This document discusses the effects of radiation on oral tissues. It begins by explaining radiation chemistry and how radiation directly and indirectly damages biological molecules. It then discusses the deterministic effects of radiation on cells, tissues, and organs. Specific oral tissues that are discussed include the oral mucosa, salivary glands, teeth, bone, and the risks of oral complications like mucositis, xerostomia, and osteoradionecrosis. The document provides detailed information on the histological changes caused by radiation exposure in these oral structures.

1. DR SHABIL MOHAMED MUSTAFA
ASSOCIATE PROFESSOR
MALABAR DENTAL COLLEGE AND RESEARCH CENTRE

2. CONTENTS
RADIATION CHEMISTRY
DETERMINISTIC EFFECTS
On Cells
On Tissues And Organs
Radiotherapy In Oral Cavity
Radiation Effects On Oral Tissues
On Whole Body Irradiation
Radiation Effect On Embryos&fetuses
STOCHASTIC EFFECTS
Carcinogenesis
Heritable Effects

3. Radiobiology is the
study of the effects of
ionizing radiation on
living systems

4. The initial interaction ->first 10 -13
second after exposure.
modification of biologic molecules within
the ensuing seconds to hours.
alterations in cells and organisms that
persist for hours, decades, and possibly
even generations.
may result in injury or death

5. RADIATION CHEMISTRY
• When the energy of a photon or
secondary electron ionizes biologic
macromolecules
DIRECT
• a photon may be absorbed by water in
an organism, ionizing some of its water
molecules. The resulting ions form free
radicals (radiolysis of water) that in turn
interact with and produce changes in
biologic molecules
INDIRECT

6. DIRECT
IONIZING RADIATION+BIO.MOLECULE
(10-10SEC)
FREE RADICAL(unstable+ reactive)
Stablity
BREAKING APART CROSSLINKING
ALTERED BIO.MOLECULE- Structurally&functionally
1/3rd of biologic effects
Particulate radiation: neutrino& alpha particle

7. Indirect
XRAY PHOTONS + WATER IN CELLS
FREE RADICALS
TOXINS(H₂O₂)
CELLULAR DYSFUNCTION &BIOLOGIC DAMAGE
 More chance –CELLS80-70%H₂O
 May take hours to decades to become evident

8. CHANGES IN DNA
BREAKAGE OF ONE /BOTH DNA STRANDS
BASE PAIR CHANGE
HYDROGEN BOND DISRUPTION
CROSSLINK WITHIN
HELIX/OTHER DNA/PROTEIN

10.  SINGLE STRAND BREAKAGE
 DOUBLE STRAND BREAKAGE

11. DETERMINISTIC EFFECT
 Radiation injury to organisms results from either the
killing of large numbers of cells
STOCHASTIC EFFECTS
 sublethal damage to individual cells that results in
cancer formation or heritable mutation

12. DETERMINISTIC EFFECTS
ON CELLS
INTRACELLULAR STRUCTURES
NUCLEUS
CHROMOSOME
CELL REPLICATION
DNA DAMAGE
BYSTANDER EFFECT
APOPTOSIS
RECOVERY

14. RADIOSENSITIVITY OF CELLS

15. DETERMINISTIC EFFECT
ON TISSUES &ORGANS
SHORT TERM EFFECTS
o effects seen in the first days or weeks after exposure
o determined primarily by the sensitivity of its
parenchymal cells
o When continuously proliferating tissues (e.g., bone
marrow, oral mucous membranes) are irradiated with
a moderate dose, cells are lost primarily by
reproductive death, bystander effect, and apoptosis.
o rarely or never divide (e.g., neurons or muscle)
demonstrate little or no radiation-induced hypoplasia
over the short term

16. LONG TERM EFFECTS
o seen months and years after exposure
o are a loss of parenchymal cells and replacement
with fibrous connective tissue.
o These changes are caused by reproductive death of
replicating cells and by damage to the fine
vasculature.
o impairs the transport of oxygen, nutrients, and
waste products and results in cell death
o Thus both dividing (radiosensitive) and nondividing
(radioresistant) parenchymal cells are replaced by fi
brous connective tissue, a progressive fi broatrophy
of the irradiated tissue

17. RADIOSENSITIVITY OF ORGANS

18. MODIFYING FACTORS
Dose
 severity depends on the amount of radiation received.
 Very often a clinical threshold dose exists below which
no adverse effects are seen.
 In all individuals receiving doses above the threshold
level, the amount of damage is proportional to the
dose.

19. Dose Rate
 indicates the rate of exposure.
 For example, a total dose of 5 Gy may be given at a
high dose rate (5 Gy/min) or a low dose rate (5
mGy/min). Exposure of biologic systems to a given
dose at a high dose rate causes more damage than
exposure to the same total dose given at a lower dose
rate.
 lower dose rates-> a greater opportunity exists for
repair of damage, thereby resulting in less net damage.

20. Oxygen
 The radioresistance of many biologicsystems increases
by a factor of 2 or 3 when the exposure is made with
reduced oxygen (hypoxia).
 The greater cell damage sustained in the presence of
oxygen is related to the INCREASEDamounts of
hydrogen peroxide and hydroperoxyl free radicals
formed.
 important clinically because hyperbaric oxygen
therapy may be used during radiation therapy of
tumors having hypoxic cells

21. Linear Energy Transfer
In general, the dose required to produce a certain
biologic effect is reduced as the linear energy transfer
(LET) of the radiation is increased.
 higher-LET radiations (e.g., α particles) are more
effi cient in damaging biologic systems because their
high ionization density is more likely than x rays to
induce double-strand breakage in DNA.
Low-LET radiations such as x rays deposit their energy
more sparsely, or uniformly, in the absorber and thus
are more likely to cause single-strand breakage and
less biologic damage.

22. RADIOTHERAPY IN THE
ORAL CAVITY
 radiation therapy of radiosensitive oral malignant
tumors, usually squamous cell carcinomas.
 when the lesion is radiosensitive, advanced, or deeply
invasive and cannot be approached surgically.
 Combined surgical and radiotherapeutic treatment
often provides optimal treatment.
 chemotherapy+ radiation therapy +surgery.

23. Fractionation of the total x-ray dose into multiple small doses
provides greater tumor destruction than is possible with a
large single dose
 Allows increased cellular repair of normal tissues, which
are believed to have an inherently greater capacity for
recovery than tumor cells
 Increases the mean oxygen tension in an irradiated tumor,
rendering the tumor cells more radiosensitive.
killing rapidly dividing tumor cells and shrinking the tumor
mass after the first few fractions
reducing the distance that oxygen must diffuse from the fine
vasculature through the tumor to reach the remaining
viable tumor cells.
The fractionation schedules established empirically.

24. RADIATION
EFFECT ON
ORAL TISSUES

25.  Typically 2 Gy is delivered daily, bilaterally through 8-
× 10-cm fi elds over the oropharynx, for a weekly
exposure of 10 Gy. This continues typically for 6 to 7
weeks until a total of 64 to 70 Gy is administered.
 Cobalt the source of γ radiation; however, on
occasion small implants containing radon or iodine 125
are placed directly in a tumor mass. Such implants
deliver a high dose of radiation to a relatively small
volume of tissue in a short time.
 Recently a threedimensional technique called
intensity-modulated radiotherapy (IMRT) has been
used to control the dose distribution with high
accuracy.

26. Oral Mucous Membrane
 contains a basal layer composed of rapidly dividing,
radiosensitive stem cells.
 end of the second week of therapy
MUCOSITIS > some cells die
mucous membranes begin to show areas of redness and
inflammation
As the therapy continues
PSEUDOMEMBRANE (THE DESQUAMATED EPITHELIAL
LAYER)
the irradiated mucous membrane begins to separate from the
underlying connective tissue(white/yellow)
At the end of therapy
SEVERE MUCOSITIS +MAXIMUM DISCOMFORT+DYSPHAGIA

27. AFTER IRRADIATION IS COMPLETED,
 the mucosa begins to heal rapidly->completed by about 2
months.
 the mucous membrane tends to become ATROPHIC,
THIN, AND RELATIVELY AVASCULAR.(Due to progressive
obliteration of the fine vasculature and fibrosis of the
underlying connective tissue)
 complicate denture wearing cause ORAL ULCERATIONS
of the compromised tissue
 Ulcers may also result from radiation necrosis or tumor
recurrence.
 biopsy may be required to make the differentiation.
Good oral hygiene minimizes infection.
 Topical anesthetics may be required at mealtimes.
 Secondary yeast infection by Candida albicans is a common
complication and may require treatment

29. TASTE BUDS
 are sensitive to radiation.
 therapeutic dose-cause extensive degeneration of the
normal histological architecture of taste buds.
 loss of taste acuity during the second or third week of
radiotherapy.
 Bitter and acid flavors posterior two thirds of the tongue
is irradiated
 salt and sweet anterior third of the tongue is irradiated.
Taste acuity usually decreases by a factor of 1000 to 10,000
during the course of radiotherapy.
 Alterations in the saliva may partly account for this
reduction, state of virtual insensitivity.
 Taste loss is reversible and recovery takes 60 to 120 days.

30. Salivary Glands
 The major salivary glands exposed to 20 to 30 Gy during radiotherapy
for cancer in the oral cavity or oropharynx.
 parenchymal component of the salivary glands is rather radiosensitive
(parotid glands more so than submandibular or sublingual glands).
 progressive loss of salivary secretion (hyposalivation) is usually seen in
the fi rst few weeks after initiation of radiotherapy.
 fl ow is dose dependent and reaches  zero at 60 Gy.
 Dry mouth (xerostomia) ,tender, and swallowing is difficult and
painful.
 irradiation of both parotid glands complain of dry mouth and diffi
culty with chewing and swallowing than are those with unilateral
irradiation.
 saliva substitutes are available to help restore function.


31.  Reduced salivary flow that persists beyond a year is
unlikely to show significant recovery.
 Histologically, an acute inflammatory response may
occur soon after the initiation of therapy, particularly
involving the serous acini.
 In the months after irradiation the inflammatory
response becomes more chronic, and the glands
demonstrate PROGRESSIVE FIBROSIS, ADIPOSIS,
LOSS OF FINE VASCULATURE, AND
CONCOMITANT PARENCHYMAL DEGENERATION
accounting for the xerostomia.

32.  IMRT spare the contralateral salivary glands + minimize
the loss of salivary function.
 serous cells are more radiosensitive than mucous cells, the
residual saliva is more viscous.+has a pH value 1 unit below.
 initiate decalcifi cation of normal enamel+ the buffering
capacity of saliva ---44% during radiation therapy
 If some portions of the major salivary glands are spared,
dryness of the mouth usually subsides in 6 to 12 months
because of compensatory hypertrophy of residual salivary
gland tissue

33. Teeth
Children receiving radiation therapy to the jaws
may show defects in the permanent dentition 
 retarded root development,
 dwarfed teeth,
 failure to form one or more teeth
 EXPOSURE PRECEDES CALCIFI CATION
 may destroy the tooth bud.
 IRRADIATION AFTER CALCIFI CATION
 may inhibit cellular differentiation, causing malformations and
arresting general growth
 may retard or abort root formation
 but the eruptive mechanism of teeth is relatively radiation
resistant. Irradiated teeth with altered root formation still erupt.

34.  the severity of the damage is dose dependent.
 Adult teeth are resistant to the direct effects of radiation
exposure
 Pulpal tissue demonstrates long-term fibroatrophy after
irradiation.
 Radiation has no discernible effect on the crystalline
structure of enamel, dentin, or cementum, and radiation
does not increase their solubility.

35. Radiation Caries
 rampant form of dental decay occur in individuals who receive
a course of radiotherapy that includes exposure of the salivary
glands
REASON:the major salivary glands, the microflora undergo a
pronounced change
rendering them acidogenic in the saliva and plaque.
 Patients receiving radiation therapy to oral structures have
increases in Streptococcus mutans, Lactobacillus, and
Candida .
changes in the salivary glands and saliva,
 including reduced flow, decreased pH, reduced buffering
capacity, increased viscosity, and altered flora.
 The residual saliva in individuals with xerostomia also has a low
concentration of Ca+2 ion
 greater solubility of tooth structure and reduced
remineralization.
 reduced or absent cleansing action of normal salivadebris
accumulates quickly

36.  . Clinically, three types of radiation caries exist.
I. The most common is WIDESPREAD SUPERFI CIAL
LESIONS attacking buccal, occlusal, incisal, and palatal
surfaces.
II. INVOLVING PRIMARILY THE CEMENTUM AND
DENTIN IN THE CERVICAL REGION may progress
around the teeth circumferentially and result in loss of
the crown.
III. DARK PIGMENTATION OF THE ENTIRE CROWN.
incisal edges may be markedly worn.
IV Combinations of these lesions
• The histologic features are similar to those of typical
carious lesions.
• rapid course &widespread attack distinguish radiation
caries.

38.  The best method daily application for 5 minutes of a
viscous topical 1% neutral sodium fluoride gel in custom-
made applicator trays
 causes a 6month delay in the irradiation-induced elevation
of S. mutans.
 Avoidance of dietary sucrosereduces the concentrations
of S. mutans and Lactobacillus.
 The best result 
 combination of restorative dental procedures, excellent
oral hygiene, a diet restricted in cariogenic foods, and
topical applications of sodium fluoride.
 Patient cooperation in maintaining oral hygiene is
extremely important because radiation caries is a lifelong
threat.
 Teeth with gross caries or periodontal involvement are
often extracted before irradiation.

39. Bone
Oral cancer Rxirradiation of the mandible or maxilla.
The primary damage to the vasculature of the periosteum and cortical bone,
which are normally already sparse.
Radiation also acts by destroying osteoblasts and, to a lesser extent, osteoclasts.
Subsequent to irradiation
normal marrow may be replaced with fatty marrow and fibrous connective tissue.
The marrow tissue becomes hypovascular, hypoxic, and hypocellular
the endosteum becomes atrophic- showing a lack of osteoblastic and osteoclastic
activity, and some lacunae of the compact bone are empty, an indication of
necrosis.
The degree of mineralization may be reduced, leading to brittleness, or little
altered from normal bone.
bone death results and the bone is exposed, the condition is termed
OSTEORADIONECROSIS.

40. OSTEORADIONECROSIS
most serious clinical complication after bone
irradiation.
radiation-induced breakdown of the oral mucous
membrane, by mechanical damage to the weakened
oral mucous membrane such as from a denture sore or
tooth extraction, through a periodontal lesion, or from
radiation caries.
 The decreased vascularity of the mandible renders it
easily infected by microorganisms from the oral cavity

41. This infection may cause a nonhealing wound in
irradiated bone that is diffi cult to treat.
more common in the mandible than in the richer
vascular supply to the maxilla +mandible is more
frequently irradiated.
The higher the radiation dose absorbed by the bone,
the greater the risk for osteoradionecrosis.
Patients should be referred for dental care before
undergoing a course of radiation therapy to minimize
radiation caries and osteoradionecrosis

42.  The risk for osteoradionecrosis and infection can be
minimized by
 removing all teeth with extensive caries or with poor
periodontal support (allowing suff i cient time for the
extraction wounds to heal before beginning radiation
therapy)
adjusting dentures to minimize the risk of denture
sores.
Removal of teeth after irradiation should be avoided
when possible.
 When teeth must be removed from irradiated jaws,
the dentist should use
atraumatic surgical technique to avoid elevating the
periosteum +antibiotic coverage

43.  Often patients who have had radiation therapy require
a radiographic examination to supplement clinical
examinations
 Whenever possible, it is desirable to avoid taking
radiographs during the first 6 months after completion
of radiotherapy, however, to allow time for the mucous
membrane to heal.

44. Musculature
• Radiation may causes inflammation and fibrosis
resulting in contracture and trismus in the muscles of
mastication.
• Usually the masseter/pterygoid musclesinvolved
• Restriction in mouth opening usually starts about 2
months after radiotherapy is completed and progresses
thereafter.
• An exercise program may be helpful in increasing
opening distance.

46. Deterministic
Effects of Whole-
Body Irradiation

48. ACUTE RADIATION
SYNDROME
 collection of signs and symptoms experienced by persons after acute
whole-body exposure to radiation.
 animal experiments and human exposures in the course of medical
radiotherapy, atom bomb blasts, and radiation accidents.
 PRODROMAL PERIOD
 fi rst minutes to hours 1.5 Gy,
 anorexia, nausea, vomiting, diarrhea, weakness, and fatigue
 Cause – not clear; ANS involvement
 Higher dose,rapid onset&greater the severity of symptoms.
 Latent Period
 apparent wellbeing no signs or symptoms of radiation sickness occur.
 dose related.
 hours or days after supralethal exposures (greater than approximately 5
Gy) to a few weeks after exposures of about 2 Gy.

49. Hematopoietic Syndrome
 2 to 7 Gy cause injury to the hematopoietic stem cells of the
bone marrow and spleen.
 The high mitotic activity  a highly radiosensitive tissue.
 cause a rapid fall in the numbers of circulating granulocytes,
platelets, and fi nally erythrocytes
 Although mature circulating granulocytes, platelets, and
erythrocytes are radioresistant because they are nonreplicating
cells, their paucity in the peripheral blood after irradiation
reflects the radiosensitivity of their precursors.
 signs
 infection (from lymphopenia and granulocytopenia),
 hemorrhage (from loss of platelets)
 anemia (from erythrocyte depletion).
 The probability of death is low after exposures at the low end of
this range but much higher at the high end.
 When death results from the hematopoietic syndrome, it usually
occurs 10 to 30 days after irradiation.

51. Gastrointestinal
Syndrome
 range of 7 to 15 Gy, which causes extensive damage to
the gastrointestinal system in addition to the
hematopoietic damage
 injury to the rapidly proliferating basal epithelial cells of
the intestinal villi and leads to rapid loss of the epithelial
layer of the intestinal mucosa.
 there is loss of plasma and electrolytes, loss of effi cient
intestinal absorption, and ulceration of the mucosal
lining with hemorrhaging into the intestines.
 are responsible for the diarrhea, dehydration, and loss of
weight
 Endogenous intestinal bacteria readily invade the
denuded surface, producing septicemia.

52.  At about the time that developing damage to the
gastrointestinal system reaches a maximum, the effect
of bone marrow depression is beginning to be
manifested.
 marked lowering of the body ’ s defense against
bacterial infection and a decrease in effectiveness of
the clotting mechanism.
 The combined effects of damage to these
hematopoietic and gastrointestinal stem cell systems
cause DEATH within 2 weeks from fluid and
electrolyte loss, infection, and possibly nutritional
impairment.
 Thirty of the firefighters at the accident site at
Chernobyl, Ukraine, died in the first few months of
the hematopoietic or gastrointestinal syndrome.

53. Cardiovascular and Central
Nervous System Syndrome
 50 Gy usually cause death in 1 to 2 days.
 collapse of the circulatory system with a precipitous
fall in blood pressure in the hours preceding death.
 Autopsy revealed necrosis of cardiac muscle.
 intermittent stupor, incoordination, disorientation,
and convulsions suggestive of extensive damage to the
nervous system. Although the precise mechanism is
not fully understood, these latter symptoms most
likely result from radiation-induced damage to the
neurons and fi ne vasculature of the brain..

54. Management of Acute Radiation
Syndrome The presenting clinical problems
govern the management
 Antibiotics are indicated when the granulocyte count
falls.
 Fluid and electrolyte replacement is used as necessary.
 Whole blood transfusions are used to treat anemia,
and platelets may be administered to arrest
thrombocytopenia.
 Bone marrow grafts are indicated between identical
twins because there is no risk for graft-versus-host
disease

55. RADIATION EFFECTS ON EMBRYOS
AND FETUSES
 Embryos and fetuses are considerably more radiosensitive than adults most
embryonic cells are relatively undifferentiated and rapidly mitotic.
 Exposures in the range of 2 to 3 Gy during the fi rst few days after conception
are thought to cause undetectable death of the embryo.
 The cells in the embryo are dividing rapidly and are highly sensitive to
radiation.
 Lethality is common and many of these embryos fail to implant in the uterine
wall.
 The fi rst 15 weeks includes the period of organogenesis when the major organ
systems form.
 The most common abnormalities among the Japanese children exposed early
in gestation were reduced growth that persists through life and reduced head
circumference (microcephaly), often associated with mental retardation.
 Other abnormalities included small birth size, cataracts, genital and skeletal
malformations, and microphthalmia.

56.  LATE EFFECTS
 impairment of growth and development.
 reduced height, weight, and skeletal development.
 The younger the individual was at the time of exposure, the
more pronounced the effects.
 Cataracts The threshold ranges from about 0.6 Gy when
the dose is received in a single exposure to more than 5 Gy
when the dose is received in multiple exposures over a
period of weeks
 Most affected individuals are unaware of their presence.
 Life Span Shortening -decrease in median life expectancy
with increasing radiation dose.
 Survivors demonstrate increased frequency of heart
disease, stroke, and diseases of the digestive, respiratory,
and hematopoietic systems.

57. Stochastic Effects
result from sublethal changes in the DNA of individual
cells.
consequence of such damage is carcinogenesis.
Heritable effects, although much less likely, can also
occur.

58. Carcinogenesis
 Radiation causes cancer by modifying DNA.
 The most likely mechanism is RADIATION-INDUCED
GENE MUTATION.
 investigators think that RADIATION ACTS AS AN
INITIATORinduces a change in the cell so that it no
longer undergoes terminal differentiation.
 RADIATION ACTS AS A PROMOTER, stimulating cells to
multiply.
 also convert premalignant cells into malignant ones, for
instance, CONVERSION OF PROTO-ONCOGENES TO
ONCOGENES.
 Gene mutations may also involve a loss of function in the
case of tumorsuppressor genes.

59.  Data on radiation-induced cancers come primarily from
populations of people who have been exposed to high
levels of radiation; however, in principle, even low doses of
radiation may initiate cancer formation in a single cell.
 Estimation of the number of cancers induced by radiation
is difficult.
 Radiation-induced cancers are not distinguishable from
cancers produced by other causes.
 estimated only as the number of excess cases found in
exposed groups compared with the number in unexposed
groups of people.

60.  The group of individuals most intensively studied for estimating the
cancer risk from radiation is the Japanese atomic bomb survivors
 .
 The cases of more than 120,000 individuals have been followed since
1950, of whom 91,000 were exposed.
 The incidences of deaths from leukemias and solid cancers.
 The risk for most solid cancers increases linearly with dose.
 Most individuals in these studies received exposures far in excess of
the diagnostic range.
 Thus the probability that a cancer will result from a small dose can be
estimated only by extrapolation from the rates observed after exposure
to larger doses shows the radiosensitivity of various tissues in terms of
susceptibility to radiation-induced cancer.

62. Leukemia
 . The incidence of leukemia (other than chronic lymphocytic leukemia)
rises after exposure of the bone marrow to radiation.
 Atomic bomb survivors and patients irradiated for ankylosing
spondylitis show a wave of leukemias beginning soon after exposure
and peaking at around 7 years. For individuals exposed under age 30
years, the risk for development of leukemia ceases after about 30 years.
For individuals exposed as adults, the risk persists throughout life.
Leukemias appear sooner than solid cancers because of the higher rate
of cell division and differentiation of hematopoietic stem cells
compared with the other tissues. Persons younger than 20 years are
more at risk than adults are. Evidence also exists for a slightly increased
risk for childhood cancer, both leukemia and solid tumors, after
diagnostic irradiation in utero. The level of the risk is uncertain but
thought to increase the absolute risk by about 0.06% per 0.1 Gy.

63. Thyroid Cancer
 The incidence of thyroid carcinomas (arising from the
follicular epithelium) increases in humans after exposure.
 10%-die.
 The beststudied groups are Israeli children irradiated to
the scalp for ringworm; children in Rochester, New York,
irradiated to the thymus gland; and survivors of the atomic
bombs in Japan.
 Susceptibility greater early in childhood children are
more susceptible
 Females-2-3 times more susceptible.
 Chernobyl nuclear power plant, primarily iodine 131-
caused about 4000 cases of thyroid cancer in children
and 15 fatalities.

64. Esophageal Cancer
 Data -relatively sparse.
 Japanese atomic bomb survivors &ankylosing
spondylitis.

65. Brain and Nervous System
 Cancers Patients exposed to diagnostic x-ray
examinations in utero and to therapeutic doses in
childhood or as adults (average midbrain dose of about
1 Gy) show excess numbers of malignant and benign
brain tumors.
 The strongest association was with a history of
exposure to full-mouth dental radiographs when
younger than 20 years
 Because of their age, it is likely that these patients
received substantially more exposure than is the case
today with contemporary imaging techniques

66. Salivary Gland Cancer
Japanese atomic bomb survivors -irradiation for diseases of the
head and neck&persons exposed to diagnostic x radiation.
An association with dental radiography has been shown, the risk
full-mouth examinations before the age of 20 years.
parotid dose of 0.5 Gy significant correlation between dental
radiography and salivary gland tumors.
Cancer of Other Organs Other organs such as the skin, paranasal
sinuses, and bone marrow also show excess neoplasia after
exposure.
However, the mortality and morbidity rates expected after head
and neck exposure are much lower than for the organs described
previously

68. HERITABLE EFFECTS
 are changes seen in the offspring of irradiated
individuals.
 They are the consequence of damage to the genetic
material of reproductive cells
 At low levels of exposure, such as encountered in
dentistry, they are far less important than
carcinogenesis.

69. Effects on Humans
 Studies on the atomic bomb survivors.
 To date, no such radiation related genetic damage has
been demonstrated
 No increase has occurred in adverse pregnancy outcome,
leukemia or other cancers, or impairment of growth and
development in the children of atomic bomb survivors.
 Similarly, studies of the children of patients who received
radiotherapy show no detectable increase in the frequency
of genetic diseases.
 not exclude the possibility that such damage occurs but do
show that it must be at a very low frequency.

70. Doubling Dose
measure the risk from genetic exposure
the doubling dose
 which is the amount of radiation a
population requires to produce in the
next generation as many additional
mutations as arise spontaneously.

71.  In humans, the genetic doubling dose is estimated to
be approximately 1 sievert (Sv).
 Because the average person receives far less gonadal
radiation, radiation contributes relatively little to
genetic damage in populations.
 For comparison, the background dose is about 0.003
Sv per year and the gonadal dose to males from a full-
mouth radiographic examination is about 0.001 Sv or
less.
 This exposure is contributed largely by the maxillary
views, which are angled caudally.
 The dose to the ovaries is about 50 times less, in the
range of 0.00002 Sv.