radiation biology / dental implant courses by Indian dental academy

Seminar
INDIAN DENTAL ACADEMY
Leader in continuing Dental Education
www.indiandentalacademy.com

Purpose statement
At the end of the session the
learners should be able to
describe the mechanism and
effects of radiation on oral
tissues

S/No Learning objectives Domain Level Criteria Condition
1 Define radiation biology Cognitive Must know all -
2 Describe the mechanism,
theory and sequence of
radiation injury
Cognitive Must know all -
3 Discuss genetic and somatic
effects of radiation
Cognitive Must know all -
4 Discuss the changes caused by
radiation on biologic
molecules and on cellular
level.
Cognitive Must Know all
5 Describe the effects of
radiation on oral cavity and
their treatment.
Cognitive &
Pschymotor
Must know - -

CONTENTS:
 Definition of radiation biology
 Radiation injury and its mechanism
 Theories of radiation injuries
 Sequence of radiation injury
 Somatic and genetic effects
 Radiosensitivity & cell type
 Radiation effects
-At tissue & organ level
-On oral cavity
 Effects on whole body irradiation

Introduction
 Soon after the x rays was discovered in 1895, there were
reports of erythema, dermatitis, ulcerations and neoplastic
changes in the tissue brought about by exposure to the x rays.
 Many dentists who were ignorant of early warnings or chose
to ignored them suffered the loss of one or more fingers to
hold the film in the patients mouth and thus exposed the
fingers to repeated doses of x-radiation.
 Since those days information about biologic effects of
radiation upon man has continually increased along with
good technics for good oral radiography and safe handling of
x ray radiation in dentistry.

What is Radiation Biology ?
 “Radiation Biology” is defined as the study of effects of
ionizing radiation on living systems.
 Initial interaction of the ionizing radiation with the biological
molecule occurs within the first 10-13 seconds after exposure.
 Subsequent modification of biologic molecules within the
following seconds to hours.
 Later these molecular changes may result in alterations in
cells and organisms that may perists for hours, decades and
possibly for generations.

Radiation Injury
 In diagnostic radiography some X-rays reach the film while
others are absorbed by patients tissues.
 Absorption refers to total transfer of energy from the X –ray
photons to the patients tissues.
 X ray absorption by patient tissues causes chemical changes
in them leading to biologic damage.
 Radiation injury can occur by following two mechanisms:
Ionization or by Free radical formation

Mechanism of Radiation Injury
X ray photon interacts Ionization
with tissue Excitation Chemical
Breaks bond change
Biologic
changes

Theories of radiation injuries
Damage to living tissues caused by exposure to ionizing
radiation may result from:
1.Direct hit and absorption of X-ray photon within the cell.
2.Absorption of photon by water in the cell causing
formation of free radical.

Direct Theory or target action theory
 It states that the effect which occurs when the energy of a
photon or secondary electron ionizes biological
macromolecules.
 This states that the changes occur due to-
 Absorption of energy by biologic molecule
 Transfer of energy between unstable intermediate
molecules
 Formation of damaged stable molecules
 Resultant molecules are rearrangements resulting from
dissociation of molecules into free radicals and subsequently
reformed stable configuration by dissociation and cross
linking

 Free radical production:
RH + X-Radiation R.+ H+ + e-
 Free radical Fates:
Dissociation : R. X+Y
Cross linking : R.+S. RS
 Free radicals are atoms or molecules that have unpaired
electron in their valance shell ,with extreme reactivity and
very short life approx. 10-10 seconds .
 The resultant molecule differs from the original molecule
highlighting biologic change in irradiated organism.

The subsequent effects include:
 Inability to pass information
 Abnormal replication
 cell death
 Temporary changes as the DNA is repaired before further cell
division.
 If radiation hits somatic cells, it could result in radiation
induced malignancy.
 If reproductive stem cells are hit the result could be radiation
induced congenital abnormalities.

Factors on which results of direct effect
depend are:-
1. Type and number of nucleic acid bonds that are broken
2. The intensity and type of radiation.
3. Time between exposures.
4. The ability of cell to repair the damage.

INDIRECT OR POISON CHEMICAL THEORY
 Suggests that X-ray photons absorbed within the cells cause
formation of toxins which in turn damage the cells.
 Water-predominant molecule of biologic system absorbs
photon, ionizes and releases free radicals produced by the
action of radiation on water which further interact with
organic molecules and produce changes in biologic
molecules.

Radiolysis of Water
 Human body has up to 70% of water content.
 A complex series of chemical changes occur in water after
exposure to ionizing radiation known as radiolysis of water
resulting in formation of free radicals.
 Ionization of water results in production of hydrogen and
hydroxyl free radicals.
 First step in this process is absorption of energy by water
molecule causing displacement of a electron from it resulting
in a positively charged water molecule and a electron pair
Photon +H2Oe- + H2O+
OR e- +H2O2e- +H2O+www.indiandentalacademy.com

e- + H2OH2O-
H2O- H* + OH-
H2O+ + H2O  H2O++ OH*.
Photon +H
2
O H2O*H*.+OH*
The positively charged water
molecule reacts with another
water molecule to form
hydroxyl free radical.
Water molecule may also be
excited and dissociate into
hydroxyl ion and hydrogen
free radical

 Although radiolysis of water is extremely complex on balance
water is largely converted to hydrogen and hydroxyl free
radicals
 When dissolved molecular oxygen is present in irradiated
water, hydroperoxyl free radicals may also be formed
H*+ O2 H2O
Hydroperoxyl free radicals also may contribute to the formation
hydrogen peroxide in tissues:
HO2* + H* H2O2
HO2 + HO2 O2+ H2O2

 The generation of free radicals occur in less than 10
-10
secs
after passage of photon.
 Both peroxyl radical and hydrogen peroxide are oxidizing
agents that can cause significant alteration in biological
molecule and even cell destruction and are considered as
major toxins formed in the biological tissues by ionizing
radiation.

EFFECT ON BIOLOGIC MOLECULES
Proteins
 Denaturation
 Inter and intramolecular cross linking
 Enzymes get inactivated leading to failure or
conversion of substrate to product.
Nucleic acids
 change or loss of base
 disruption of hydrogen bonds between DNA
strands
 breakage of DNA strands
 cross linking of DNA strands

Effects at cellular level
Intracellular
 Nucleus :
inhibition of cell division
Chromosomes : single or double
armed chromosomal aberrations
GAP 1
S
GAP 2
MITOSIS
proliferating cell moves in the cycle from
mitosis to gap 1(G1) to the period of DNA
synthesis (S) to gap 2 (G2) to the next
mitosiswww.indiandentalacademy.com

CELL CYTOPLASM
 Increased permeability of plasma membrane to sodium
and potassium ions.
 Swelling and disorganisation of mitochondria
 Focal cytoplasmic necrosis

EFFECTS ON CELL KINETICS
 Effects seen on cell division and cell maturation process and
depends upon:
-Dose of radiation: High / Low
-Period of radiation: acute/chronic
-Nature of dose of radiation: fractionalised / at one time
-Interval period between doses

Effects seen are
MITOTIC DELAY
Inhibition of progression of cell through cell cycle.
Larger the dose, the greater the reduction in mitotic activity
with incomplete recovery.
CELL DEATH
Mitosis linked cell death in a cell population is loss of capacity
for mitotic division.
Cell death is caused by damage to the nucleus that result in
chromosome aberrations.
Reproductive death occurs in dividing cells after exposure to
moderate dose of radiation

• RECOVERY
Cell recovery involves enzymatic repair of single strand breaks
of DNA.
Because of this repair, a higher total dose is required to achieve
a given degree of cell killing when multiple fractions are used
than when the same total dose is given in a brief exposure.
Damage to both strands of DNA at same site is usually lethal to
the cell.

ACUTE EXPOSURE
When a large dose of radiation
is absorbed in a short
period of time.
eg. Nuclear accident
.
CHRONIC EXPOSURE
This occurs when small
amount of radiations are
absorbed repeatedly over a
long period of time

Dose-Response Curve
 All ionizing radiation are considered potentially harmful and
can produce biological damage.
 To establish acceptable level of radiation exposure it is useful
to plot the dose administered and damage produced
 A dose-response curve can be used to correlate the response
or damage of tissues with the “dose” or amount of radiation
received.

Threshold Curve
• This curve indicates that below a certain level
[threshold] no response is seen.

Linear Curve
• This curve indicates that response is
proportional to dose.

Linear Nonthreshold Curve
• This dose response curve indicates that a
response is seen at any dose.

SEQUENCE OF RADIATION INJURY
LATENT PERIOD:
The time that elapses between exposure to ionizing radiation
and the appearance of observable clinical signs.
It may be short or long depending on the total dose of radiation
received.
PERIOD OF INJURY:
Cell injury including cell death, changes in cell death,
changes in cell function, formation of giant cells and
cessation of mitotic activity.

Recovery period:
The last event in the sequence of radiation injury is the
recovery period. Not all cellular radiation injuries are
permanent. After each exposure, cellular damage is followed
by repair e.g. Damage caused by low level radiations within
the body.

Types of radiation effects
 Somatic Effect:
The radiation effects produced in an exposed individual
during his or her life time are termed as somatic effects .
Somatic cells include cells of the body excluding reproductive
cells.
Somatic effects are of following two types:
Deterministic effect
Stochastic effect

Deterministic effects:
 The severity of the effect is proportional to the dose received.
 These are damaging effects that will definitely result from a
specific high dose of radiation.
 Threshold dose exists below which there will be no effect.
 eg . skin reddening and cataract formation.

Stochastic effect:
 There is increase in probability of occurrence of biological
effect with increasing absorbed dose rather than its severity.
 There is no threshold dose i.e. every exposure to ionizing
radiation carries a possibility of inducing a stochastic effect.
Eg. cancer

Genetic Stochastic Effect
 Mutations result from any sudden change to a gene or a
chromosome. They can be caused by external factors like
such as radiations or occur spontaneously.
 Radiation to the reproductive organs can damage their DNA
and can result in congenital abnormality in offspring.
However there is no certainty that these events will happen,
so all genetic effects are described as stochastic.
 The reproductive cells are prone to damage with
comparatively smaller doses than amount needed to produce
radiation effect on other organs of the body. Genetic effects
are not seen in the person affected but are transferred to the
future generations. www.indiandentalacademy.com

 Radiation induced mutation affects the health of the offspring.
eg. Congenital abnormality in the offspring, retardation of
growth rate.
 Damage can be caused to either dominant or recessive genes.
If dominant genes are damaged , effect is seen on next
generation. If recessive genes are damaged effects may be seen
after several generations.
 Genetic changes are cumulative and it cannot be repaired.
 Changes in somatic cells are not passed to the progeny.

Radiosensetivity of different types of cells
Mammalian cells are divided into following categories based on
histological observation of early cell death.
 Vegetative Intermitotic cells:
eg. Precursor stem cells in spermatogenic or erythroblastic
series, basal cells of oral mucous membrane.
 Differentiating intermitotic cells:
eg inner enamel epithelium of developing teeth, hematopoitic
cells.
 Multipotential connective tissue cells:
eg fibroblasts.

 Reverting Postmitotic cells:
eg. Acinar and ductal cells of salivary glands, cells of liver,
kidney and thyroid.
 Fixed post mitotic cells:
eg. Neurons, striated muscle cells

Acute or short term radiation effect
 Following the latent period the effects which are seen within
minutes, days or weeks are termed as acute or short term
effects.
 These are determined primarily by sensitivity of parenchymal
cells .
 When continuously proliferating tissues are irradiated by
moderate dose, cells are lost primarily by temporary or
permanent inhibition of mitosis and by extensive mitosis
linked death.
 These effects become apparent relatively quickly as reduction
in number if final cells in the serieswww.indiandentalacademy.com

CHRONIC OR LONG TERM EFFECT
 It depends upon extent of damage to fine vasculature.
 The relatively radiosensitivity of capillaries and connective
tissue is intermediate between that of differentiating
intermitotic cells and reverting postmitotic cells.
 Irradiation of capillaries causes swelling, degeneration and
necrosis. These changes increase capillary permeability and
initiate a slow progressive fibrosis around the blood vessel.
 The net result is progressive fibroatrophy of irradiated tissue,
loss of function and reduced resistance of irradiated tissue to
infection and trauma.

Factors influencing radiation effect on the body
Following factors determine the degree of radiation injury:
 Type of Radiation:
 Sparsely ionizing radiation like X- rays or gamma rays
deposit their energy over wide range of area as compared to
alpha rays.
 Alpha rays deposit energy over small area so ionizing effect of
alpha rays will be comparatively more.
 Total dose:
 Quantity of radiation received or the total amount of
radiation energy absorbed.
 More damage occurs when tissue absorb large quantity of
radiations.

 Dose rate:
 Rate at which exposure to radiation occurs and absorption
takes place.
 Dose rate-- dose/time.
 More radiation damage takes place with high dose rates
because a rapid delivery of radiation damage does not allow
time for cellular damage to be repaired.
 Amount of tissue irradiated:
 Total –body irradiation produces more adverse systemic
effects than if small localized areas of the body are exposed.

 Cell Sensitivity:
More damage occurs in cells that divide rapidly.
 Age:
Children are more susceptible to radiation damage than
adults.
 Oxygen :
The radioresistance of many biologic systems increases by
factor 2 or 3 when irradiation is conducted with reduced
oxygen.
The greater cell damage sustained is related to the increase
amounts of hydrogen peroxide and hydroperoxyl free
radicals formed.

RADIATION EFFECTS ON ORAL
CAVITY

Oral mucous membrane:
 Near the end of the second week reddening and inflammation.
 Formation of white to yellow pseudomembrane, sloughing.
Secondary infection by candida albicans.
 At the end of the therapy the mucositis is severe, discomfort is
maximum food intake is difficult.
 After termination of therapy healing may be complete after two
months
 But the mucous membrane tend to become thin, and relatively
atrophic and avascular
 Obliteration of fine vasculature and fibrosis of connective tissue.

Patients are prone to ulcerations and unable to tolerate dentures.
Radiation has more marked effect on non-keratinized
mucosa.
PREVENTION
 Eating a well balanced soft diet.
 Maintaining good oral hygiene.
 Chlorhexidine mouth rinse.

MANAGEMENT
 Topical
 Diluting agents- Saline, bicarbonate rinses.
 Coating agents- aluminium hydroxide, magnesium
hydroxide, sucralfate.
 Topical anesthetics- Diphenhydramine hydrochloride.
 Lip lubricants- water based lubricants are preferred than oil
based.
 Systemic
 Amifostine (ethyol)- sulphydryl compound acts by
scavenging free radicals generated in tissues exposed to
radiation & promotes repair of damaged DNA.

TASTE BUDS:
 These are sensitive to radiation and patient experiences loss
of taste in 2nd or 3rd week of radiotherapy.
 Posterior 2/3rd of tongue when irradiated affects bitter and
acid flavors.
 Anterior 1/3rd of tongue when irradiated affects sweet and
salty flavors.
 These changes may also be attributed to salivary changes
post radiation.

Salivary glands
 Their parenchymal component is sensitive to radiation.
 Acute response - inflammatory serous acini
Chronic response- progressive fibrosis, loss of fine
vasculature and simultaneous parenchymal degeneration.
 There are changes in salivary composition, increase in
sodium, calcium, mg & proteins and other mineral contents.
 Decreased pH (5.5) & more acidogenic microflora causes
decalcification of teeth.
 Mouth becomes dry and tender due to xerostomia.

 Xerostomia may subside after six to twelve months if
persistent beyond that it is less likely to return to normal.
 Increase in the number of streptococci, lactobaccili and
candida.
 Because of small, thick, acidic and viscous saliva such
patients are quite prone to radiation caries.

Prevention
 Frequent sips of water
 Sucking ice chips
 Increase fluid intake
Management
 Saliva stimulants-sugar free gums, mints, candy.
 Saliva substituites- Hydroxyethyl cellulose.
 Pilocarpine – 5 to 10 mg thrice daily
 Bethnacol- 75 to 200 mg per day in divided dose
 Civemilline- 30 mg thrice daily

Teeth:
 Adult teeth are mostly resistant to radiation effects.
 During developing stage if teeth are irradiated :
 prior to calcification the tooth buds get destroyed .
 after initial calcification further differentiation is inhibited
causing malformation or arrest of growth.
 pulp shows decreased vascularity and increased cellularity
making it more prone to pulpitis.

Radiation caries:
 Is a rampant form of caries .
 The lesion occurs secondary to changes in salivary gland and
saliva due to:
 decrease in salivary pH,
 decreased flow,
 increased viscosity.
 Leading to decalcification of enamel and accumulation of
food debris.

Clinically three types of radiation caries are seen:
1. Involving cementum and dentin in cervical areas.
These lesion progresses around the tooth circumferences
and results in amputation of crown.
2. Generalized superficial lesions affecting buccal, occlusal,
incisal and palatal surfaces of teeth.
3. Dark pigmentation of crown.
 Radiotherapy decreases secretory immunoglobulin A, pH &
bicarbonate conentration.
 Decreased concentration of salivary antimicrobial proteins,
reduced remineralizing potential of teeth & loss of buffering
capacity contribute to dental caries.www.indiandentalacademy.com

Prevention
 Optimal oral hygiene should be maintained.
 Daily application of fluoride
Management
 Use of fluorides & remineralizing agents.
 Patients not able to effectively comply with use of fluoride
trays should be instructed to use brush-on gels and rinses.

Bone
The primary damage to the mature bone is-
1. Due to damage to vasculature of the periosteum and cortical
bone which is already sparse in a dense bone such as
mandible.
2. Endosteum becomes atrophic- lack of osteoblastic &
osteoclastic activity
 Bone infection & necrosis following irradiation is called
osteoradionecrosis. The bone becomes hypoxic,
hypovascular and hypocellular.
 Osteoradionecrosis most serious complication of
radiotherapy that usually occurs due to infection or necrosis
of the bone following tooth extraction or a chronic denture
sore.

 Osteoradionecrosis involves
mandible more commonly
than maxilla due to greater
bone density & unilateral
vascular supply to each half of
mandible

Prevention:
 Elimination of trauma
 Removing all poorly supported teeth allowing sufficent time
for extraction wound to heal before beginning radiotherapy.
 Discontinuation of tobacco and alcohol use
 Hyperfractionation & IMRT can reduce risk of
osteoradionecrosis.
Treatment
 Topical antibiotics (e.g. tetracycline) or antiseptics (e.g.
chlorhexidine), Systemic antibiotics- Penicillin/Clindamycin.
 Hyperbaric oxygen therapy (HBO).
 Surgical removal of necrotic bone, if required.
 Partial mandibulectomy for severe cases of ORN

EFFECTS ON WHOLE BODY IRRADIATION
 When the whole body is exposed to low or moderate doses of
radiation characteristic changes develops which is called as
Acute radiation syndrome.
 Acute radiation syndrome is collection of signs and symptoms
experienced by patient after acute whole body exposure to
radiation.

Stage Dose (Gy) Clinical picture
Prodromal symptoms 1 to 2
Anorexia, diarrhea, vomitting,
weakness and fatigue
Latent period 2 to 4 No signs and symptoms
Haematopoietic
symptoms
4 to 7
Increase susceptibility to
haemorrhage, anaemia
Gastrointestinal
symptoms 7 to 15
Diarrhea, dehydration,
intestinal ulceration and
bleeding
Cardiovascular and
central nervous system 50
Fall in blood pressure
Intermittent stupor,
incoordination, diorientation
and convulsion

Late somatic effects
 Somatic effects are those seen in the irradiated individual .
The most important are radiation induced cancers.
 Such lesions are stochastic effect of radiation in that the
probability of an individual getting cancer depends upon the
amount of radiation exposure.

Carcinogenesis:
 Radiation causes cancer by modifying the DNA. Although
most such damage is repaired, imperfect repair may be
transmitted to the daughter cells and result in cancer.
 Radiation acts as a initiator ,it produces change in the cell so
that it no longer undergoes terminal differentiation.
 Evidence are also there that radiation acts a promoter
stimulating cells to multiply
 It may convert premalignant cells to malignant
Eg- thyroid cancer, esophageal cancer, brain & nervous system
cancers, salivary gland cancer, leukemia andcancer of other
organs

Other somatic effects
1. Growth & development
2. Mental retardation
3. Cataracts

Conclusion
 All ionizing radiations are harmful and produce biologic
changes in living tissue. Although the amount of x-radiation
used in dental radiography is small, biologic changes does
occur.
 The dental radiographer must have a working knowledge of
radiation biology, the study of the study of effects of ionizing
radiation on living tissue, to understand the harmful effects
of x-radiation.

REFERENCES
 Oral Radiology Principles and interpretation – Radiation
Biology, White and Pharoah 5th Edition.
 Dental Radiology –Principles and Technique, Radiation
biology – Haring Howerton 3rd Edition.
 Textbook of dental and maxillofacial radiology 2nd edition,
Radiation biology, Freny R Kajodkar
 Essential of Dental Radiography and Radiology Eric Whaites –
Radiation biology, Third Edition
 Fundamentals of dental radiography, Lincoln R Manson,
Biologic effects, x-ray protection and radiobiologic health
 Oral Radiology Principles and interpretation – Radiation
Biology, Goaz and White 5th Edition.
 Burket’s textbook of oral medicine- Oral Cancer, eleventh
edition. www.indiandentalacademy.com

Whether the source of
radiation is natural or
man-made, whether it is
a small dose of radiation
or a large dose, there
will be some biological
effects.
Thank You

radiation biology / dental implant courses by Indian dental academy

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