exposure of a person or population to radiation increases the probability of cancer but not its severity. Stochastic effects are believed not to have dose thresholds.
ICRP introduced another term ‘detriment’ to measure the harmful health effects of low-dose radiation to individuals and their offsprings. The detriment in a population is defined as the mathematical expectation of the induction of cancer and hereditary damage caused by an exposure to radiation. Detriment is a complex concept combining the probability, severity and time of expression of radiation harm.
Early precursor cells of blood cells and spermatogenic cells, and basal cells of oral mucous membrane are all cells which divide regularly and do not undergo differentiation. These cells are extremely radiosensitive.
Intermediate precursors of blood cells, spermatocytes and oocytes, dividing cells in inner enamel epithelium are cells that divide less frequently and undergo some differentiation. These cells are less radiosensitive than the first group.
Connective tissue cells such as fibroblasts, vascular endothelial cells, and mesenchymal cells are cells that divide when there is a need for more cells. These cells have an intermediate radiosensitivity.
Cells such as acinar and ductal cells of salivary glands, and parenchymal cells of liver, kidney and thyroid are cells which are differentiated and specialized in their function. These are divided infrequently and hence are usually radioresistant.
It refers to the various effects on the health of an individual exposed to high doses of radiation. These effects present within 24 hours of irradiation and may last for months. These have been classified into gastrointestinal, hemato-poietic and neural/vascular presentations.
It occurs after exposure to 2–7 Gy of radiation. It occurs due to the exposure to active hematopoietic areas such as sternum and pelvis. This results in destruction of the blood cell precursors, which in turn leads to lower levels of peripheral blood cells. Circulating blood cells themselves are not affected by radiation. Granulocytes which have a short lifespan, are not replaced by maturation of precursor cells. This predisposes to infections. As thrombocytes disappear in peripheral blood, bleeding ensues. As erythrocytes, which have a long lifespan, disappear, anemia occurs.
It occurs after an exposure of about 7–15 Gy. Exposure of the stomach and intestines to radiation results in injury to the rapidly dividing basal epithelial cells. This results in ulceration of the mucosa, resulting in loss of plasma and electrolytes, bleeding, and diarrhea. The normal microbial flora invades the mucosa resulting in septicemia. The combined effects of gastrointestinal and hematopoietic syndromes result in death within 2 weeks.
Cells and tissues in embryos and fetuses are more radiosensitive than adult cells. In the early fetus, radiation exposure has an all-or-none effect, i.e. there is either spontaneous abortion or normal development. The most sensitive period for the occurrence of developmental anomalies is between 18 and 45 days of gestation. The period of brain development, from 8 to 15 weeks post conception is also a very sensitive period. Radiation exposure during this period may result in microcephaly and mental retardation. Exposure after this period may result in general growth retardation and an increased risk for childhood cancer. However, all these changes occur after exposure to radiation levels of about 1 Gy, whereas full mouth dental radiography using a lead apron results in an exposure of just 0.25 μGy.
Radiation exposure to germ cells may result in chromosomal alterations which are heritable. The major genetic effect of radiation is due to microdeletions, which refer to the deletion of multiple, functionally unrelated but contiguous genes. These effects do not cause death of the individual but result in several malformations such as mental and physical retardation and various malformations. These diseases are rare. It has been estimated that the risk of these multi-organ congenital disorders after exposure to 1 Gy is approximately 0.1%.
Exposure to ionizing radiation is an established cancer risk factor. Cancer risk has been described based on the linear non-threshold hypothesis, according to which, at low doses and dose rates, total radiation-related cancer risk is proportional to dose. The mechanism of carcinogenesis is thought to be due to gene mutations. These may not be repaired and the unrepaired genes may be transmitted to daughter cells, which may lead to the development of cancer. It has been suggested that radiation acts as both an initiator and a promoter of carcinogenesis.
One of the modalities used in the treatment of cancer is radiotherapy. Irradiation of a high dose given to patients suffering from cancer in the orofacial region invariably exposes the oral tissues. The source of radiation is usually gamma rays from external source, while brachytherapy with inserted radon or iodine-125 implants may occasionally be used. The dose of radiation is about 50 Gy, given in divided doses of 2 Gy/day.
The basal layer of the oral mucosa consists of dividing cells which are susceptible to radiation damage. Death of these cells results in mucositis. Mucositis begins 12–17 days after initiation of radiotherapy.
Salivary glands are frequently in the path of radiation and are exposed during radiotherapy. The parenchyma of these glands is radiosensitive, which finally results in a fibrosis of the gland. This results in a progressive decrease in salivary secretion, termed xerostomia. This decrease is dose dependent and secretion reaches zero at about 60 Gy. Patients complain of dry mouth and difficulty in swallowing. As lubricating properties of saliva are lost and its pH decreases, demineralization of enamel begins.
Mature teeth are not affected by radiation, however, radiation doses as low as 400 cGy may retard the development of incompletely formed teeth. Irradiation to developing teeth may result in short roots, incomplete calcification, dilaceration, and delayed or arrested eruption.
It is a form of rampant caries that occurs in individuals exposed to curative radiation. Radiation causes a change in saliva by decreasing its secretion, lowering its pH, and reducing its buffering capacity. This reduces the cleansing action of saliva on teeth and results in accumulation of debris, demineralization, and finally, rampant caries.
It refers to the secondary infection of irradiated bone. Radiation exposure to bone affects the vascularity of bone, destroys osteoblasts and some osteoclasts. The normal vascular bone marrow is converted to fatty and fibrous marrow. Thus, the marrow tissue becomes hypoxic, hypovascular and hypocellular.
If secondary infection is then superimposed on irradiated bone, the bone readily undergoes necrosis. Infection may occur from sequelae of caries, periodontitis, denturesore or a tooth extraction. Osteonecrosis is more common in mandible than the maxilla, presumably because of the rich vascular supply of maxilla, and also since the mandible is irradiated more frequently.
Thus, before the initiation of radiotherapy, the dental status of a patient should be assessed. Any pre-existing disease such as caries, periodontal disease, third molar pathology, defective restoration, etc. should be treated.
It is imperative that dental professionals as well as the public are aware of the potential hazards of the ionizing radiation and have adequate knowledge regarding the methods to minimize unnecessary exposure to radiation. This section will attempt to highlight various measures to protect the patient, radiation personnel and public from the long-term hazards of diagnostic radiology.
Radiation is the transmission of energy through space and matter. It is natural and part of our lives. The radioactive materials present naturally in the earth’s crust can be encountered in the building construction materials, food substances and the air we breathe. Muscles, bones, and tissues of our own bodies contain naturally occurring radioactive elements. It is estimated that about four-fifths of the average annual radiation dose worldwide is the contribution from natural radiation.
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