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Oral Radiology Principles Interpretation 4th Edition
White S. Digital Instant Download
Author(s): White S., Pharoah M.
ISBN(s): 9780815194910, 0815194919
Edition: 4
File Details: PDF, 43.00 MB
Language: english
A Harcourt Health Sciences Company

Publisher.John Scbrefer
Editor: Penny Rudolph
Associate Developmental Fditor. Kimberly Frare
Project Manager: Linda McKinley
Production Fditor: Jennifer Furey
Designer: Renee Duenow
CoverDesign: Elizabeth Rohne Rudder

FOURTH EDITION

Copyright © 2000 by Mosby, Inc.

Previous editions copyrighted 1982, 1987, and 1994

All rights reserved. No part of this publication may be reproduced or transmitted in any form or
by any means, electronic or mechanical, including photocopy, recording, or any information
storage and retrieval system, without permission in writing from the publisher.

Permission to photocopy or reproduce solely for internal or personal use is permitted for li-
braries or other users registered with the Copyright Clearance Center, provided that the base fee
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Mosby, Inc.
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Printed in United States

Library of Congress Cataloging-in-Publication Data

Oral radiology : principles and interpretation / [edited by] Stuart C.

White, Michael J. Pharoah. - 4th ed.
p. cm.
Includes bibliographical references and index.
ISBN 0-8151-9491-9
1. Teeth-Radiography. 2. Jaws-Radiography. 3. Mouth-Radiography.
I. White, Stuart C. 11. Pharoah, M. J.
[ DNLM: 1. Radiography, Dental. WN 230 G573o 1999]
RK309.07 1999
617.6' 07572-dc21
DNLM/DLC
98-53444

01 02 03 / 9 8 7 6 5 4
Contributors

KATHRYN A. ATCHISON, DDS, MPH STEPHEN R. MATTESON, DDS

Professor, Professor and Chairman,
University of California School of Dentistry, Department of Dental Diagnostic Science,
Center for the Health Sciences, University of Texas Health Science Center,
Los Angeles, California Dental School,
San Antonio, Texas
BYRON W. BENSON, DDS, MS
Professor, C. GRACE PETRIKOWSKI, DDS, MSC, DIP. ORAL
Department of Diagnostic Sciences, RAD, FRCD(C)
Baylor College of Dentistry, Assistant Professor,
Texas A&M University System, Department of Radiology,
Dallas, Texas Faculty of Dentistry, University of Toronto,
Toronto, Ontario,
SHARON L. BROOKS, DDS, MS Canada
Professor,
Department of Oral Medicine/Pathology/Oncology, AXEL RUPRECHT, DDS, MSCD, FRCD(C)
University of Michigan School of Dentistry; Professor and Director, Oral and Maxillofacial Radiology,
Associate Professor, Department of Oral Pathology, Radiology, and Medicine,
Department of Radiology, College of Dentistry;
University of Michigan School of Medicine, Professor,
Ann Arbor, Michigan Department of Radiology,
College of Medicine,
NEIL L. FREDERIKSEN, DDS, PhD University of Iowa,
Professor and Director, Oral and Maxillofacial Radiology, Iowa City Iowa
Department of Diagnostic Sciences,
Baylor College of Dentistry, VIVEK SHETTY, DDS, DR IVIED DENT
Texas A&M University System, Associate Professor,
Dallas, Texas Department of Oral and Maxillofacial Surgery,
University of California School of Dentistry,
BARTON M. GRATT, DDS, PhD Los Angeles, California
Professor of Oral Radiology,
Department of Oral Medicine, ROBERT E. WOOD, DDS, MSC, PhD, FRCD(C)
University of Washington, Assistant Professor,
Seattle, Washington Radiology Department,
University of Toronto;
LINDA LEE, DDS, MSC, DIPL, ABOP, FRCD(C) Active Staff Dentist,
Assistant Professor, Department of Dentistry,
Department of Radiology, Princess Margaret Hospital,
Faculty of Dentistry, University of Toronto; Toronto, Ontario,
Active Staff Dentist, Canada
Department of Dentistry,
Ontario Cancer Institute,
Princess Margaret Hospital,
Toronto, Ontario,
Canada

V
To our wives and children

Liza
Heather and Kelly

Linda
Jayson, Edward, and Lian
 "Man erblickt nur, was man shon weiss and versteht. "

Johann Wolfgang von Goethe

Gesprache mit EV. Miiller
24.4.1819

One recognizes only what one already knows and understands.

Preface

A s we close this century, we reflect on the

changes and new opportunities in our lives,
tempt to be an encyclopedia. We endeavor to convey the
core body of knowledge required for dental students to
be able to use imaging thoughtfully for the diagnosis
profession, and the world. This book inevitably reflects
many of these changes. In the two decades since work and management of disease in the oral and maxillofa-
on the first edition began, dentistry has experienced in- cial region. Our intent is to describe the practical appli-
creasing awareness of the importance of infection con- cation of radiology as well as its underlying principles.
trol; the risks associated with exposure to ionizing radi- This gives the student the knowledge to provide state-of-
ation; the introduction of faster films; improved film/ the-art care as well as the insight to evaluate the efficacy
screen combinations; improved technology for complex of future developments in this field.
motion tomography; rapid developments in new imag- Even as many aspects of oral and maxillofacial radi-
ing modalities such as digital radiography, computed ology change, others stay constant. We cannot overem-
tomography (CT), and magnetic resonance imaging phasize the importance of a sound knowledge of nor-
( MRI); and the development of new therapies, includ- mal anatomy for radiographic interpretation. Only with
ing osseous integrated implants. Our understanding of a clear appreciation for the range of normal can abnor-
the molecular mechanisms and pathophysiology of dis- mality be identified. Just as critical for effective radio-
eases affecting the oral cavity is becoming increasingly graphic interpretation is knowledge of the mechanisms
sophisticated, as is our awareness of a growing range of disease and the effects of pathologic processes on
of radiographic manifestations, especially those con- normal structures. By understanding the radiographic
tributed by new imaging modalities (e.g., CT, MRI) for changes associated with disease processes, the clinician
oral disease. Because of these continuous changes, oral can classify lesions into general categories of disease,
and maxillofacial radiology is an especially exciting field which results in a logical interpretation and treatment
of study and practice. As we look to the future, we see plan. With this edition we have made a special effort to
only an acceleration of these trends. We can anticipate, standardize the presentation of the cardinal radio-
for instance, that the field of digital imaging is in its in- graphic features of each condition considered, includ-
fancy and will play an increasingly important role in im- ing its location, periphery, shape, internal structure, and
age acquisition, display, and disease identification in the effects on surrounding structures. As before, this infor-
new millennium. mation is placed in context with clinical features, differ-
It is a particular pleasure for me (SCW) to welcome ential diagnosis. and management.
Michael J. Pharoah as a co-editor of this text. He has
made significant contributions to this new edition, es-
pecially the chapters concerned with the interpretation Acknowledgments
of disease, and brings the benefit of knowledge acquired
from teachers that included Drs. Harry Worth, Guy This book is the product of the generous contributions
Poyton, and Douglas Stoneman. of many. Twelve of the chapters of this edition are con-
In this edition of the book, as before, we seek to bring tributed in whole or part by colleagues. We thank them
to the reader a clear presentation of the basic principles for sharing their expertise in this endeavor. We are also
of oral and maxillofacial radiology. This text does not at- pleased to acknowledge the insightful comments of

ix
X PREFACE

other colleagues, including Drs. Peter Hirschmann, UCLA made invaluable contributions to the quality of
Susan Kinder, Alan Lurie, Colin Price, and Donald new illustrations. And, of course, our students are a help-
Tyndall, who have reviewed parts of this work in draft ful and continuing source of inspiration for better ways
form. Messrs. David Allen and Thomas Russell of East- to present the material.
man Kodak Company made valuable suggestions re-
garding film and film processing. Also, Ms. Karen Strebel Stuart C. White
and Mr. Patrick Mason of the Media Department at Michael J. Pharoah
Contents

SECTION ONE 8 Intraoral Radiographic Examinations, 122

The Physics of Ionizing Radiation, 1
9 Normal Radiographic Anatomy, 169
1 Radiation Physics, 2
I n collaboration with ALBERT G. RICHARDS 10 Extraoral Radiographic Examinations, 194

11 Panoramic Radiography, 205

SECTION TWO
1 2 Specialized Radiographic Techniques, 217
Biologic Effects of Radiation, 21 NEIL L. FREDERIKSEN

2 Radiation Biology, 22 1 3 Guidelines for Prescribing Dental

Radiographs, 241
KATHRYN A. ATCHISON
SECTION THREE
SHARON L. BROOKS
Radiation Safety and Protection, 41

3 Health Physics, 42 SECTION FIVE

NEIL L. FREDERIKSEN
Radiographic Interpretation
of Pathology, 255
SECTION FOUR
14 Principles of Radiographic
Imaging Principles and Techniques, 67 Interpretation, 256

4 X-Ray Film, Intensifying Screens, 1 5 Dental Caries, 271

and Grids, 68 I n collaboration with BARTON M. GRATT

5 Projection Geometry, 83 16 Periodontal Diseases, 290

6 Processing X- Ray Film, 91 1 7 Dental Anomalies, 303

7 Radiographic Quality Assurance 18 Inflammatory Lesions of the jaws, 338

and Infection Control, 109 LINDA LEE

xi
19 Cysts of the laws, 355 26 Soft Tissue Calcification
and Ossification, 552
20 Benign Tumors of the laws, 378
STEPHEN R. MATTESON 27 Trauma to Teeth and Facial Structures, 566

21 Malignant Diseases of the laws, 420 28 Developmental Disturbances of the Face

ROBERT E. WOOD and laws, 588

22 Diseases of Bone Manifested in the laws, 444 29 Salivary Gland Radiology, 604
BYRON W. BENSON
23 Systemic Diseases Manifested
in the laws, 472 30 Orofacial Implants, 622
VIVEK SHETTY
24 Disorders of the Temporomandibular BYRON W. BENSON
Joint, 493
C. GRACE PETRIKOWSKI

25 Paranasal Sinuses, 529

AXEL RUPRECHT

xii
Oral Radiology
Principles and Interpretation
Radiation
Physics
In collaboration with
ALBERT G. RICHARDS

Composition of Matter
All things are composed of matter. Matter is anything
that occupies space and has inertia. It has mass and can
exert force or be acted on by a force. It occurs in three
states-solid, liquid, and gas-and may be divided into
elements and compounds. Atoms, the fundamental
units of elements, and cannot be subdivided by ordinary
chemical methods but may be broken down into smaller
(subatomic) particles by special high-energy techniques.
More than 100 subatomic particles have been described;
the so-called "fundamental" particles (electrons, pro-
tons, and neutrons) are of greatest interest in radiology
because the generation, emission, and absorption of ra-
diation occurs at the subatomic level.

ATOMIC STRUCTURE
Because the atom cannot be directly observed, various
models are used to describe its structure, each of which
is capable of explaining observable actions. The phe-
nomena associated with radiology employ the quantum
mechanical model proposed by Niels Bohr in 1913.
Bohr conceived the atom as a miniature solar system, at
the center of which is the nucleus, analogous to the sun.
Electrons revolve around this nucleus at high speeds,
analogous to the planets orbiting the sun. In all atoms
except hydrogen, the nucleus consists of two primary
subatomic particles: protons and neutrons. A single pro-
ton constitutes the nucleus of the hydrogen atom. Elec-
trons orbit the nucleus of all atoms. All electrons are
alike, as are all protons and neutrons.
 Fig. 1-1, A, illustrates Bohr's model using a stylized
rendering of three atoms. The paths of the electrons are
drawn as sharply defined orbits to facilitate graphic rep-
resentation of the generation of x-rays and their interac-
tion with matter. In reality the orbit should be repre-
sented by broad parameters defining a space in which
Hydrogen atom Helium atom Lithium atom
the electron is most likely to be found. The orbits, or 2 Electrons 3 Electrons
1 Electron
shells, lie at defined distances from the nucleus and are 1 Proton 2 Neutrons 3 Protons
identified by a letter (Fig. 1-1, B). The innermost shell is 2 Protons 3 Neutrons
the K shell, and the next in order are the L, M, N, O, P,
and Q shells. The shells also have numbers for identifi-
cation: 1 for the K shell, 2 for the L shell, and so on.
These are the principal quantum numbers, represented
by the letter n. No known atom has more than seven
shells. Only two electrons may occupy the K shell, with
increasingly larger numbers of electrons occupying the
outer shells. The maximal number of electrons in a given
shell is 2(n 2 ), where n is the principal quantum number.
Electrons, protons, and neutrons have unique charac-
teristics. The electron carries an electrical charge of -1,
the proton a charge of +1, and the neutron no charge at
all. The mass of an electron at rest is about 9.1 X 10 -28 g.
In contrast, the mass of a proton is 1.67 X 10 -24 g, which
is 1838 times the mass of an electron. The mass of a neu-
tron is 1.68 x 10 -24 g, making it 1841 times heavier than
an electron and slightly heavier than a proton. Most of
the mass of an atom consists of protons and neutrons con-
centrated in the nucleus. The nucleus contributes only a
small fraction (about 1/100,000) of the total size of an atom;
most of the size of an atom is contributed by the cloud of
electrons orbiting it. FIG. 1-1 A, Atomic structures of hydrogen, helium, and
The number of protons contained in the nucleus de- lithium showing orbiting electrons surrounding neutrons and
termines the positive charge. Because any atom in its protons in the nucleus. B, Atom showing the structure and
ground state is electrically neutral, the total number of i dentification of electron shells around the nucleus.
protons and electrons it carries must be the same. The
number of protons in the nucleus also determines the
identity of an element. This is its atomic number, which
is designated by the symbol Z. Consequently, each of the from a given shell must exceed the electrostatic force of
more than 100 types of atoms (elements) has a definitive attraction between it and the nucleus. This is called the
atomic number, a corresponding number of orbital elec- binding energy of the electron and is specific for each
trons, and unique chemical and physical properties. shell of each atom. Electrons in the K shell of a given
Nearly the entire mass of the atom consists of the pro- atom have the greatest binding energy because they are
tons and neutrons in the nucleus. The total number of closest to the nucleus. The binding energy of the elec-
protons and neutrons in the nucleus of an atom is its trons in each successive shell decreases. To move an
atomic mass, designated by the symbol A. electron from a specific orbit to another orbit farther
The electrostatic attraction between a positively from the nucleus, energy must be supplied in an
charged nucleus and its negatively charged electrons bal- amount equal to the difference in binding energies be-
ances the centrifugal force of the rapidly revolving elec- tween the two orbits. In contrast, in moving an electron
trons and maintains them in their orbits. Consequently, from an outer orbit to one closer to the nucleus, energy is
the amount of energy required to remove an electron lost and given up in the form of electromagnetic radia-

3
4 SECTION ONE THE PHYSICS OF IONIZING RADIATION

tion. (See "Characteristic Radiation," p. 12.) The Kshell lighter and carry a single negative charge; therefore they
electrons or any other electrons of large (high-Z) atoms have a much lower probability of interacting with matter
have greater binding energies than those in comparable than alpha particles. They ionize matter much less
shells of smaller (low-Z) atoms. This is because large densely than alpha particles. Beta particles are used in
atoms have more protons and thus bind the orbital elec- radiation therapy for treatment of skin lesions.
trons more tightly to the nucleus than do small atoms. The capacity of particulate radiation to ionize atoms
depends on its kinetic energy, which equals 1/2 ( mass X
I ONIZATION velocity2 ), and its charge. The rate of loss of energy from
a particle as it moves along its track through matter (tis-
If the number of orbiting electrons in an atom is equal sue) is its linear energy transfer (LET). A particle loses ki-
to the number of protons in its nucleus, the atom is elec- netic energy at each ionization; the greater its physical
trically neutral. If an electrically neutral atom loses an size and charge and the lower its velocity, the greater is its
electron, it becomes a positive ion, and the free electron LET. For example, alpha particles (with their high charge
is a negative ion. This process of forming an ion pair is and low velocity) have a high LET (are densely ionizing)
termed ionization. Heating or interactions (collisions) and as a consequence lose kinetic energy rapidly and
with high-energy x-rays or particles such as protons can have short path lengths. Beta particles (which are much
remove electrons from an atom. Such ionization re- less densely ionizing because of their lighter mass and
quires sufficient energy to overcome the electrostatic lower charge) have a lower LET than alpha particles
force binding the electrons to the nucleus. The elec- and thus penetrate through tissue more readily.
trons in the inner shells (K, L, and M) are so tightly
bound to the nucleus that only x-rays, gamma rays, and
ELECTROMAGNETIC RADIATION
high-energy particles can remove them. In contrast, the
electrons in the outer shells have such low binding en- Electromagnetic radiation is the movement of energy
ergies that they can be easily displaced by photons of through space as a combination of electric and mag-
lower energy (e.g., ultraviolet or visible light). netic fields. It is generated when the velocity of an elec-
trically charged particle is altered (Fig. 1-2). Gamma
rays, x-rays, ultraviolet rays, visible light, infrared radia-
Nature of Radiation tion (heat), microwaves, and radio waves are all exam-

Radiation is the transmission of energy through space

and matter. It may occur in two forms: particulate and
electromagnetic.

PARTICULATE RADIATION
Particulate radiation consists of atomic nuclei or sub-
atomic particles moving at high velocity. Alpha rays, beta
rays, and cathode rays are examples of particulate radi-
ation. Alpha rays are high-speed doubly ionized helium
nuclei consisting of two protons and two neutrons. They
result from the decay of many radioactive elements. Af-
ter acquiring two electrons, they become neutral helium
atoms. Because of their double charge and heavy mass,
they densely ionize matter through which they pass. Ac-
cordingly, they quickly give up their energy and pene-
trate only a few microns of body tissue. (An ordinary
sheet of paper absorbs them.)
Beta and cathode rays are both high-speed electrons.
Beta rays are emitted by radioactive nuclei, and cathode
rays are produced by manufactured devices (e.g., x-ray
tubes). The very high-speed beta particles are able to
FIG. 1-2 A vibrating negatively charged particle generates
penetrate matter to a greater depth than alpha particles, electromagnetic radiation. Oscillations of the particle are
to a maximum of 1.5 cm in tissue. This deeper penetra- traced on a strip recorder; they are equal in frequency to the
tion occurs because beta particles are smaller and electromagnetic waves produced.
CHAPTER 1 RADIATION PHYSICS 5

ples of electromagnetic radiation (Fig. 1-3). Gamma rays most successfully described by quantum theory. The
are photons having the same energy range as x-rays, but wave theory of electromagnetic radiation maintains that
they originate in the nuclei of radioactive atoms. X-rays, radiation is propagated in the form of waves, not unlike
in contrast, originate from the interaction of electrons the waves resulting from a disturbance in water. Such
and nuclei in a manufactured device, an x-ray machine waves consist of electrical and magnetic fields oriented
for example. The types of radiation in this spectrum are in planes at right angles to one another that oscillate
ionizing or nonionizing depending on their energy. If perpendicular to the direction of motion (Fig. 1-4).
sufficient energy is associated with the radiation to re- They move forward much as a ripple moves over the sur-
move orbital electrons from the atoms in the irradiated face of water. All electromagnetic waves travel at the ve-
matter, the radiation is ionizing. locity of light (3.0 X 108 m per sec; the velocity of light
Some of the properties of electromagnetic radiation is represented by the letter c) in a vacuum. Waves of all
are best expressed by wave theory, whereas others are kinds exhibit the properties of wavelength (,\) and fre-

Photon energy
FIG. 1-3 Electromagnetic spectrum showing the relationship among wavelength, pho-
ton energy, and physical properties of various portions of the spectrum. Photons with shorter
wavelengths have higher energy. Photons used in dental radiography have a wavelength of
0.1 to 0.001 nm.

FIG. 1-4 The electric and magnetic fields associated with a photon.
6 SECTION ONE THE PHYSICS OF IONIZING RADIATION

quency (v). Wavelength and frequency of electromag-

netic radiation are related as follows:

where .\ is in meters and v is in cycles per second

(hertz). Wave theory is more useful for considering ra-
diation in bulk when millions of quanta are being ex-
amined, as in experiments dealing with refraction, re-
flection, diffraction, interference, and polarization.
Quantum theory depicts electromagnetic radiation as
s mall bundles of energy called photons. Each photon
travels at the speed of light and contains a specific
amount of energy. The unit of photon energy is the elec-
tron volt (eV) (Fig. 1-5). The relationship between wave-
FIG. 1-5 An electron volt is the amount of energy acquired
by one electron accelerating through a potential difference length and photon energy is as follows:
of 1 volt (1.602 x 10 -19 joules).

where E is energy in kiloelectron volts (keV), h is Planck's

constant (6.626 X 10 -34 joule-seconds), c is the velocity
of light, and A is wavelength in nanometers. This expres-
sion may be simplified as follows:

The quantum theory of radiation has been successful

in correlating experimental data on the interaction of
radiation with atoms, the photoelectric effect, and the
production of x-rays.
Typically, high-energy photons such as x-rays are
characterized by their energy, whereas lower-energy pho-
tons (ultraviolet through radio waves) are characterized
by their wavelength.

FIG. 1-6 Tube head (including the recessed x-ray tube),

components of the power supply, and the oil that conducts
heat away from the x-ray tube.
The X-Ray Machine
The heart of an x-ray machine is the x-ray tube and its
power supply. The x-ray tube is positioned within the
tube head along with some components of the power
supply (Fig. 1-6). Often the tube is recessed within the
tube head to improve the quality of the radiographic
i mage. (See Chapter 5.) The tube head is supported by
an arm that is usually mounted on a wall. A control panel
allows the operator to adjust the time of exposure and
often the energy and exposure rate of the x-ray beam.

X-RAY TUBE
The basic apparatus for generating x-rays, the x-ray tube,
is composed of a cathode and an anode (Fig. 1-7). The
cathode serves as a source of electrons to be directed at
the anode. The cathode and anode lie within an evacu-
ated glass envelope or tube. When electrons from the
cathode strike the target in the anode, they produce
FIG. 1-7 X-ray tube with the major components labeled. x-rays. For the x-ray tube to function, a power supply
CHAPTER 1 RADIATION PHYSICS 7

is necessary to establish high voltage potentials be- The filament lies in a focusing cup (see Figs. 1-7 and
tween the anode and cathode to accelerate the electrons 1-9, A), a negatively charged concave reflector made of
(Fig. 1-8). molybdenum. The focusing cup electrostatically focuses
the electrons emitted by the incandescent filament into
a narrow beam directed at a small rectangular area on
CATHODE
the anode called the focal spot (see Figs. 1-7 and 1-9, B).
The cathode (see Fig. 1-7) of an x-ray tube consists of a The electrons move in this direction because they are
filament and a focusing cup. The filament is the source repelled by the negatively charged cathode and at-
of electrons within the x-ray tube. It is a coil of tungsten tracted to the positively charged anode. The x-ray tube is
wire about 2 mm in diameter and 1 cm or less in length. evacuated as completely as possible to prevent collision
It is mounted on two stiff wires that support it and carry of the moving electrons with gas molecules, which would
the electric current. These two mounting wires lead significantly reduce their speed. It also prevents oxida-
through the glass envelope and connect to both the tion and "burnout" of the filament.
high- and low-voltage electrical sources. The filament is
heated to incandescence by the flow of current from the
ANODE
low-voltage source and emits electrons at a rate propor-
tional to the temperature of the filament. The anode consists of a tungsten target embedded in a
copper stem (see Fig. 1-7). The purpose of the target in
an x-ray tube is to convert the kinetic energy of the elec-
trons generated from the filament into x-ray photons.
The target is made of tungsten, a material that has many
characteristics of an ideal target material. It has a high
atomic number, high melting point, and low vapor pres-
sure at the working temperatures of an x-ray tube. A tar-
get material with a high atomic number is best because it
is most efficient for the production of x-rays. Only a small
amount of the KE of electrons coming from the filament
generates x-ray photons when the electrons strike the
focal spot of the target. Because this is an inefficient
process, with more than 99% of the electron kinetic en-
ergy converted to heat, the requirement for a high melt-
FIG. 1-8 Dental x-ray machine circuitry with the major
ing point is clear. Although the atomic number of tung-
components labeled. A, Filament step-down transformer;
B, filament current control (mA switch); C, autotransformer, sten (74) is lower than that of some other metals, its
D, kVp selector dial (switch); E, high-voltage transformer; melting point is much higher. The low vapor pressure of
F, x-ray timer (switch); G, tube voltage indicator (volt-meter); tungsten at high temperatures also helps maintain the
H, tube current indicator (ammeter); I, x-ray tube. vacuum in the tube at high operating temperatures.

FIG. 1-9 A, Focusing cup (arrow) containing a filament in the cathode of the tube from
a dental x-ray machine. B, Focal spot area (arrows) on the target of the tube. The size and
shape of the focal area approximate those of the focusing cup.
8 SECTION ONE THE PHYSICS OF IONIZING RADIATION

Because the thermal conductivity of tungsten is rela- ing the heat over this expanded area. As a conse-
tively low, the tungsten target is typically embedded in a quence, small focal spots can be used with tube cur-
large block of copper. Copper, a good thermal conduc- rents of 100 to 500 milliamperes (mA), 10 to 50 times
tor, dissipates heat from the tungsten, thus reducing the that possible with stationary targets. The target and ro-
risk of target melting. In addition, an insulating oil may tor (armature) of the motor lie within the x-ray tube,
circulate between the glass envelope and the protective and the stator coils (which drive the rotor at about
tube housing carrying away heat from the copper stem. 3000 revolutions per minute) lie outside the tube. Such
This type of anode is a stationary anode. rotating anodes are not used in intraoral dental x-ray
The focal spot is the area on the target to which the machines but may be used in cephalometric units and
focusing cup directs the electrons from the filament. in medical x-ray machines requiring higher radiation
The sharpness of the radiographic image increases as output.
the size of the radiation source-the focal spot-
decreases. (See Chapter 5.) The heat generated per
unit target area, however, becomes greater as the focal
POWER SUPPLY
spot decreases in size. To take advantage of the smaller A brief review of some aspects of an electric circuit may
focal spot while distributing the electrons over the sur- be useful in understanding the power supply in an x-ray
face of a larger target, the target is placed at an angle to machine. An electric current is the movement of elec-
the electron beam (Fig. 1-10). The projection of the fo- trons in a conductor, for example, a wire. The rate of
cal spot perpendicular to the electron beam (the effec- the current flow-the number of electrons moving past
tive focal spot) is smaller than the actual size of the a point in a second-is measured in amperes. It depends
focal spot. Typically the target is inclined about 20 de- on two factors: the pressure, or voltage, of the current
grees to the central ray of the x-ray beam. This causes measured in volts, and the resistance of the conductor
the effective focal spot to be almost 1 X 1 mm, as op- to the flow of electricity, measured in ohms. These units
posed to the actual focal spot, which is about 1 X 3 mm. are related by Ohm's law:
The effect is a small apparent source of x-rays and an
V=IXR
increase in sharpness of the image (see Fig. 5-2) with a
larger actual focal spot for heat dissipation. where Vis the electric potential in volts, I is the current
Another method of dissipating the heat from a small flow in amperes, and R is the resistance of the conductor
focal spot is to use a rotating anode. In this case the i n ohms. Such an electric circuit is often compared to a
tungsten target is in the form of a beveled disk that ro- simple water supply system in which the rate of water
tates when the tube is in operation (Fig. 1-11). As a re- flow through a pipe (amperes) depends both on the wa-
sult, the electrons strike successive areas of the target,
widening the focal spot by an amount corresponding
to the circumference of the beveled disk and distribut-

FIG. 1-10 The angle of the target to the central ray of the FIG. 1-11 X-ray tube with a rotating anode, which allows
x-ray beam has a strong influence on the apparent size of heat at the focal spot to spread out over a large surface
the focal spot. The projected effective focal spot is much area.
smaller than the actual focal spot size.
CHAPTER 1 RADIATION PHYSICS 9

ter pressure (volts) and the pipe resistance or diameter fore the intensity of x-ray pulses tends to be sharply
(ohms). peaked at the center of each cycle (Fig. 1-12, C). During
The primary functions of the power supply of an x-ray the following half (or negative half) of the cycle, the po-
machine are to (1) provide a low-voltage current to heat larity of the AC reverses, and the filament becomes pos-
the x-ray tube filament by use of a step-down trans- itive and the target negative (see Fig. 1-12, B). At these
former and (2) generate a high potential difference be- times the electrons stay in the vicinity of the filament
tween the anode and cathode by use of a high-voltage and do not flow across the gap between the two ele-
transformer. These transformers and the x-ray tube lie ments of the tube. This half of the cycle is called inverse
within an electrically grounded metal housing called the voltage or reverse bias (see Fig. 1-12, B). No x-rays are gen-
head of the x-ray machine. An electrical insulating mat- erated during this half of the voltage cycle (see Fig.
erial, usually oil, surrounds the transformers. 1-12, C. Therefore when an x-ray tube is powered with
The filament step-down transformer (see Fig. 1-8, A) 60-cycle AC, 60 pulses of x-rays are generated each sec-
reduces the voltage of the incoming alternating current ond, each having a duration of %120 second. This type of
(AC) to about 10 volts. Its operation is regulated by the fil- power supply circuitry, in which the alternating high
ament current control (mA switch) (see Fig. 1-8, B), which voltage is applied directly across the x-ray tube, limits
adjusts the resistance and thus the current flow through x-ray production to half the AC cycle. It is called self-
the low voltage circuit, including the filament. This in turn rectified or half-wave rectified. Almost all conventional dental
regulates the temperature of the filament and thus the x-ray machines are self-rectified.
quantity of electrons emitted. The electrons emitted by A tube energized with a self-rectifying power supply
the filament travel to the anode and constitute the tube must not be operated for extended periods. With overuse
current. The mA setting on the filament current control the target may get so hot that it emits electrons, and dur-
refers to the tube current, which is measured by the am- ing the negative half cycle, the inverse voltage may drive
meter (see Fig. 1-8, H). The tube current is the flow of electrons from the target to the filament, causing the fil-
electrons from the filament to the anode and then back to ament to overheat and melt. The glass envelope also may
the filament through the wiring of the power supply. be damaged if the electrons are driven in the wrong di-
The output of the autotransformer (see Fig. 1-8, C) rection by the reverse bias on the tube.
is regulated by the kilovolts peak (kVp) selector dial Recently, some dental x-ray manufacturers have pro-
(see Fig. 1-8, D). The kVp dial selects varying voltages duced machines that replace the conventional 60-cycle
from different levels on the autotransformer and applies AC high-voltage current of the x-ray tube with a high-
them across the primary winding of the high-voltage frequency power supply. This effect is an essentially con-
transformer. The kVp dial therefore controls the volt- stant potential between the anode and cathode. The re-
age between the anode and cathode of the x-ray tube. sult is that the mean energy of the x-ray beam produced
The high-voltage transformer (see Fig. 1-8, E) provides by these x-ray machines is higher than that from a con-
the high-voltage required by the x-ray tube to acceler- ventional half-wave rectified machine operated at the
ate the electrons from the cathode to the anode and gen- same voltage. This is because the number of lower-
erate x-rays. It accomplishes this by boosting the peak energy (nondiagnostic) x-rays is reduced. These photons
voltage of the incoming line current to up to 60 to are produced as the voltage across the x-ray tube rises
100 kV and thus the peak energy of the electrons passing from zero to its peak and then decreases back again to
through the tube to up to 60 to 100 keV. zero during the voltage cycle in the half-wave rectified
Because the line current is AC (60 cycles per second), machine (see the "Production of X-Rays" section). For a
the polarity of the x-ray tube alternates at the same fre- given voltage setting and radiographic density, the im-
quency (Fig. 1-12, A). When the polarity of the voltage ages resulting from these constant-potential machines
applied across the tube is such that the target anode is have a longer contrast scale and lower patient dose com-
positive and the filament is negative, the electrons pared with conventional x-ray machines.
around the filament accelerate toward the positive tar-
get and current flows through the tube (Fig. 1-12, B). As
TIMER
the tube voltage is increased, the speed of the electrons
toward the anode increases. Because the line voltage is A timer is built into the high-voltage circuit to control
variable, the voltage potential between the anode and the duration of the x-ray exposure (see Fig. 1-8, I+). The
cathode varies. The kVp selector dial setting controls the timer controls the time that high voltage is applied to the
peak kilovoltage across the tube (see Fig. 1-8, I) during tube and therefore the time during which tube current
one cycle. When the electrons strike the focal spot of the flows and x-rays are produced. Before the high voltage is
target, some of their energy converts to x-ray photons. applied across the tube, however, the filament must be
X-rays are produced at the target with greatest efficiency brought to operating temperature to ensure an adequate
when the voltage applied across the tube is high. There- rate of electron emission. Subjecting the filament to con-
10 SECTION ONE THE PHYSICS OF IONIZING RADIATION

FIG. 1-12 A, A 60-cycle AC line voltage at a primary transformer. B, Voltage at the anode
varies up to the kVp setting (70 in this case). C, The intensity of radiation produced at the
anode increases as the anode voltage increases. (Modified from Johns HE, Cunningham JR:
The physics of radiology, ed 3, Springfield, III, 1969, Charles C Thomas.)

tinuous heating at normal operating current is not prac- exposure (e.g., 3, 6, 9, 15). The number of impulses di-
tical because maintaining the filament at a high temper- vided by 60 (the frequency of the power source) gives
ature for a long period shortens its life. Failure of the fil- the exposure time in seconds. Therefore 30 impulses is
ament is a common source of malfunction of x-ray tubes. equivalent to a half-second exposure.
To minimize filament burnout, the timing circuit first
sends a current through the filament for about half a sec-
TUBE RATING AND DUTY CYCLE
ond to bring it to the proper operating temperature. Af-
ter the filament is heated, the timer then applies power Each x-ray machine comes with tube rating specifica-
to the high-voltage circuit. In some circuit designs, a con- tions that describe the maximal exposure time that the
tinuous low-level current passing through the filament tube can be energized without risk of damage to the tar-
maintains it at a safe low temperature. In this case the de- get from overheating. These specifications describe in
lay to preheat the filament before each exposure is even graph form the maximal safe intervals (seconds) that
shorter. Accordingly, the machine should be left on con- the tube can be used for a range of voltages (kVp) and
tinuously during working hours. filament current (mA) values. These tube ratings gen-
Some x-ray machine timers are calibrated in fractions erally do not impose any restrictions on tube use for
and whole numbers of seconds. The time intervals on dental periapical radiography. If a dental x-ray unit is to
other timers are expressed as number of impulses per be used for extraoral exposures, however, the tube rat-
CHAPTER 1 RADIATION PHYSICS 11

ing chart should be mounted by the machine for easy

reference.
The duty cycle relates to the frequency with which
successive exposures can be made. The heat buildup at
the anode is measured in heat units defined by the fol-
lowing equation: heat units (HU) = kVp X mA X sec
( watt-sec), an actual measure of energy. The heat stor-
age capacity for anodes of various diagnostic tubes
ranges from 100,000 to 250,000 HU. Because of heat
generated at the anode, the interval between succes-
sive exposures must be long enough for its dissipation.
This characteristic is a function of the size of the an-
ode and the method used to cool it. The cooling char-
acteristics of anodes are described by the maximal
number of heat units it can store without damage and
the heat dissipation rate, which can be determined
from the cooling curves provided by the manufacturer
of each tube.

Production of X-Rays
Electrons traveling from the filament to the target con-
vert some of their KE into x-ray photons by the forma-
tion of bremsstrahlung and characteristic radiation.

BREMSSTRAHLUNG RADIATION
Bremsstrahlung interactions, the primary source of x-ray
photons from an x-ray tube, are produced by the sudden
stopping or slowing of high-speed electrons at the target.
When the electrons from the filament strike the tungsten
FIG. 1-13 Bremsstrahlung radiation is produced by the di-
target, x-ray photons are created if they either hit a target rect hit of electrons on the nucleus in the target (A) or by
nucleus directly or their path takes them close to a nu- the passage of electrons near the nucleus, which results in
cleus. If a high-speed electron hits the nucleus of a target electrons' being deflected and decelerated (B).
atom, all its kinetic energy is transformed into a single
x-ray photon (Fig. 1-13, A). The energy of the resultant
photon (in keV) is numerically equal to the energy of the ample, applies a fluctuating voltage of as much as 70 kVp
electron. This in turn is equal to the kilovoltage applied across the tube. This tube therefore produces x-ray pho-
across the x-ray tube at the instant of its passage. tons with energies ranging to a maximum of 70,000 eV
Most high-speed electrons, however, have near or (70 keV). Fig. 1-14 demonstrates the continuous spec-
wide misses with atomic nuclei (Fig. 1-13, B). In these trum of photon energies produced by an x-ray machine
interactions, a negatively charged high-speed electron is operating at 100 kVp. The reasons for this continuous
attracted toward the positively charged nuclei and loses spectrum are as follows:
some of its velocity. This deceleration causes the elec-
tron to lose some kinetic energy, which is given off in the 1. The continuously varying voltage difference between
form of a photon. The closer the high-speed electron the target and filament, which is characteristic of half-
approaches the nuclei, the greater is the electrostatic wave rectification, causes the electrons striking the
attraction on the electron, the braking effect, and the target to have varying levels of kinetic energy.
energy of the resulting bremsstrahlung photon. 2. Most electrons participate in many interactions
Bremsstrahlung interactions generate x-ray photons before all their kinetic energy is expended. As a con-
with a continuous spectrum of energy. The energy of an sequence, an electron carries differing amounts
x-ray beam may be described by identifying the peak op- of energy at the time of each interaction with a tung-
erating voltage (in kVp). A dental x-ray machine oper- sten atom that results in the generation of an x-ray
ating at a peak voltage of 70,000 volts (70 kVp) for ex- photon.
12 SECTION ONE THE PHYSICS OF IONIZING RADIATION

3. The bombarding electrons pass at varying distances of characteristic photons are a function of the energy lev-
around tungsten nuclei and are thus deflected to vary- els of various electron orbital levels and hence are char-
ing extents. As a result, they give up varying amounts acteristic of the target atoms. Characteristic radiation is
of energy in the form of bremsstrahlung photons. only a minor source of radiation from an x-ray tube.

CHARACTERISTIC RADIATION
Characteristic radiation occurs when an electron from Factors Controlling
the filament displaces an electron from a shell of a tung- the X-Ray Beam
sten target atom, thereby ionizing the atom. When this
happens, another electron in an outer shell of the tung- The x-ray beam emitted from an x-ray tube may be mod-
sten atom is quickly attracted to the void in the deficient ified to suit the needs of the application by altering the
inner shell (Fig. 1-15). When the displaced electron is re- beam exposure length (timer), exposure rate (mA),
placed by the outer-shell electron, a photon is emitted beam energy (kVp and filtration), beam shape (colli-
with an energy equivalent to the difference in the two mation), and target-patient distance.
orbital binding energies. Characteristic radiation from
the K shell occurs only above 70 kVp with a tungsten tar-
EXPOSURE TIME
get and occurs as discrete increments compared with
bremsstrahlung radiation (see Fig. 1-14). The energies Figure 1-16 portrays the changes in the x-ray spectrum
that result when the exposure time is increased while
the tube current (mA) and voltage (kVp) remain con-
stant. When the exposure time is doubled, the number
of photons generated is doubled, but the range of
photon energies is unchanged. Therefore changing the
time simply controls the "quantity" of the exposure,
the number of photons generated.

TUBE CURRENT (mA)

Fig. 1-17 illustrates the changes in the spectrum of pho-
tons that result from increasing tube current (mA) while
maintaining constant tube voltage (kVp) and exposure
ti me. As the mA setting is increased, more power is ap-
plied to the filament, which heats up and releases more
electrons that collide with the target to produce radia-
FIG. 1-14 Spectrum of photons emitted from an x-ray tion. Theoretically, a linear relationship exists between
beam generated at 100 kVp. The vast preponderance of mA and radiation output. Therefore the quantity of ra-
radiation is bremsstrahlung, with a minor addition of char- diation produced by an x-ray tube (i.e., the number of
acteristic radiation. photons that reach the patient and film) is directly pro-

FIG. 1-15 Characteristic radiation. A, An incident electron in an inner orbit ejects a pho-
toelectron, creating a vacancy. B, This vacancy is filled by an electron from an outer orbit.
C, A photon is emitted with energy equal to the difference in energy levels between the
two orbits. D, Electrons from various orbits may be involved, giving rise to other photons.
The energies of the photons thus created are characteristic of the target atom.
CHAPTER 1 RADIATION PHYSICS 13

portional to the tube current and the time the tube is op- difference between the cathode and anode, thus in-
erated. The quantity of radiation produced is expressed creasing the energy of each electron when it strikes the
as the product of time and tube current. The quantity of target. This results in an increased efficiency of conver-
radiation remains constant regardless of variations in mA sion of electron energy into x-ray photons, and thus an
and time as long as their product remains constant. For increase in (1) the number of photons generated, (2)
i nstance, a machine operating at 10 mA for 1 second their mean energy, and (3) their maximal energy. The
(10 mAs) produces the same quantity of radiation when increased number of high-energy photons produced per
operated at 20 mA for 0.5 second (10 mAs). Although unit time by use of higher kVp results from the greater
this is generally true, in practice some dental x-ray ma- efficiency in the production of bremsstrahlung photons
chines fall slightly short of this ideal. that occurs when increased numbers of higher-energy
electrons interact with the target.
The ability of x-ray photons to penetrate matter de-
TUBE VOLTAGE (kVp)
pends on their energy. High-energy x-ray photons have
Fig. 1-18 shows the way the spectrum of photon energies a greater probability of penetrating matter, whereas rel-
in a x-ray beam increases through increases in tube volt- atively low-energy photons have a greater probability of
age (kVp). Increasing the kVp increases the potential being absorbed. Therefore the higher the kVp and
mean energy of the x-ray beam, the greater the pene-
trability of the beam through matter. A useful way to
characterize the penetrating quality of an x-ray beam is
by its half-value layer (HVL). The HVL is the thickness
of an absorber, such as aluminum, required to reduce
by one half the number of x-ray photons passing
through it. As the average energy of an x-ray beam in-
creases, so does its HVL. The term quality refers to the
mean energy of an x-ray beam.

FILTRATION
An x-ray beam consists of a spectrum of x-ray photons
of different energies, but only photons with sufficient
energy to penetrate through anatomic structures and
reach the image receptor (usually film) are useful for di-
FIG. 1-16 Spectrum of photon energies showing that as agnostic radiology. Those that are of low energy (long
exposure time increases, so does the total number of pho- wavelength) contribute to patient exposure but do not
tons, but the mean energy and maximal energy of the beams have enough energy to reach the film. Consequently, to
are unchanged. reduce patient dose, the less-penetrating photons
should be removed. This can be accomplished by plac-

FIG. 1-17 Spectrum of photon energies showing that two FIG. 1-18 Spectrum of photon energies showing that as the
1 0-mA exposures result in slightly more radiation than one kVp is increased (with mA held constant), a corresponding
20-mA exposure. The difference, however, is slight. i ncrease occurs in the mean energy of the beam, the total
number of photons emitted, and the maximal energy of the
photons.
14 SECTION ONE THE PHYSICS OF IONIZING RADIATION

i ng an aluminum filter in the path of the beam. Fig. 1-19 escaping through the x-ray port. The inherent filtration
illustrates how the addition of an aluminum filter alters of most x-ray machines ranges from the equivalent of 0.5
the energy distribution of the unfiltered beam. The alu- to 2 mm of aluminum. Total filtration is the sum of the
minum preferentially removes many of the lower-energy inherent filtration plus any added external filtration sup-
photons with lesser effect on the higher-energy photons plied in the form of aluminum disks placed over the
that are able to penetrate to the film. port in the head of the x-ray machine. Governmental
In determinations of the amount of filtration re- regulations require the total filtration in the path of a
quired for a particular x-ray machine, kVp and inherent dental x-ray beam to be equal to the equivalent of 1.5
filtration of the tube and its housing must be consid- mm of aluminum to 70 kVp, and 2.5 mm of aluminum
ered. Inherent filtration consists of the materials that for all higher voltages. (See Chapter 3.)
x-ray photons encounter as they travel from the focal spot
on the target to form the usable beam outside the tube
enclosure. These materials include the glass wall of the
COLLIMATION
x-ray tube, the insulating oil that surrounds many dental A collimator is a metallic barrier with an aperture in
tubes, and the barrier material that prevents the oil from the middle used to reduce the size of the x-ray beam
(Fig. 1-20, A, B) and therefore the volume of irradiated
tissue within the patient. Round and rectangular colli-
mators are most frequently used in dentistry. Dental x-ray
beams are usually collimated to a circle 2 3/4 inches (7 cm)
in diameter. The round collimator (see Fig. 1-20, A) is a
thick plate of radiopaque material (usually lead) with a
circular opening centered over the port in the x-ray
head through which the x-ray beam emerges. Typically,
round collimators are built into open-ended aiming
cylinders. Rectangular collimators (see Fig. 1-20, B) fur-
ther limit the beam to a size just larger than that of the
x-ray film. The size of the beam should be reduced to
the size of the film being exposed to reduce further un-
necessary patient exposure. Some types of film-holding
instruments also provide rectangular collimation of the
x-ray beam. (See Chapters 3 and 9.)
FIG. 1-19 Filtration of an x-ray beam with aluminum results Use of collimation also improves image quality. When
i n the preferential removal of low-energy photons, reducing an x-ray beam is directed at a patient, about 90% of the
the intensity of the beam but increasing its mean energy. x-ray photons are absorbed by the tissues and 10% of

FIG. 1-20 Collimation of an x-ray beam (dotted area) is achieved by restricting its useful
size. A, Circular collimator. B, Rectangular collimator restricts area of exposure to just larger
than the detector size.
CHAPTER 1 RADIATION PHYSICS 15

the photons pass through the patient and reach the intensity is that the x-ray beam spreads out as it moves
film. Many of the absorbed photons generate scattered from the source. The relationship is as follows:
radiation within the exposed tissues by a process called
Compton scattering. These scattered photons travel in all
directions (Fig. 1-21). Many fog the film and thereby de-
grade image quality. The detrimental effect of scattered
radiation on the images can be minimized by collimat- where I is intensity and D is distance. Therefore if a dose
i ng the beam to reduce the number of scattered pho- of 1 gray (Gy) is measured at a distance of 2 m, a dose of
tons reaching the film. 4 Gy will be found at 1 m, and 0.25 Gy at 4 m.
Therefore changing the distance between the x-ray
tube and patient has a marked effect on beam intensity.
I NVERSE SQUARE LAW Such a change requires a corresponding modification
The intensity of an x-ray beam at a given point (number of the kVp or mAs if the exposure of the film is to be
of photons per cross-sectional area per unit exposure kept constant.
time) depends on the distance of the measuring device
from the focal spot. For a given beam the intensity is in-
versely proportional to the square of the distance from
the source (Fig. 1-22). The reason for this decrease in Interactions of X-Rays
with Matter
The intensity of an x-ray beam is reduced by interac-
tion with the matter it encounters. This attenuation re-
sults from interactions of individual photons in the
beam with atoms in the absorber. The x-ray photons
are either absorbed or scattered out of the beam. In
absorption, photons ionize absorber atoms and convert
their energy into KE of the absorber electrons. In scat-
tering, photons are ejected out of the primary beam as
a result of interactions with the orbital electrons of ab-
sorber atoms. In the case of a dental x-ray beam, three
mechanisms exist by which these interactions take
place: (1) coherent scattering, (2) photoelectric ab-
sorption, and (3) Compton scattering. In addition,
about 9% of the primary photons pass through the pa-
FIG. 1-21 Scattered radiation resulting from Compton in- tient without interaction (Table 1-1).
teraction (A) may strike the film and degrade the radio-
graphic image by causing film fog. Photons may also be ab-
sorbed (8) or pass through the object without interacting (C).

FIG. 1-22 The intensity of an x-ray beam is inversely pro-

portional to the square of the distance between the source *Scattered photons result from primary, Compton, and coherent interactions.
and the point of measure. From Gibbs SJ: Personal communication, 1986.
16 SECTION ONE THE PHYSICS OF IONIZING RADIATION

COHERENT SCATTERING
bration causes the electron to radiate energy in the form
Coherent scattering (also known as classical scattering) of another x-ray photon with the same frequency and
may occur when a low-energy incident photon passes energy as in the incident beam. Usually the secondary
near an outer electron of an atom (which has a low bind- photon is emitted at an angle to the path of the incident
ing energy). The photon may not be absorbed but scat- photon. In effect, the direction of the incident x-ray pho-
tered without a loss of energy (Fig. 1-23). The incident ton is altered. This interaction accounts for only about
photon interacts with the electron by causing it to vibrate 8% of the total number of interactions (per exposure)
momentarily at the same frequency as the incoming pho- in a dental examination (see Table 1-1). Coherent scat-
ton. The incident photon then ceases to exist. The vi- tering contributes very little to film fog because the total
quantity of scattered photons is small and its energy level
is too low for much of it to reach the film.

PHOTOELECTRIC ABSORPTION
Photoelectric absorption occurs when an incident pho-
ton collides with a bound electron in an atom of the ab-
sorbing medium. At this point the incident photon
ceases to exist. The electron is ejected from its shell and
becomes a recoil electron (photoelectron) (Fig. 1-24).
The kinetic energy imparted to the recoil electron is
equal to the energy of the incident photon minus that
used to overcome the binding energy of the electron.
The absorbing atom is now ionized because it has lost
an electron. In the case of atoms with low atomic num-
bers (e.g., those in most biologic molecules), the bind-
ing energy is small. As a result the recoil electron ac-
quires most of the energy of the incident photon. Most
FIG. 1-23 Coherent scattering resulting from the interac- photoelectric interactions occur in the K shell because
tion of a low-energy incident photon with an outer electron, the density of the electron cloud is greater in this region
causing it to vibrate momentarily. After this, a scattered pho- and a higher probability of interaction exists. About
ton of the same energy is emitted at a different angle from 30% of photons absorbed from a dental x-ray beam are
the path of the incident photon. absorbed by the photoelectric process.

FIG. 1-24 A, Photoelectric absorption occurs when an incident photon gives up

all its energy to an inner electron ejected from the atom (a photoelectron). B, An
electron vacancy in the inner orbit results in ionization of the atom. C, An elec-
tron from a higher energy level fills the vacancy and emits characteristic radiation.
D, All orbits are subsequently filled, completing the energy exchange.
CHAPTER 1 RADIATION PHYSICS 17

An atom that has participated in a photoelectric in- tal radiographs. It is this difference in the absorption
teraction is ionized. This electron deficiency (usually in that makes the production of a radiographic image
the K shell) is instantly filled, usually by an L-shell elec- possible.
tron, with the release of characteristic radiation (see Fig.
1-15). Whatever the orbit of the replacement electron,
COMPTON SCATTERING
the characteristic photons generated are of such low en-
ergy that they are absorbed within the patient and do Compton scattering occurs when a photon interacts with
not fog the film. an outer orbital electron (Fig. 1-25). In this interaction
The recoil electrons ejected during photoelectric the incident photon collides with an outer electron,
absorptions travel only a short distance in the absorber which receives kinetic energy and recoils from the point
before they give up their energy. As a consequence, all of impact. The incident photon is then deflected by its
the energy of incident photons that undergo photo- interaction and is scattered from the site of the collision.
electric interaction is deposited in the patient. This is The energy of the scattered photon equals the energy of
beneficial in producing high-quality radiographs, be- the incident photon minus the kinetic energy gained by
cause no scattered radiation fogs the film, but poten- the recoil electron plus its binding energy. As with photo-
tially deleterious for patients because of increased electric absorption, Compton scattering results in the
radiation absorption. loss of an electron and ionization of the absorbing atom.
The frequency of photoelectric interaction varies Scattered photons travel in all directions. The higher
directly with the third power of the atomic number of the energy of the incident photon, however, the greater
the absorber. For example, because the effective the probability that the angle of scatter of the secondary
atomic number of compact bone (Z = 13.8) is greater photon will be small and its direction will be forward.
than water (Z = 7.4), the probability that a photon will Approximately 30% of the scattered photons formed
be absorbed by a photoelectric interaction in bone is during a dental x-ray exposure (primarily from Comp-
approximately 6.5 times greater than in an equal dis- ton scattering) exit the patient's head. This is advanta-
tance of water. This difference is readily seen on den- geous to the patient because some of the energy of the

FIG. 1-25 Compton absorption occurs when an incident photon interacts with an outer
electron, producing a scattered photon of lower energy than the incident photon and a re-
coil electron ejected from the target atom.
18 SECTION ONE THE PHYSICS OF IONIZING RADIATION

i ncident x-ray beam escapes the tissue, but it is disad- intensity by half, in the preceding example, the HVL is
vantageous because it causes nonspecific film darken- 1.5 cm. The absorption of the beam depends primarily
i ng. Scattered photons darken the film while carrying on the thickness and mass of the absorber and the en-
no useful information to it because their path is altered. ergy of the beam.
The probability of Compton scattering is directly pro- The spectrum of photon energies (as illustrated by the
portional to the electron density. The number of electrons kVp setting) in an x-ray beam is wide. In such a hetero-
in bone (5.55 X 10 23 per cc) is greater than in water geneous beam the probability of absorption of individual
(3.34 X 10 23 per cc); therefore the probability of Comp- photons depends on their energy. Low-energy photons
ton scattering is correspondingly greater in bone than are much more likely than high-energy photons to be
in tissue. In a dental x-ray beam, approximately 62% of absorbed. As a consequence the superficial layers of an
the photons undergo Compton scattering. absorber tend to remove the low-energy photons and
The importance of photoelectric absorption and transmit the higher-energy photons. Therefore as an
Compton scattering in diagnostic radiography relates to x-ray beam passes through matter, the intensity of the
differences in the way photons are absorbed by various beam decreases but the mean energy of the resultant
anatomic structures. The number of photoelectric and beam increases. In contrast to the absorption of a mono-
Compton interactions is greater in hard tissues than in chromatic beam, an x-ray beam is absorbed less and less
soft tissues. As a consequence, more photons in the by each succeeding unit of absorber thickness. For ex-
beam exit the patient after passing through soft tissue ample, the first 1.5 cm of water might absorb about 40%
than through hard tissue. This allows a radiograph to of the photons in an x-ray beam with a mean energy of
provide a clear image of enamel, dentin, bone, and soft
tissues.

SECONDARY ELECTRONS
In both photoelectric absorption and Compton scatter-
ing, electrons are ejected from their orbits in the absorb-
ing material after interaction with x-ray photons. These
secondary electrons give up their energy in the absorber
by either of two processes: (1) collisional interaction with
other electrons, resulting in ionization or excitation of
the affected atom, and (2) radiative interactions, which
produce bremsstrahlung radiation resulting in the emis-
sion of low-energy x-ray photons. Secondary electrons
eventually dissipate all their energy, mostly as heat by col-
lisional interactions, and come to rest.

BEAM ATTENUATION
As a dental x-ray beam travels through matter, individ-
ual photons are removed, primarily through photoelec-
tric and Compton interactions. The reduction of beam
intensity is predictable because it depends on physical
characteristics of the beam and absorber. A monochro-
matic beam of photons, a beam in which all the photons
have the same energy, provides a good example. When
just the primary (not scattered) photons are considered,
a constant fraction of the beam is attenuated as the
beam moves through each unit thickness of an absorber.
Therefore 1.5 cm of water may reduce a beam intensity
FIG. 1-26 Exponential decay of intensity in a homoge-
by 50%, the next 1.5 cm by another 50% (to 25% of the neous photon beam through the absorber, where the HVL is
original intensity), and so on. This is an exponential pat- 1.5 cm of absorber. The curve for a heterogeneous x-ray
tern of absorption (Fig. 1-26). The HVL described ear- beam does not drop quite as precipitously because of the
lier in this chapter is a measure of beam energy describ- preferential removal of low-energy photons and the increased
ing the amount of an absorber that reduces the beam mean energy of the resulting beam.
CHAPTER 1 RADIATION PHYSICS 19

,50 kVp. The mean energy of the remnant beam might in- ability to produce ionization in air under standard con-
crease 20% as a result of the loss of lower-energy photons. ditions of temperature and pressure (STP).
The next 1.5 cm of water removes only about 30% of the
photons as the average energy of the beam increases an-
UNITS OF MEASUREMENT
other 10%. If the water test object is thick enough, the
mean energy of the remnant beam approaches the peak Table 1-2 presents some of the more frequently used
voltage applied across the tube and absorption becomes units for measuring quantities of radiation. In recent
similar to that of a monochromatic beam. years a move has occurred to use a modernized version
The attenuation of a beam depends on both the en- of the metric system called the SI system (Systeme
ergy of the incident beam and the composition of the International d'Unites). This book uses SI units.
absorber. In general, as the energy of the beam in-
creases, so does the transmission of the beam through Exposure
the absorber. When the energy of the incident photon Exposure is a measure of radiation quantity, the capacity
is raised to the binding energy of the K -shell electrons of radiation to ionize air. The roentgen (R) is the tradi-
of the absorber, however, the probability of photoelec- tional unit of radiation exposure measured in air; 1 R is
tric absorption increases sharply and the number of that amount of x-radiation or gamma radiation that pro-
transmitted photons is greatly decreased. This is called duces 2.08 X 10`3 ion pairs in 1 cc of air (STP). It measures
K-edge absorption. (The probability that a photon will in- the intensity of radiation to which an object is exposed.
teract with an orbital electron is greatest when the en- No specific SI unit is equivalent to the R, but in terms of
ergy of the photon equals the binding energy of the other SI units it is equal to coulombs per kilogram (C/kg);
electron; it decreases as the photon energy increases.) 1 R = 2.58 X 10-4 C/kg, and 1 C/kg equals 3.88 X 103 R.
Photons with energy less than the binding energy of' The roentgen applies only for x-rays and gamma rays. In
K-shell electrons interact photoelectrically only with recent years the roentgen has been replaced by air kerma,
electrons in the L shell and in shells even farther from an acronym for kinetic energy released in matter. Kerma
the nucleus. Rare earth elements are sometimes used as measures the KE transferred from photons to electrons
filters because their K edges (50.2 keV for gadolinium) ans is expressed in units of dose (Gy).
greatly increase the absorption of high-energy photons.
This is desirable because these high-energy photons are Absorbed Dose
not as likely to contribute to a radiographic image as Absorbed dose is a measure of the energy absorbed by
mid-energy photons. any type of ionizing radiation per unit mass of any type
of matter. The SI unit is the gray (Gy)-1 Gy equals
l joule/kg. The traditional unit of absorbed dose is the
Dosimetry rad (radiation absorbed dose), where 1 rad is equivalent
to 100 ergs/g of absorber. One gray equals 100 rads.
Determining the quantity of radiation exposure or dose
is termed dosimetry. The term dose is used to describe the Equivalent Dose
amount of energy absorbed per unit mass at a site of in- The equivalent dose (H T) is used to compare the bio-
terest. Exposure is a measure of radiation based on its logic effects of different types of radiation on a tissue or
20 SECTION ONE THE PHYSICS OF IONIZING RADIATION

organ. It is the sum of the products of the absorbed dose The tissue weighting factors include gonads, 0.20; red
( D T ) averaged over a tissue or organ and the radiation bone marrow, 0.12; esophagus, 0.05; thyroid, 0.05; skin,
weighting factor (WR ): 0.01; and bone surface, 0.01. The unit of effective dose
is the sievert (Sv). The use of this term is described more
fully in Chapter 3.
It is expressed as a sum to allow for the possibility that
the tissue or organ has been exposed to more than one Radioactivity
type of radiation. The radiation weighting factor is cho- The measurement of radioactivity (A) describes the de-
sen for the type and energy of the radiation involved. cay rate of a sample of radioactive material. The SI unit
Therefore high-LET radiations (which are more damag- is the becquerel (Bq); 1 Bq equals 1 disintegration/
i ng to tissue than low-LET radiations) have a corre- second. The traditional unit is the curie (Ci), which cor-
spondingly higher WR. For example, the WR of photons is responds to the activity of 1 g of radium (3.7 X 10'° dis-
1; of 5-keV neutrons and high-energy protons, 5; and integrations/sec).
of alpha particles, 20. The unit of equivalent dose is the
sievert (Sv). For diagnostic x-ray examinations, 1 Sv
equals 1 Gy. The traditional unit of equivalent dose is BIBLIOGRAPHY
the rem (roentgen equivalent man). One sievert equals Bushberg JT et al: The essential physics of medical imaging; Balti-
100 rem. more, 1994, Williams & Wilkins.
Bushong SC: Radiologic science for technologists: physics, biology,
Effective Dose and protection, ed 5, St Louis, 1993, Mosby.
The effective dose (E) is used to estimate the risk in hu- Curry TS, DowdeyJE, Murry RC: Christensen's introduction to the
mans. It is the sum of the products of the equivalent physics of diagnostic radiology, ed 4, Philadelphia, 1990, Lea &
dose to each organ or tissue (H T ) and the tissue weight- Febiger.
i ng factor (WT): International Commission on Radiological Protection: Radia-
tion protection, I CRP Publ. 60, Oxford, England, 1990, Author.
Radiation
Biology

adiation biology is the study of the effects of

ionizing radiation on living systems. This disci-
pline requires studying many levels of organization within
biologic systems spanning broad ranges in size and tem-
poral scale. The initial interaction between ionizing radi-
ation and matter occurs at the level of the electron within
the first 10-13 second after exposure. These changes result
in modification of biologic molecules within the ensuing
seconds to hours. In turn, the molecular changes may
lead to alterations in cells and organisms that persist for
hours, decades, and possibly even generations. They may
result in injury or death of the cell or organism.
Biologic effects of ionizing radiation may be divided into
two broad categories: deterministic effects and stochastic
effects. Deterministic effects are those effects in which the
severity of response is proportional to the dose. These ef-
fects 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 and radiation
sickness after whole-body irradiation. By contrast, stochastic
effects are those for which the probability of occurrence of
the change, rather than its severity, is dose dependent. Sto-
chastic effects are all-or-none: 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.

Radiation Chemistry
Radiation acts on living systems through direct and in-
direct effects. When the energy of a photon or sec-
ondary electron ionizes biologic macromolecules, the
effect is termed direct. Alternatively, the photon may be
absorbed by water in an organism, ionizing the water
molecules. The resulting ions form free radicals (radi- These molecules are not stable and dissociate rapidly
olysis of water) that in turn interact with and produce to form a hydroxyl ion and hydrogen free radical:
changes in the biologic molecules. Because intermedi-
ate changes involving water molecules are required, this
series of events is termed indirect. The positively charged water molecule reacts with an-
other water molecule to form a hydroxyl free radical:

DIRECT EFFECT
Direct alteration of biologic molecules (RH, where R is Water may also be excited and dissociate directly into
the molecule and His a hydrogen atom) by ionizing ra- hydrogen and hydroxyl free radicals:
diation begins with absorption of energy by the biologic
molecule and formation of unstable free radicals (atoms
or molecules having an unpaired electron in the valence Whereas the radiolysis of water is extremely complex,
shell). They are extremely reactive and have very short in balance water is largely converted to hydrogen and
lives, quickly reforming into stable configurations by dis- hydroxyl free radicals.
sociation (breaking apart) or cross-linking (joining of The generation of free radicals occurs in less than
two molecules). 10-10 second after the passage of a photon. These radi-
Free radical production: cals play a dominant role in producing molecular
changes in biologic molecules.
When dissolved molecular oxygen (0 2 ) is present in
irradiated water, hydroperoxyl free radicals may also be
formed:

Hydroperoxyl free radicals also may contribute to the

formation of hydrogen peroxide in tissues:

Because the altered molecules differ structurally and

functionally from the original molecules, the conse-
quence is a biologic change in the irradiated organism.
Approximately one third of the biologic effects of x-ray exposure Both peroxyl radicals and hydrogen peroxide are
result from direct effects. oxidizing agents that can significantly alter biologic mol-
ecules and cause cell destruction. They are considered
to be major toxins produced in the tissues by ionizing
RADIOLYSIS OF WATER radiation.
A complex series of chemical changes occurs in water
after exposure to ionizing radiation. Collectively these
I NDIRECT EFFECTS
reactions result in the radiolysis of water. The first step is
ionization of water resulting from the absorption of a Because water is the predominant molecule in biologic
photon or interaction with a photoelectron or Compton systems (about 70% by weight), it frequently participates
electron. Displacement of an electron from the water in the interactions between x-ray photons and the biologic
molecule results in an ion pair, a positively charged wa- molecules of an organism. About two thirds of radiation-
ter molecule (H 2 0+) and the displaced electron: induced biologic damage results from indirect effects.
The interaction of hydrogen and hydroxyl free radicals
with organic molecules can result in the formation of or-
ganic free radicals. Such reactions may involve the re-
The displaced electron is usually captured by a water moval of hydrogen:
molecule to form a negatively charged water molecule
( H 20 - ):

23
24 SECTION TWO BIOLOGIC EFFECTS OF RADIATION

The OH' free radical is more important in causing tion required to induce significant amounts of protein
such damage. denaturation (or enzyme inactivation) is much higher
Organic free radicals are unstable and transform into than that required to induce gross cellular changes or
stable altered molecules as described in the earlier sec- cell death. Such data suggest that radiation-induced
tion in this chapter on direct effects (p. 23). These al- changes in protein structure and function are not the
tered molecules have different chemical and biologic major cause of radiation effects after absorption of mod-
properties from the original molecules. The important erate doses (2 to 4 Gy) of radiation.
role of water radiolysis and the indirect action of radia-
tion may be seen by comparing the radiation dose re-
quired to inactivate enzymes when dry or in solution.
The dose required to inactivate 37% of dry yeast inver-
Radiation Effects
tase is 110 kGy but only 60 kGy when the enzyme is irra- at the Cellular Level
diated in solution.
EFFECTS ON INTRACELLULAR
STRUCTURES
CHANGES IN BIOLOGIC MOLECULES
The effects of radiation on intracellular structures result
Nucleic Acids from radiation-induced changes in their macromole-
The last few decades have seen a growing appreciation cules. Although the initial molecular changes are pro-
for the crucial role of nucleic acids in determining cel- duced within a fraction of a second after exposure, cel-
lular functions. It is clear that damage to the deoxyri- lular changes resulting from moderate exposures usually
bonucleic acid (DNA) molecule is primarily responsible require a minimum of hours to become apparent. These
for cell death after radiation exposure. Radiation pro- changes are manifest initially as structural and func-
duces a number of different types of alterations in DNA, tional changes in cellular organelles. Later, cell death
including the following: may occur.
1. Change or loss of a base
2. Disruption of hydrogen bonds between DNA strands Nucleus
3. Breakage of one or both DNA strands A wide variety of radiobiologic data indicate that the nu-
4. Cross-linking of DNA strands within the helix, to cleus is more radiosensitive (in terms of lethality) than
other DNA strands, or to proteins the cytoplasm, especially in dividing cells. The sensitive
site in the nucleus is the DNA within chromosomes.
The amount of radiation required to cause disrup-
tion of DNA molecules (e.g., an average of one single- Chromosome Aberrations
strand break per molecule) is much higher than is re- Chromosomes serve as useful markers for radiation in-
quired to cause cell death. Such evidence suggests that if jury. They may be easily visualized and quantified, and
DNA is the molecular target in a cell, relatively few bio- the extent of their damage is related to cell survival.
chemical lesions of the types just listed may be required Chromosome aberrations are observed in irradiated
to result in cell death. DNA sensitivity to radiation re- cells at the time of mitosis when the DNA condenses to
sults from its complex replication mechanism in mitoti- form chromosomes. The type of damage that may be ob-
cally active cell populations. served depends on the stage of the cell in the cell cycle
at the time of irradiation.
Proteins Fig. 2-1 shows the stages of the cell cycle. If radiation
Irradiation of proteins in solution usually leads to exposure occurs after DNA synthesis (i.e., in G 2 or
changes in their secondary and tertiary structures mid and late S), only one arm of the affected chromosome
through disruption of side chains or the breakage of hy- is broken (chromatid aberration) (Fig. 2-2, A). If the
drogen or disulfide bonds. Such changes lead to denat- radiation-induced break occurs before the DNA has repli-
uration. The primary structure of the protein is usually cated (i.e., in G1 or early S), the damage manifests as a
not significantly altered. Irradiation may also induce in- break in both arms (chromosome aberration) at the next
termolecular and intramolecular cross-linking. When an mitosis (Fig. 2-2, B). Most simple breaks are repaired by
enzyme is irradiated, the biologic effect of the radiation biologic processes and go unrecognized. Fig. 2-3 illustrates
may become amplified. For example, inactivation of an several common forms of chromosome aberrations re-
enzyme molecule results in its failure to convert many sulting from incorrect repair. Such radiation-induced
substrate molecules to their products. Thus many mole- aberrations may result in unequal distribution of chro-
cules become subsequently affected, although only a matin material to daughter cells or prevent completion of
small number were initially damaged. The dose of radia- a subsequent mitosis. Chromosome aberrations have been
CHAPTER 2 RADIATION BIOLOGY 25

changes probably play only a minor role in the cellular

changes seen in rapidly dividing cells after exposure to
moderate doses of radiation (2 to 4 Gy).

EFFECTS ON CELL KINETICS

The effects of radiation on the kinetics (turnover rate)
of a cell population have been studied in rapidly divid-
ing cell systems such as skin and intestinal mucosa and
in cell culture systems. Irradiation of such cell popula-
tions will cause a reduction in size of the irradiated tis-
sue as a result of mitotic delay (inhibition of progression
of the cells through the cell cycle) and cell death (usu-
ally during mitosis).

FIG. 2-1 Cell cycle. A proliferating cell moves in the cycle Mitotic Delay
from mitosis to gap 1 (G1) to the period of DNA synthesis Mitotic delay occurs after irradiation of a population of
(S) to gap 2 (G 2 ) to the next mitosis. dividing cells. Fig. 2-4 illustrates the effect of radiation
on mitotic activity. A low dose of radiation induces mild
mitotic delay in G2 cells. The delayed cells subsequently
pass through mitosis with other (nondelayed) cells, giv-
ing rise to an elevated mitotic index. A moderate dose
results in a longer mitotic delay (G 2 block) and some
cell death. The area under the curve of the following
supranormal mitotic index is smaller than that of the
preceding mitotic delay, indicating some cell death.
Larger doses may cause a profound mitotic delay with
incomplete recovery.

Cell Death
Mitosis-linked death in a cell population is loss of the ca-
pacity for mitotic division. Cell death results from dam-
age to the nucleus that results in chromosome aberra-
tions. This damage causes the cell to die, usually while
FIG. 2-2 Chromosome aberrations. A, I rradiation of the attempting to complete the first few mitoses after irra-
cell after DNA synthesis results in a single-arm chromatid diation. Reproductive death occurs in a dividing cell
aberration. B, Irradiation before DNA synthesis results in a population after exposure to a moderate dose of radia-
double-arm aberration.
tion, which accounts for the radiosensitivity of tissues.
When a population of nondividing cells is irradiated,
much larger doses and longer time intervals are re-
detected in peripheral blood lymphocytes of patients ex- quired for induction of interphase death.
posed to medical diagnostic procedures. Moreover, the Survival curves are used to study the response of repli-
survivors of the atom bombings of Hiroshima and Na- cating cells exposed in culture. Single cells grown in tis-
gasaki have demonstrated chromosome aberrations in sue culture are dispersed onto plates, where they form
circulating lymphocytes more than two decades after the colonies. The plates are irradiated before colony growth,
radiation exposure. The frequency of aberrations is gen- and the effect of the irradiation on the reproductivity of
erally proportional to the radiation dose received. the cells is studied.
Fig. 2-5 shows typical survival curves for cells exposed
Cytoplasm to x-radiation in which the fraction of surviving cells is
Radiation effects occur in cellular structures other than compared with the absorbed dose. The value n is the ex-
nuclei and chromosomes. After relatively large doses of trapolation number and measures the size of the shoul-
radiation (30 to 50 Gy), mitochondria demonstrate in- der. The shoulder in the survival curve represents either
creased permeability, swelling, and disorganization of the accumulation of sublethal damage before cells die or
the internal cristae. Such permeability and structural a measure of the repair process active early in the period
26 SECTION TWO BIOLOGIC EFFECTS OF RADIATION

FIG. 2-3 Chromosome aberrations. A, Ring formation; B, dicentric formation; C, translo-

cation. In D and E the arrows point to tetracentric exchange and chromatid exchange tak-
i ng place in Trandescontia, an herb. (D and E courtesy Dr. M. Miller, Rochester, N.Y.)
CHAPTER 2 RADIATION BIOLOGY 27

of irradiation. DO indicates the slope of the straight por-

tion of the curve. It measures the amount of radiation re-
quired to reduce the number of colony-forming cells to
37% and thus is the dose required to deliver an average of
one cell-killing event per cell. Survival curves have helped
researchers understand the response of cells to irradia-
tion under various conditions.

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 (e.g., in radiation ther-
apy) than when the same total dose is given in a single
brief exposure. Damage to both strands of DNA at the
FIG. 2-4 Radiation-induced mitotic delay. The degree of
same site (usually caused by particulate radiation) is usu-
delay in a replicating cell population depends on the amount ally lethal to the cell.
of exposure. A large dose severely depresses mitosis and pro-
l ongs recovery. RADIOSENSITIVITY AND CELL TYPE

Different cells from various organs of the same individ-

ual may respond to irradiation quite differently. This
variation was recognized as early as 1906 by the French
radiobiologists Bergonie and Tribondeau. They ob-
served that the most radiosensitive cells are those that
(1) have a high mitotic rate, (2) undergo many future
mitoses, and (3) are most primitive in differentiation.
These findings are still true except for lymphocytes and
oocytes, which are very radiosensitive even though they
are highly differentiated and nondividing.
Mammalian cells may be divided into five categories
of radiosensitivity on the basis of histologic observations
of early cell death:

1. Vegetative intermitotic cells are the most radiosensitive.

They divide regularly, have long mitotic futures, and
do not undergo differentiation between mitoses.
These are stem cells that retain their primitive prop-
erties and whose function is to replace themselves.
Examples include early precursor cells, such as those
in the spermatogenic or erythroblastic series, and
basal cells of the oral mucous membrane.
2. Differentiating intermitotic cells are somewhat less
radio-sensitive than vegetative intermitotic cells be-
cause they divide less often. They divide regularly,
although they undergo some differentiation be-
tween divisions. Examples of this class include in-
termediate dividing and replicating cells of the in-
ner enamel epithelium of developing teeth, cells of
FIG. 2-5 Survival curve for mammalian cells grown in cul-
ture after irradiation. I n this case the cells have an extrapo-
the hematopoietic series that are in the intermedi-
l ation number (n) of about 2 and a D o of about 3.6 Gy. The ate stages of differentiation, spermatocytes, and
n value is a measure of the size of the shoulder; D o i s the oocytes.
amount of radiation required to reduce the surviving popu- 3. Multipotential connective tissue cells have intermediate
l ation to 37% of its former size. radiosensitivity. They divide irregularly, usually in re-
28 SECTION TWO BIOLOGIC EFFECTS OF RADIATION

sponse to a demand for more cells, and are also ca-

pable of limited differentiation. Examples are vas-
cular endothelial cells, fibroblasts, and mesenchy-
mal cells.
4. Reverting postmitotic cells are generally radioresistant
because they divide infrequently. They also are gen-
erally specialized in function. Examples include the
acinar and ductal cells of the salivary glands and pan-
creas as well as parenchymal cells of the liver, kidney,
and thyroid.
5. Fixed postmitotic cells are most resistant to the direct
action of radiation. They are the most highly differ-
entiated cells and, once mature, are incapable of di-
vision. Examples of these cells include neurons, stri-
ated muscle cells, squamous epithelial cells that have
differentiated and are close to the surface of oral mu-
cous membrane, and erythrocytes.
LONG-TERM EFFECTS
The long-term deterministic effects of radiation on tis-
sues and organs depend primarily on the extent of dam-
Radiation Effects at the Tissue age to the fine vasculature. The relative radiosensitivity
and Organ Level of capillaries and connective tissue is intermediate be-
tween that of differentiating intermitotic cells and re-
The radiosensitivity of a tissue or organ is measured by verting postmitotic cells. Irradiation of capillaries causes
its response to irradiation. A fairly small number of lost swelling, degeneration, and necrosis. These changes in-
cells results in no clinical effect. With an increased num- crease capillary permeability and initiate a slow pro-
ber of lost cells, all affected organisms display a clinical gressive fibrosis around the vessels. As a result, deposi-
result. The severity of this change depends on the dose tion of fibrous scar tissue is increased around the vessels,
and thus the amount of cell loss. The following discus- leading to premature narrowing and eventual oblitera-
sion pertains to the effect of irradiation of tissues and tion of vascular lumens. This impairs the transport of
organs when the exposure is restricted to a small area. oxygen, nutrients, and waste products and results in
Moderate doses to a localized area may lead to repairable death of all cell types. The net result is progressive fibro-
damage. Comparable doses to a whole organism may re- atrophy of the irradiated tissue.
sult in death from damage to the most sensitive systems Such progressive atrophic changes lead to a loss of cell
in the body. function and a reduced resistance of irradiated tissue to
infection and trauma. These cellular changes are the basis
for long-term radiation-induced atrophy of tissues and or-
SHORT-TERM EFFECTS
gans. Death of parenchymal cells after moderate exposure
The short-term effects of radiation on a tissue are de- is thus the result of (1) mitotic-linked death of rapidly di-
termined primarily by the sensitivity of its parenchymal viding cells in the short term and (2) the consequences of
cells. If continuously proliferating tissues (e.g., bone progressive fibroatrophy on all cell types over time.
marrow, oral mucous membranes) are irradiated with
a moderate dose, cells are lost primarily by mitosis-
MODIFYING FACTORS
linked death. The extent of cell loss depends on dam-
age to the stem cell pools and the proliferative rate The response of cells to irradiation depends on varia-
of the cell population. The effects of irradiation of tions in exposure parameters and the environment of
such tissues become apparent relatively quickly as a re- the cell.
duction in the number of mature cells in the series.
Tissues composed of cells that rarely or never divide Dose
(e.g., muscle) demonstrate little or no radiation- The severity of deterministic damage seen in irradiated
induced hypoplasia over the short term. The relative tissues or organs depends on the amount of radiation
radiosensitivity of various tissues and organs is shown received. Very often a clinical threshold dose exists be-
in Table 2-1. low which no adverse effects are seen. All individuals re-
CHAPTER 2 RADIATION BIOLOGY 29

FIG. 2-6 Survival curve for mammalian cells grown in cul- FIG. 2-7 Survival curve for mammalian cells grown in cul-
ture after irradiation at low and high dose rates. A high ture after irradiation with and without oxygen. The presence
dose rate kills more cells because less time exists for repair of of oxygen increases the cells' sensitivity to radiation: the D o
sublethal damage. value is reduced from 3.6 Gy when irradiated without oxy-
gen to 1.8 Gy in the presence of oxygen. The oxygen en-
hancement ratio measures the influence of oxygen.

ceiving doses above the threshold level show damage in sustained in the presence of oxygen is related to the in-
proportion to the dose. creased amounts of hydrogen peroxide and hydroper-
oxyl free radicals formed. The oxygen enhancement
Dose Rate ratio measures the extent of this damage. It is the dose
The term dose rate indicates the rate of exposure. For ex- required to achieve a given endpoint (e.g., 50% survival
ample, a total dose of 5 Gy may be given at a high dose of a cell population) under anoxic conditions divided
rate (5 Gy/min) or a low dose rate (5 mGy/min). Expo- by the dose required to produce the same endpoint un-
sure of biologic systems to a given dose at a high dose rate der fully oxygenated conditions. Fig. 2-7 demonstrates
causes more damage than exposure to the same total oxygen's influence on cell survival curves.
dose given at a lower dose rate. When organisms are ex-
posed at lower dose rates, a greater opportunity exists for Linear Energy Transfer
repair of damage, thereby resulting in less net damage. In general, the dose required to produce a certain bio-
Fig. 2-6 illustrates the effects of dose rate schematically. logic effect is reduced as the linear energy transfer
(LET) of the radiation is increased. Thus higher-LET
Oxygen radiations (e.g., alpha particles) are more efficient in
The radioresistance of many biologic systems increases damaging biologic systems because their high ionization
by a factor of 2 or 3 when irradiation is conducted with density is more likely than x-rays to induce double-
reduced oxygen (hypoxia). The greater cell damage strand breakage in DNA.
30 SECTION TWO BIOLOGIC EFFECTS OF RADIATION

Radiation Effects mation of a white to yellow pseudomembrane (the

desquamated epithelial layer). At the end of therapy the
on the Oral Cavity mucositis is usually most severe, discomfort is at a maxi-
mum, and food intake is difficult. Good oral hygiene
RATIONALE OF RADIOTHERAPY minimizes infection. Topical anesthetics may be re-
The oral cavity is irradiated during the course of treating quired at mealtimes. Secondary yeast infection by Can-
radiosensitive oral malignant tumors, usually squamous dida albicans is a common complication and may require
cell carcinomas. The specific treatment of choice for a treatment.
lesion depends on many tumor variables such as radio- After irradiation is completed, the mucoua begins to
sensitivity, histology, size, location, invasion into adjacent heal rapidly. Healing is usually complete by about 2
structures, and duration of symptoms. Radiation ther- months. At later intervals (months to years) the mucous
apy for malignant lesions in the oral cavity is usually in- membrane tends to become atrophic, thin, and relative-
dicated when the lesion is radiosensitive, advanced, or ly avascular. This long-term atrophy results from pro-
deeply invasive and cannot be approached surgically. gressive obliteration of the fine vasculature and fibrosis
Combined surgical and radiotherapeutic treatment of- of the underlying connective tissue. These atrophic
ten provides optimal treatment. Increasingly, chemo- changes complicate wearing of dentures because they
therapy is being combined with radiation therapy and may cause oral ulcerations of the compromised tissue.
surgery. Ulcers can result from a denture sore, radiation necro-
Fractionation of the total x-ray dose into multiple small sis, or tumor recurrence. A biopsy may be required to
doses provides greater tumor destruction than is possible make the differentiation.
with a large single dose. Fractionation characteristically
also allows increased cellular repair of normal tissues, Taste Buds
which are believed to have an inherently greater capacity Taste buds are sensitive to radiation. Doses in the thera-
for recovery than tumor cells. Fractionation also increases peutic range cause extensive degeneration of the nor-
the mean oxygen tension in an irradiated tumor, render- mal histology architecture of taste buds. Patients often
ing the tumor cells more radiosensitive. This results from notice a loss of taste acuity during the second or third
rapid killing of tumor cells and shrinkage of the tumor week of radiotherapy. Bitter and acid flavors are more
mass after the first few fractions, reducing the distance severely affected when the posterior two thirds of the
that oxygen must diffuse through the tumor to reach the tongue is irradiated, and salt and sweet when the ante-
remaining viable tumor cells. The fractionation schedules rior third of the tongue is irradiated. Taste acuity usu-
currently in use have been established empirically. ally decreases by a factor of 1000 to 10,000 during the
course of radiotherapy. Alterations in the saliva may ac-
count partly for this reduction, which may proceed to a
RADIATION EFFECT ON ORAL TISSUES
state of virtual insensitivity, with recovery to near-normal
The following sections describe the deterministic effects levels some 60 to 120 days after irradiation.
of a course of radiotherapy on the normal tissue of the
oral cavity. This discussion assumes that 2 Gy is delivered Salivary Glands
daily, bilaterally through 8 X 10 cm fields over the The major salivary glands are at times unavoidably ex-
oropharynx, for a weekly exposure of 10 Gy. This con- posed to 20 to 30 Gy during radiotherapy for cancer in
tinues typically until a total of 50 Gy is administered. the oral cavity or oropharynx. The parenchymal com-
Cobalt is often the source of gamma radiation; how- ponent of the salivary glands is rather radiosensitive
ever, on occasion small implants containing radon or (parotid glands more so than submandibular or sublin-
iodine-12,5 are placed directly in a tumor mass. Such im- gual glands). The first few weeks after initiation of ra-
plants deliver a high dose of radiation to a relatively diotherapy usually sees a marked and progressive loss of
small volume of tissue in a short time. salivary secretion. The extent of reduced flow is dose de-
pendent and reaches essentially zero at 60 Gy. The
Oral Mucous Membrane mouth becomes dry (xerostomia) and tender, and swal-
The oral mucous membrane contains a basal layer com- lowing is difficult and painful because the residual saliva
posed of radiosensitive vegetative and differentiating in- also loses its normal lubricating properties.
termitotic cells. Near the end of the second week of Patients with irradiation of both parotid glands are
therapy, as some of these cells die, the mucous mem- more likely to complain of dry mouth than are those
branes begin to show areas of redness and inflammation with unilateral irradiation. The small volume of viscous
(mucositis). As the therapy continues, the irradiated saliva that is secreted usually has a pH value 1 unit below
mucous membrane begins to break down, with the for- normal (i.e., an average of 5.5 in irradiated patients
CHAPTER 2 RADIATION BIOLOGY 31

compared with 6.5 in unexposed individuals). This pH is

low enough to initiate decalcification of normal enamel.
In addition, the buffering capacity of saliva falls as
much as 44% during radiation therapy. If some portions
of the major salivary glands have been spared, dry-
ness of the mouth usually subsides in 6 to 12 months be-
cause of compensatory hypertrophy of residual salivary
gland tissue. Reduced salivary flow that persists beyond
a year is unlikely to show significant recovery.
Histologically an acute inflammatory response may oc-
cur soon after the initiation of therapy, particularly in-
volving 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 de-
generation (Fig. 2-8), thus accounting for the xerostomia.
Salivary changes have a profound influence on the
oral microflora and secondarily on the dentition, often
leading to radiation caries. After radiotherapy that in-
cludes the major salivary glands, the microflora under-
go 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. Because of their small
volume of thick, viscous, acidic saliva, such patients are
quite prone to radiation caries.

Teeth
Irradiation of teeth with therapeutic doses during their
development severely retards their growth. Such irradi-
ation may be for local disease (e.g., eosinophilic granu-
loma) or a generalized condition (leukemia being
treated with whole-body irradiation followed by bone
marrow transplantation). If it precedes calcification, it
may destroy the tooth bud. Irradiation after calcification
has begun may inhibit cellular differentiation, causing
malformations and arresting general growth. Children
receiving radiation therapy to the jaws may show defects
in the permanent dentition such as retarded root devel-
opment, dwarfed teeth, or failure to form one or more FIG. 2-8 Radiation effects on human submandibular sali-
vary glands. A, Normal gland. B, A gland 6 months after
teeth (Fig. 2-9). Teeth irradiated during development
exposure to radiotherapy. Note the loss of acini and pres-
may complete calcification and erupt prematurely. In
ence of chronic inflammatory cells. C, A gland 1 year after
general, the severity of the damage is dose dependent. exposure to radiotherapy. Note the loss of acini and exten-
Irradiation of teeth may retard or abort root formation, sive fibrosis.
but the eruptive mechanism of teeth is relatively radia-
tion resistant. Irradiated teeth with altered root forma-
tion still erupt. Radiation Caries
Adult teeth are very resistant to the direct effects of Radiation caries is a rampant form of dental decay that
radiation exposure. Pulpal tissue, which consists pri- may occur in individuals who receive a course of radio-
marily of reverting and fixed postmitotic cells, demon- therapy that includes exposure of the salivary glands. The
strates long-term fibroatrophy after irradiation. Radia- carious lesions result from changes in the salivary glands
tion has no discernible effect on the crystalline structure and saliva, including reduced flow, decreased pH, re-
of enamel, dentin, or cementum, and radiation does not duced buffering capacity, and increased viscosity. Because
i ncrease their solubility. of the reduced or absent cleansing action of normal
32 SECTION TWO BIOLOGIC EFFECTS OF RADIATION

FIG. 2-9 Dental abnormalities after radiotherapy in two patients. The first, a 9-year-old
girl who received 35 Gy at the age of 4 years because of Hodgkin's disease, had severe
stunting of the incisor roots with premature closure of the apices at 8 years (A) and
retarded development of the mandibular second premolar crowns with stunting of the
mandibular incisor, canine, and premolar roots at 9 years (B). The other patient, C, a 10-
year-old boy who received 41 Gy to the jaws at age 4 years, had severely stunted root
development of all permanent teeth with a normal primary molar. (A and B courtesy Mr.
P. N. Hirschmann, Leeds, England; C courtesy Dr. James Eischen, San Diego, Calif.)

saliva, debris accumulates quickly. Irradiation of the teeth sodium fluoride gel in custom-made applicator trays.
by itself does not influence the course of radiation caries. Use of topical fluoride causes a 6-month delay in the
Clinically, three types of radiation caries exist. The irradiation-induced elevation of Streptococcus mutans.
most common is widespread superficial lesions attack- Avoidance of dietary sucrose in addition to the use of a
ing buccal, occlusal, incisal, and palatal surfaces. An- topical fluoride further reduces the concentrations of
other type involves primarily the cementum and dentin S. mutans and Lactobacillus. The best result comes from a
in the cervical region. These lesions may progress combination of restorative dental procedures, excellent
around the teeth circumferentially and result in loss of oral hygiene, and topical applications of sodium fluoride.
the crown. A final type appears as a dark pigmentation Patient cooperation in maintaining oral hygiene is ex-
of the entire crown. The incisal edges may be markedly tremely important. Teeth with gross caries or periodon-
worn. Some patients develop combinations of all these tal involvement are often extracted before irradiation.
lesions (Fig. 2-10). The histologic features of the lesions
are similar to those of typical carious lesions. It is the Bone
rapid course and widespread attack that distinguish ra- Treatment of cancers in the oral region often includes
diation caries. irradiation of the mandible. The primary damage to ma-
The best method of reducing radiation caries is daily ture bone results from radiation-induced damage to the
application for 5 minutes of a viscous topical 1 % neutral vasculature of the periosteum and cortical bone, which is
CHAPTER 2 RADIATION BIOLOGY 33

FIG. 2-10 Radiation caries. Note the extensive loss of

tooth structure resulting from radiation-induced xerostomia.

normally already sparse. Radiation also acts by destroy-

ing osteoblasts and, to a lesser extent, osteoclasts. Subse-
quent to irradiation, normal marrow may be replaced
with fatty marrow and fibrous connective tissue. The mar-
row tissue becomes hypovascular, hypoxic, and hypocel-
lular. In addition, the endosteum becomes atrophic,
showing a lack of osteoblastic and osteoclastic activity,
and some lacunae of the compact bone are empty, an in-
dication of necrosis. The degree of mineralization may
be reduced, leading to brittleness, or little altered from FIG. 2-11 Osteoradionecrosis. A, Area of exposed man-
normal bone. These changes are so severe that bone dible after radiotherapy. Note the loss of oral mucosa. B,
death results. The condition is termed osteoradionecrosis. De-struction of irradiated bone resulting from the spread of
Osteoradionecrosis is the most serious clinical com- i nfection.
plication that occurs in bone after irradiation. The de-
creased vascularity of the mandible renders it easily in-
fected by microorganisms from the oral cavity. This can be minimized by removing all poorly supported
bone infection may result from radiation-induced break- teeth, allowing sufficient time for the extraction wounds
down of the oral mucous membrane, by mechanical to heal before beginning radiation therapy, and adjusting
damage to the weakened oral mucous membrane such dentures to minimize risk of denture sores. When teeth
as from a denture sore or tooth extraction, through a pe- must be removed from irradiated jaws, the dentist should
riodontal lesion, or from radiation caries. This infection use atraumatic surgical technique to avoid elevating the
may cause a nonhealing wound in irradiated bone that periosteum, provide antibiotic coverage, and use low-
is difficult to treat (Fig. 2-11). It is more common in concentration epinephrine-containing local anesthetics
the mandible than in the maxilla, probably because of the that do not contain lidocaine.
richer vascular supply to the maxilla and the fact that Often patients require a radiographic examination
the mandible is more frequently irradiated. The high- to supplement the clinical examination. These radio-
er the radiation dose absorbed by the bone, the greater graphs are especially important because untreated caries
the risk of osteoradionecrosis. leading to periapical infection can be quite severe with
Patients must be referred for dental care before un- the compromised vascular supply to bone. The amount
dergoing a course of radiation therapy to reduce the of added radiation is negligible compared with the
severity of or prevent radiation caries and osteoradio- amount received during therapy and should not serve as
necrosis. Radiation caries can be minimized by restoring a reason to defer radiographs. Whenever possible, how-
all carious lesions before radiation therapy and initiating ever, it is desirable to avoid taking radiographs during
preventive techniques of good oral hygiene and daily top- the first 6 months after completion of radiotherapy to al-
ical fluoride. The risk of osteoradionecrosis and infection l ow the mucosal membrane time to heal.
34 SECTION TWO BIOLOGIC EFFECTS OF RADIATION

Effects of Whole-Body Irradiation

When the whole body is exposed to low or moderate
doses of radiation, characteristic changes (called the
acute radiation syndrome) develop. The clinical picture
after whole-body exposure is quite different from
that seen when a relatively small volume of tissue is
exposed.

ACUTE RADIATION SYNDROME

The acute radiation syndrome is a collection of signs and
symptoms experienced by persons after acute whole-
body exposure to radiation. Information about this syn-
drome comes from animal experiments and human ex-
posures in the course of medical radiotherapy, atom bers of circulating granulocytes and platelets, and finally
bomb blasts, and radiation accidents. Individually the erythrocytes. The mature circulating granulocytes,
clinical symptoms are not unique to radiation exposure, platelets, and erythrocytes themselves are very radiore-
but taken as a whole, the pattern constitutes a distinct en- sistant, however, because they are nonreplicating cells.
tity (Table 2-2). The following discussion pertains to Their paucity in the peripheral blood after irradiation
whole-body exposure at a relatively high dose rate. reflects the radiosensitivity of their precursors.
The differential changes in the blood count do not
Prodromal Period all appear at the same time (Fig. 2-12). Rather, the rate
Within the first minutes to hours after exposure to of fall in the circulating levels of a cell depends on the
whole-body irradiation of about 1.5 Gy, symptoms char- life span of that cell in the peripheral blood. Granulo-
acteristic of gastrointestinal tract disturbances may oc- cytes, with short lives in circulation, fall off in a matter of
cur. The individual may develop anorexia, nausea, vom- days, whereas red blood cells, with their long lives in cir-
iting, diarrhea, weakness, and fatigue. These early culation, fall off only slowly.
symptoms constitute the prodromal period of the acute The clinical consequences of the depression of these
radiation syndrome. Their cause is not clear but proba- cellular elements become evident as the circulating lev-
bly involves the autonomic nervous system. The severity els decline. Hence, in the weeks after radiation injury,
and time of onset may be of significant prognostic value infection appears first, followed later by anemia. The
because they are dose related: the higher the dose, the clinical signs of the hematopoietic syndrome include in-
more rapid the onset and the greater the severity of fection (in part from the lymphopenia and granulocy-
symptoms. topenia), hemorrhage (from the thrombocytopenia),
and anemia (from the erythrocyte depletion). Individu-
Latent Period als may survive exposure in this range if the bone mar-
After this prodromal reaction comes a latent period of row and spleen recover before the patient dies of one or
apparent well-being during which no signs or symptoms more clinical complications. The probability of death is
of radiation sickness occur. The extent of the latent pe- l ow after exposures at the low end of this range but
riod is also dose related. It extends from hours or days much higher at the high end. When death results from
at supralethal exposures (greater than approximately the hematopoietic syndrome, it usually occurs 10 to 30
5 Gy) to a few weeks at sublethal exposures (less than days after irradiation.
2 Gy). Symptoms follow the latent period when individ- Because periodontitis results in a likely source of en-
uals are exposed in the lethal range (approximately 2 to try for microorganisms into the bloodstream, the role
5 Gy) or supralethal range. of the dentist is important in preventing infection in
hematopoietic syndrome. After moderate injury, about
Hematopoietic Syndrome 7 to 10 days pass before clinically significant leukopenia
Whole-body exposures of 2 to 7 Gy cause injury to the develops. During this time the dentist should remove
hematopoietic stem cells of the bone marrow and spleen. all sites of infection from the mouth. The removal of
The high mitotic activity of these cells and the presence sources of infection, the vigorous administration of anti-
of many differentiating cells make the bone marrow a biotics, and in some cases the transplantation of bone
highly radiosensitive tissue. As a consequence, doses in marrow have saved individuals suffering from the acute
this range cause a rapid and profound fall in the num- radiation syndrome.
CHAPTER 2 RADIATION BIOLOGY 35

FIG. 2-12 Radiation effects on blood cells. When whole-body exposure inhibits the re-
placement of circulating cells by stem cell proliferation, the duration of the circulating cells'
survival is largely determined by their life span.

Gastrointestinal Syndrome
Whole-body exposures in the range of 7 to 15 Gy cause effect of bone marrow depression is just beginning to be
extensive damage to the gastrointestinal system. This manifested. By the end of 24 hours, the number of cir-
damage, in addition to the hematopoietic damage de- culating lymphocytes falls to a very low level. This is fol-
scribed previously, causes signs and symptoms called the lowed by decreases in the number of granulocytes and
gastrointestinal syndrome. Individuals exposed in this then of platelets (see Fig. 2-12). The result is a marked
range may experience the prodromal stage within a few lowering of the body's defense against bacterial infec-
hours of exposure. Typically from the second through tion and a decrease in effectiveness of the clotting mech-
about the fifth day no symptoms are present (latent pe- anism. The combined effects on these stem cell systems
riod) and the patient feels well. Such exposure, however, cause death within 2 weeks from a combination of fac-
causes considerable injury to the rapidly proliferating tors that include fluid and electrolyte loss, infection, and
basal epithelial cells of the intestinal villi and leads to a possibly nutritional impairment. Several of the firefight-
loss of the epithelial layer of the intestinal mucosa. The ers at Chernobyl, in the former Soviet Socialist Republic
turnover time for cells lining the small intestine is nor- Ukraine, died of the gastrointestinal syndrome.
mally 3 to 5 days. Because of the denuded mucosal
surface, plasma and electrolytes are lost; efficient in- Cardiovascular and Central Nervous
testinal absorption cannot occur. Ulceration also occurs, System Syndrome
with hemorrhaging of the intestines. All these changes Exposures in excess of 50 Gy usually cause death in 1 to
are responsible for the diarrhea, dehydration, and loss 2 days. The few human beings who have been exposed at
of weight that are observed. Endogenous intestinal this level showed collapse of the circulatory system with a
bacteria readily invade the denuded surface, producing precipitous fall in blood pressure in the hours preceding
septicemia. death. Autopsy revealed necrosis of cardiac muscle. Vic-
The level of radiation required to produce the gas- ti ms also may show intermittent stupor, incoordination,
trointestinal syndrome (more than 7 Gy) is much greater disorientation, and convulsions suggestive of extensive
than that causing sterilization of the blood-forming tis- damage to the nervous system. Although the precise
sues. However, death (from destruction of the rapidly self- mechanism is not fully understood, these latter symp-
renewing cells in the intestines) occurs before the full ef- toms most likely result from radiation-induced damage
fect of the radiation on hematopoietic systems can be to the neurons and fine vasculature of the brain.
evidenced. At about the time that developing damage The syndrome is irreversible, and the clinical course
to the gastrointestinal system reaches a maximum, the may run from only a few minutes to about 48 hours be-
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ON THE BORDERLAND
On the Borderland
 By

F. Britten Austin

Garden City New York

Doubleday, Page & Company
1923

COPYRIGHT, 1923 BY
DOUBLEDAY, PAGE & COMPANY
ALL RIGHTS RESERVED, INCLUDING THAT OF TRANSLATION
INTO FOREIGN LANGUAGES, INCLUDING THE SCANDINAVIAN

COPYRIGHT, 1919, BY THE CURTIS PUBLISHING COMPANY IN THE

UNITED STATES AND
GREAT BRITAIN
COPYRIGHT, 1919, 1920, BY INTERNATIONAL MAGAZINE CO.
COPYRIGHT, 1920, BY CONSOLIDATED MAGAZINES CORPORATION
(THE RED BOOK MAGAZINE)
ALL RIGHTS RESERVED

PRINTED IN THE UNITED STATES

AT
THE COUNTRY LIFE PRESS, GARDEN CITY, N. Y.
 First Edition

TO
EDWARD CECIL

IN
OLD FRIENDSHIP
 CONTENTS
PAGE
Buried Treasure 1
A Problem in Reprisals 28
Secret Service 51
The Strange Case of Mr. Todmorden 83
Through the Gate of Horn 98
The White Dog 122
A Point of Ethics 143
The Lovers 165
Held in Bondage 187
She Who Came Back 211
From the Depths 231
Yellow Magic 253

ON THE BORDERLAND

ON THE BORDERLAND
 BURIED TREASURE
For the last twenty minutes the after-dinner talk of the little group of
men in the liner’s smoking-room had revelled in the uncanny. One
man had started it, rather diffidently, with a strange yarn. Another
had capped it. Then, no longer restrained by the fear of a
humiliating scepticism in their audience, they gave themselves up to
that mysteriously satisfying enjoyment of the inexplicably
marvellous, vying with each other in stories which, as they were
narrated, were no doubt more or less unconsciously modified to suit
the argument, but which one and all dealt with experience that in
the ultimate analysis could not be explained by the normal how and
why of life.
“What do you think of all this, doctor?” said one of the story-tellers,
turning suddenly to a keen-eyed elderly man who had been listening
in silence. “As a specialist in mental disorders you must have had a
vast experience of delusions of every kind. Is there any truth in all
this business of spiritualism, automatic writing, reincarnation and the
rest of it? What’s the scientific reason for it all?—for some reason
there must be! People don’t tell all these stories just for fun.”
The doctor shifted his pipe in his mouth and smiled, his eyes
twinkling.
“You seem to find a certain amount of amusement in it,” he
remarked, drily. “The scientific reasons you ask for so easily are
highly controversial. But many of the phenomena are undoubtedly
genuine—automatic writing, for instance. It is a fact that persons of
a certain type find their hand can write, entirely independent of their
conscious attention, coherent sentences whose meaning is utterly
strange to them. They need not even deliberately make their mind a
blank. They may be surprised by their hand suddenly writing on its
own initiative when their consciousness is fixed upon some other
occupation, such as entering up an account-book. Always they have
a vivid feeling that not their own but another distinctly separate
intelligence guides the pen. This feeling is not evidence, of course. It
may be an illusion; probably is.
“The best-analyzed reincarnation story is probably that dealt with by
Professor Flournoy in his study of the famous medium Hélène Smith
of Geneva. This lady sincerely believed herself to be a reincarnation
of Marie Antoinette—and in her trance-state she acted the part with
astonishing fidelity and dramatic power. In her normal condition she
certainly possessed neither so much detailed knowledge of the life of
the ill-fated queen nor so much histrionic ability. She also wrote
automatically, and some of her productions were amazing, to say the
least of them. Well, Professor Flournoy’s psychological investigations
proved clearly to my thinking that it was a case of her subconscious
mind dramatizing, with that wonderful faculty of impersonation
which characterizes it, a few hints accidentally dropped into it and
combining with her subconscious memory, which forgets nothing it
has ever heard or read or even casually glanced at, to produce an
almost perfect representation of Marie Antoinette. Also he proved
that her automatic writing emanated from her own subconscious
mind and nowhere else.
“Now, I am not going to say that discarnate spirits do not
communicate through this subconscious activity of which one form is
automatic writing. I am not going to say that we do not become
reincarnated through an endless cycle of lives. I do not know
enough about it to assert such a negative—no one does. All I know
about the human mind is that we know very little about it. It is like
the moon, of which you never see more than the small end. Infinite
possibilities lie in the shadow. You are only conscious of a small
fraction of your own personality. The subconscious—the unillumined
portion of your soul—is incomputably vast. It learns everything,
forgets nothing; possibly it even goes on from life to life. When it is
tapped by any of those traditional means which nowadays we call
spiritualistic one may—or may not—come across buried treasure.”
“But you yourself do not believe in the truth of spiritualism as an
actual fact, doctor?” queried one of the group, a trace of aggression
in his tone.
The doctor shrugged his shoulders.
“I accord belief to a very limited number of attested facts, my
friend,” he said. “That I am sitting here with you, for example. I am
ready to adopt provisionally all sorts of hypotheses to explain those
varied phenomena of life, the ultimate explanation of which must in
any case elude me. They are hypotheses for myself—I do not
announce them as dogmas for others. But—if you do not think it is
too late—I will tell you a story, a rather queer experience of my own,
and you can form your own hypotheses in explanation of it.”
There was a chorus of approval. The doctor waited while the
steward refilled the glasses at the instance of one of the group, relit
his pipe, and settled himself to begin.

It was in 1883. I was a young man. I had recently finished walking

the hospitals, got my degree, and before settling down into practice
at home had decided to see a little of the world. So I signed on for a
few voyages as a ship’s doctor. At the termination of one of them I
found myself at a loose end in New York. There I became friendly
with the son of a man who in his young days had been a Californian
“Fortyniner,” had made a pile, settled East, become a railroad
speculator and made millions—William Vandermeulen.
Old Vandermeulen had a delicate daughter, Pauline, then about
nineteen years of age and in the incipient stages of consumption.
Under medical advice, he was accustomed to take her each winter
for a cruise around the West Indies in his steam yacht. That year,
young Geoffrey Vandermeulen persuaded his father to ship me as
medical officer. There was nothing alarming in the young girl’s
condition, of course, or a much older and more experienced man
would have accompanied them. She was merely delicate.
We were a small party on board: the old man, his wife—a faded old
lady with no personality whatever—Pauline, Geoffrey, and myself.
Geoffrey was an ordinary, high-spirited young man, intelligent and a
pleasant companion, but not particularly remarkable. His sister was
mildly pretty but utterly devoid of attractiveness, extremely shy, and
given to sitting in blank reverie over a book. Although she always
had one in her hand, she read, as a matter of fact, very little. It was
just an excuse for day-dreaming. Of this girl the old man, otherwise
as keen as a razor and as hard as nails—commercially, I believe, he
was little better than a pirate—was inordinately fond. Outside
business, she was the absorbing passion of his life. There was no
whim of hers that he would not gratify. It was rather pathetic to see
the old scoundrel hanging over her frail innocence, all that he had of
idealism centred in her threatened life.
The cruise was pleasant but uneventful enough for some weeks. We
pottered down through the Bahamas to Jamaica and then turned
eastward with intent to visit the various ports of the Antilles as far
south as Barbados.
It was one evening while we were chugging peacefully across the
Caribbean Sea that occurred the first of the remarkable incidents
which made this voyage so memorable to me. I remember the
setting of it perfectly. We were all in the saloon; I suppose because
the night was for some reason unpleasant. The weather was calm,
at any rate. Geoffrey and I were reading. Old Vandermeulen and his
wife were playing cribbage. Pauline was sitting at a writing-table
fixed in a corner of the saloon, entering up the day’s trivial
happenings in the diary which she religiously kept. I remember
glancing at her and noticing that she was chewing the nail of her left
thumb—a habit of which I was vainly trying to break her—as she
stared vacantly at the bulkhead, no doubt ransacking her memory
for some incident to record.
Suddenly she turned round upon us with a startled cry.
“Look, Mamma!—I have scrawled all over my diary without knowing
that I did it!—Isn’t that strange!”
We all of us looked up languidly. The mother made some banal
remark, but did not withdraw her attention from her cards. The
father glanced affectionately toward her without ceasing to count up
the score he was about to peg on the board. Geoffrey and I
continued our reading.
But the girl had been puzzling over the scrawl and all at once she
jumped up from her seat and came across to us.
“Look!” she said. “Isn’t it funny? These words—they’re all like the
words on blotting-paper—they go backwards and inside out! And
there are figures, too!—Whatever could have made me do it?—And I
don’t remember doing it either, though of course I must have done
so. There was nothing on that page a minute before, I am sure of
that!”
There was something curiously uneasy in the girl’s manner, a note in
her voice that impressed me. I got up, took the open diary from her
hand and there sure enough was a large uneven scrawl, two lines of
it, diagonally across the page, and, as she said, reversed, as though
it had been blotted down upon it.
Almost without thinking, I held the open page against one of the
mirrors panelled in the saloon wall—and I could not repress a cry of
astonishment. The scrawl was a decipherable sentence, mysterious
enough, but coherent!—I’ll write it down for you as nearly as I
remember it, so as to show you how it looked. He produced pencil
and paper from his pocket, wrote: “lucia 1324 N 8127 W katalina
sculle point SWbS 3 trees digge jno dawson youre turne:” There you
are—the last two words were added like a postscript and were
followed by a rough sketch, an irregular oval over a St. Andrew’s
cross, like this—
I read out what was written, and Pauline stared at me wide-eyed.
“Whatever could have made me write that?” she exclaimed.
Geoffrey looked up, fraternally scornful.
“It’s a thin joke, Pauline! You can’t monkey us in that fashion! I
suppose you want to pretend that the ghost of some old pirate
wrote it down in your book so as to start us off on a Treasure Island
hunt.” Stevenson’s romance was then in its first success and
Geoffrey had just been reading it. “Of course, you wrote it
deliberately—what nonsense!”
She turned round upon him, her eyes filling with tears in the
vehemence of her protest.
“Geoffrey, I couldn’t!—I couldn’t write reversed like that if I tried!”
“Oh, yes, you could,” asserted Geoffrey, confidently. “It’s easy
enough.”
“Supposing we all try,” said I, curious to test its feasibility. I felt
considerably puzzled. Pauline was not at all the sort of girl one
would expect to persist in such a pointless sort of practical joke as
this, and persistent she was—tearful like a child unjustly accused of
a crime of which it protests innocence.
Her mother and father renounced their game of cribbage and bent
their heads together over the enigmatic screed, without proffering
an opinion. It was evident that they did not wish to hurt their
daughter’s feelings by open scepticism. They would have humoured
her in anything, no matter how absurd.
I reiterated my suggestion and it was accepted in the spirit of a
parlour-game. A line from a book was selected, we all tried—and we
all failed hopelessly. None of us got more than two or three
consecutive letters right. It is not so easy as it sounds. Try it for
yourselves!
At that time, although spiritualism was a great craze in America, and
D. D. Home, Eglinton, and other famous mediums, were arousing
enormous interest and controversy in England, automatic script was
an uncommon phenomenon. Table-rapping, levitation, slate-writing
and materialization were the wonders in vogue—and I had then
never heard of the “mirror-writing” which has since become a
frequent form of automatic expression. Neither, of course, à fortiori,
had the young girl who had just produced this mysterious specimen.
We all felt puzzled and impressed at our failure to imitate
deliberately the reversed script. Old Vandermeulen picked up the
diary and read the reflection of the scrawled page in the wall-mirror.
“Well, it’s sure strange!” he said in his twangy drawl. “Geoff! You
write this down in a straightaway hand and we’ll see if we can get
any sense out of it. I guess there’s some meaning in it. Pauline ain’t
joking.”
Geoffrey obeyed and read out the script again.
“‘lucia 1324 N 8127 W katalina sculle point SWbS 3 trees digge jno
dawson youre turne’—It’s exactly like the directions to a pirate’s
buried treasure, Father!” he added, excitedly. “Skull and crossbones
and all! But of course that’s ridiculous! Though I can’t understand
how Pauline could have written it like she did!”
“And I did not know even that I was writing!” asseverated Pauline,
“let alone know what I wrote! It was just as if my hand did not
belong to me—it was a sort of numbness that made me look down.”
“Tear it up, dear!” implored her mother anxiously. “I am sure it
comes from the Devil!” Mrs. Vandermeulen belonged to a particularly
strict little sect and was always ready to discern the immediate
agency of the Evil One.
“Devil or not!” said old Vandermeulen. “I guess if there’s any buried
treasure lying around here, I’m going to peg out my claim on it.” He
turned to me. “Young man, was there ever any pirates about these
parts?” The old ruffian was quite illiterate; had never, I believe, read
a book in his life.
“Why, yes,” I replied, “from the end of the sixteenth century these
seas were the chief haunt of the buccaneers and, after them, of the
pirates who were not entirely suppressed until well in the eighteenth
century. There must be any amount of their hidden treasure buried
in these islands.”
“You don’t say!” he exclaimed, his avaricious old eyes lighting up.
“And here have I been running this yacht up and down these parts
for five years at a dead loss!” His disgust would have been comic,
were it not for the ugly, ruthless lust of gold which looked suddenly
out of his face. “Guess I’m going to quit this fooling around right
away! I don’t know and don’t care if it was the Devil himself wrote
this specification in Pauline’s book—I’m darned sure she didn’t write
it herself—the handwriting’s different, d’you see?”—It was, as a
matter of fact, compared with the previous pages, quite another
hand—hers was an upright, rounded schoolgirl calligraphy, this was
a cursive old-fashioned script inclined well forward. “So as we’ve got
nothing else to start upon, we may as well see if there’s anything to
it.” He tossed Geoffrey’s transcription across to me. “What do you
make of it, young man?” he asked, with the sneering condescension
he accorded to my superior literary attainments.
I took it, rather amused at the old scoundrel’s simplicity. That there
was any authentic meaning in Pauline’s scrawl seemed to me wildly
improbable. I was a frank materialist in those days and had
Carpenter’s formula of “unconscious cerebration” glibly ready to
cover up anything psychologically abnormal. However, I considered
the sheet of paper with attention.
“Assuming this to be a genuine message,” I said, “it would appear to
give the precise latitude and longitude of some point where it is
desirable to dig. I take it that the figures stand for 13 degrees 24
minutes North, 81 degrees 27 minutes West. The world ‘lucia’
puzzles me—unless the island of St. Lucia is meant. What ‘katalina’
stands for, I do not know—it is evidently a proper name of some
kind, ‘sculle point SWbS 3 trees digge’ presumably means that one
should dig under three trees south-west-by-south of Skull Point—
wherever that is. ‘jno dawson’ is, of course, John Dawson. Assuming
this to be a spirit-message from the other world,” I could not help
smiling ironically, “it is possibly the name of the ghost who is
communicating—and who desires to indicate to some person that it
is his or her turn. He does not specify for what. I may remark that
the ghost is either ill-educated or he has an archaic taste in spelling.”
“I don’t like it,” said Mrs. Vandermeulen, querulously timid. “Do tear
it up, William! I am sure harm will come of it!—It is the Devil
tempting you!”
“So long as he’s serious, he can tempt me sure easy!” said the old
ruffian in a tone of cool blasphemy which sent the colour out of his
wife’s face. He rang the bell and the negro steward appeared. “Sam!
Ask Captain Higgins to step in here for a moment!”
Captain Higgins, the skipper of the yacht, was a level-headed
mariner of middle age whom nothing ever ruffled. He was
competence itself.
“Good evening, Captain Higgins,” said old Vandermeulen, fixing him
with the keen eyes under shaggy gray brows, eyes which defied you
to divine his purpose whilst they probed yours. “What’s the latitude
and longitude of the island of St. Lucia?”
“Fourteen North, sixty-one West,” replied Captain Higgins promptly.
Old Vandermeulen turned to me.
“Then it’s not St. Lucia, young man,” he said. He picked up
Geoffrey’s transcription. “Well, now, Captain Higgins, is there any
place thirteen-twenty-four North, eighty-one twenty-seven West?”
The skipper reflected a moment.
“No place of importance, certainly. I’ll get the chart.”
He returned with it, spread it out on the saloon table, ran his
forefinger across it.
“Here you are!” he said. “A small island called Old Providence. It
belongs to Colombia.”
Geoffrey, who was peering over his shoulder, uttered a startled
exclamation.
“And look!” he cried. “There’s your Katalina!” He pointed to a small
islet just north of Old Providence, a mere dot on the chart. “Santa
Katalina!—My hat! that is weird!”
It certainly was. From whatever stratum of Pauline’s consciousness
her writing had emanated, it was an amazing thing that she should
have written down the exact latitude and longitude of a tiny island
off the Nicaraguan coast and named it correctly. Even I could not
help feeling that it was more than a fortuitous coincidence, that it
was uncanny. The others surrendered themselves straight away.
I turned to look at Pauline. She was deathly white; evidently
frightened at being made the vehicle of this message from the
beyond. Her mother clutched at her, as though protecting her from
unseen dangers. Geoffrey’s imagination had caught fire, his eyes
were bright with excitement.
“My sakes! Pauline!” he cried. “I believe you now! You couldn’t have
written that out of your head. I’ve read of things like this before—I
guess you’re a medium and didn’t know it!—Father! We’ll track this
message down, wherever it comes from, say now?”
“It comes from the Devil! Tear it up—oh, tear it up!” implored Mrs.
Vandermeulen. “William! Tear it up—don’t follow it!”
Old Vandermeulen turned to the skipper. His jaw had set hard, his
lips were compressed, only the glitter in his eyes, peering in a
momentary fixation of thought from under his bent brows, showed
that he shared the excitement of his son. So he must have looked in
his office when he took the decisions which had made his millions.
“Captain Higgins,” he said, curtly ignoring the supplications of his
wife, “how long will it take us to reach that island?”
The skipper put his finger on the chart at a point south of Haiti.
“We’re here,” he said. He measured off the distance. “At our best
rate of twelve knots—about sixty hours steaming.”
The old man nodded.
“Put her about,” he said. His harsh tone had an odd ring about it, as
though he was secretly conscious of affronting mysterious dangers,
was all the more emphatic. “Right now!”
Captain Higgins never queried owners’ orders.
“Very good, sir,” he replied, stolidly, and walked out of the cabin.
A minute or two later we felt the yacht swing round. There is always
something impressive when a ship on the open sea goes about upon
her course, but I never felt it more powerfully than then. It seemed
that there was a fateful significance in our deliberate action.
Geoffrey meanwhile was poring over the sheet of paper on which he
had transcribed his sister’s reversed scrawl.
“It’s all perfectly clear,” he said, triumphantly. “We’ve got to make
this island of Santa Katalina, thirteen-twenty-four North, eighty-one
twenty-seven West, try and find a place called Skull Point, look for
three trees south-west-by-south of it, and dig! We understand every
word of it now!”
“All except the word ‘lucia’” I corrected, “and whose turn it is.”
“Yes—there’s that,” he said, dubiously. “I suppose every word has
some meaning.”
“You can bet it has!” I replied, half sarcastically humouring his
credulity, half surrendering myself to an uncritical acception of these
mysteriously given directions. “I wonder who this John Dawson was
—if he existed?”
“He’s a sure-enough ghost of some old pirate!” said Vandermeulen,
with complete conviction. “And I guess he’s putting us fair and good
on to his pile!”
I laughed, involuntarily, at this childishness. The old man frowned.
“There’s some things that perhaps even you all-fired clever young
fellows don’t know,” he said, crushingly. “’Tain’t the first time I’ve
heard of this sort of thing. A mate of mine in the old days at ’Frisco
was waked up one morning by the ghost of a prospector who’d died
up in the ranges. He told him just where he’d made his strike before
his grub gave out. My mate had never heard of the place but he lit
straight away on the trail—and sure enough the ghost was telling
the truth. Old Jim Hamilton it was—and he drank himself to death on
what he got out of it.” The old man looked me straight in the eyes as
though challenging me to doubt him. Of course, I could say nothing.
He grunted scornfully, and turned again to the chart still spread out
upon the table. “It’s a nice quiet out-of-the-way place,” reflected the
old ruffian, putting his thumb-nail on the lonely island. “Just the
location for a cache—guess they’d feel pretty sure of not being
interfered with there!” There was a grim undertone in his voice
which was decidedly ugly. He might, himself, have been the
reincarnation of just such a pirate as the one whose existence he
was postulating.
Well, nothing more happened that night. Mrs. Vandermeulen,
thoroughly alarmed and uneasy, hustled her daughter off to bed. Old
Vandermeulen and his son sat up in an endless discussion of the
mysterious script, referring again and again to the chart which so
startlingly confirmed its indications, and speculating optimistically as
to the nature and amount of the treasure they were convinced was
buried in the designated place. They talked themselves into a
complete faith in the supernatural origin of the message, and, father
and son alike—it was curious to note the traits of resemblance which
cropped out in them—were equally indifferent as to whether its
source was diabolic or benevolent. Enormously wealthy although
they already were, the prospect of this phantom gold waiting to be
unearthed had completely fascinated them. At last I turned in,
wearied with the thousand and one questions they asked me and to
which I could give no answer, disgusted with their avarice, and
scornfully contemptuous of their simplicity.
I found sleep no easy matter. Sceptical though I was, I could not get
Pauline’s curious production out of my head, and the more I thought
of it the more inexplicable seemed its coincidence with the chart.
The subconscious mind, with its amazing memory, its dramatic
faculty, its unexpected invasion of the surface consciousness in
certain types, was not then the commonplace of psychology that it is
now—or I should probably have referred the whole thing to the
combination of a casual, apparently unheeding, glance at the chart
with a memory of some of her brother’s remarks about “Treasure
Island,” automatically and dramatically reproduced. As it was, I could
formulate no explanation that satisfied me—though I utterly
disbelieved in the ghost of a piratical John Dawson, of which the two
Vandermeulens were now fully persuaded.
The next day found us steaming steadily westward. Father and son
could talk of nothing else but their fancied buried treasure and their
plans for digging it up without taking the crew of the yacht into their
confidence. Mrs. Vandermeulen hovered round her daughter, horribly
anxious of she knew not what, but—after having been once silenced
by a peremptory oath from her husband—afraid to make further
protest. Pauline herself sat all day in a deck-chair, more silent even
than usual, staring dreamily across the empty sea in a reverie which
ignored us all. Naturally, I watched her closely. But, except that her
eyes had a kind of haunting fear in them, she seemed perfectly
normal. Evidently the occurrence of the previous night had shocked
her profoundly, for once, when I casually mentioned it, she
shuddered and implored me not to speak of it again. The fear of the
uncanny in herself stared out of her eyes as she entreated me.
This dreamy absorption in herself continued until supper time that
evening. Throughout the meal, I do not think she uttered a single
word. She seemed not even to hear the conversation around her, but
toyed listlessly with her food and finally ceased to eat long before
the others had finished. Watching her with a professionally
interested observation, I was uneasy. She had leaned back in her
chair, was gazing straight before her with wide-open eyes. Suddenly
I noticed that they had glazed over. All expression faded out of her
face. The arm that rested on the salmon-table stiffened into a
cataleptic sort of rigidity.
Her mother was also anxiously watching her.
“Pauline!” she cried. “Are you ill?”
There was no answer. The girl sat like a statue. Mrs. Vandermeulen
glanced at me in wild alarm, silently imploring my intervention. Old
Vandermeulen and his son were hotly arguing the desirability or
otherwise of informing Captain Higgins of their plans, and took no
notice of us.
I got up from my seat and went round the table to the girl. I lifted
up her lifelessly heavy arm with my fingers on her pulse. It was
normal.
“Miss Vandermeulen!” I said, rather sharply. “Are you not well?”
She turned her head slowly round to me, like a sleep-walker faintly
aware of some sound that does not, however, wake her, and stared
me full in the face with eyes in which there was not the slightest
glimmer of recognition.
“Pauline!” almost screamed her mother, “don’t you know your own
name?”
An expression of curious intelligence dawned in her face—her aspect
changed in some subtle manner, as though another, quite different,
personality was emerging in her—she laughed in low, confident
tones utterly unlike her ordinary laugh.
“My name is Lucia!” she said, as though stating a well-known fact.
Lucia! To say that we were startled is to understate our
astonishment—we were dumbfounded. The first word of the cryptic
message! We gazed at her for a moment as at a complete stranger
from the clouds—and indeed she looked it, as she smiled at us with
bright malicious eyes. The diffident Pauline we knew had completely
disappeared.
“She is possessed!” screamed her mother. “Oh, God—restore her!
restore her!”
The girl stood up suddenly from her chair, passed her hand over her
eyes, shook herself as though shaking off sleep. She turned away
from us deliberately.
“Oh, John!” she said, and there was an odd little foreign accent in
her tone, “I have dreamed—such a strange dream! I dreamed—I
know not!—that I was not Lucia!” She laughed softly in her new low
tones, “—That strange people were asking me my name. Then I
woke—oh, John!” she sidled up in a wheedling manner to what, so
far as we could see, was vacant space. “I am Lucia, am I not?—And
you love me? You love me?” Her shoulders moved sinuously as
though she were putting herself under the caresses of a person
invisible to us. “You love me—and I love you, although you have
only that one terrible eye!” She still spoke with that curious foreign
accent which lent a certain piquancy to her speech. “You love me,
you John Dawson, you Englishman, you love me for ever, say?” She
reminded me of Carmen sidling up to Don José. “You not deceive me
—or——!” She looked up as into a tall man’s face with a sudden
expression of feline vindictiveness, her white teeth showing in an
ugly little rictus of the mouth, and slid her hand down stealthily
toward her stocking. “But no!” She smiled; her hand came up again
as though to rest upon a man’s shoulder. “You love me—and I love
you—and,” her voice dropped, “when we have killed the others we
go away with the treasure—you promise me, John Dawson?”
She appeared utterly unaware of our presence. There was a
dramatic intensity in her voice and gestures which thrilled even me,
although I had attended some hypnotic experiments in London and
was aware of the complete realism with which a somnambulist will
play a part suggested to him. I had no doubt whatever that she was
in a state of hypnosis, accidentally self-induced, and that she was
merely acting on the suggestions of the talk she had overheard.
Her mother, however, had no such consoling certitude. She hid her
face in her hands, groaning: “She is possessed! She is possessed!
Oh, God, cast out the evil spirit! cast out the evil spirit!”
Geoffrey was white to the lips, appalled, unable to utter a sound.
The old man stared at her, fascinated, a strange gleam in his eyes.
The mother turned to me in despair.
“Oh, doctor! Do something—do something!—Oh, if only we had a
minister here! She is possessed by an evil spirit! My Pauline! My
Pauline!” She sank on her knees by one of the swivel-chairs, gave
herself up to agonized prayers. “Oh, God, cast out the evil one! Oh,
God, cast out the evil one!”
Thinking that this strange incident had already lasted more than long
enough, I took a step toward the girl with a vague idea (though I
didn’t quite know how) of breaking the hypnosis. She stood looking
upward still, with a wheedling, diabolical smile, into apparent
nothingness.
“We will go together—we two—with the treasure, say, John
Dawson?” she murmured seductively, the very incarnation of a
Delilah. “Mansvelt is dead—we will run away from Simon and go
with my people before they kill us all—they are very many and you
can only hold out two-three days—but we might take the treasure,
John Dawson, the treasure you and Simon hid with Mansvelt—
Simon, we will kill him—and we will go away and be rich—rich, John
Dawson—say?” Her voice was perfidiously honeyed, her eyes
glistened, as she caressed that uncanny empty air.
“What is she talking about?” muttered Geoffrey in a low, excited
voice. “Who are these people—Mansvelt and Simon? Have you heard
of them, doctor?”
I shook my head. They were utterly unknown to me. For a moment I
hesitated, fascinated by the little drama, curious to hear more.
The mother moaned.
“Oh, do something, doctor! do something!—Save her! Save her! Oh,
God, deliver her from the evil one!”
Her agony recalled me to my professional duty. I started forward but
before I could reach her I was snatched back by a violent hand on
my shoulder.
“Stand aside!” commanded old Vandermeulen in a terrible voice.
“Evil spirit or no evil spirit, I guess it knows all about that treasure—
and I’m going to hear what it’s got to say!” Of his normal love for his
daughter there was not a trace. The man was completely
dominated, to the exclusion of any other sentiment, by the lust for
gold, more gold. He looked scarcely human as his eyes glowered
upon me, murder in them if I thwarted him. “If it’s the Devil himself
that’s got her—let her talk!”
But the mother sprang up with a wild shriek, rushed toward her
daughter.
“Do you wish her eternal damnation?” she cried, flinging her arms
about the girl. “Pauline! Pauline! For the love of God, don’t you know
me?—Oh, say a prayer—say a prayer after me!” She commenced the
Lord’s Prayer in a voice that trembled with anguish.
The girl stood rigid in her embrace, drawn up away from her, looking
down upon her with fixed and hostile eyes. She made one instinctive
movement to escape—and then suddenly crumpled in a swoon upon
the floor.
She came round easily enough under simple restoratives, looked up
at us with childish, bewildered eyes—the old Pauline again! Her
mother completely broke down over her, sobbing in almost crazy joy
at her restoration. Emotionally infected, perhaps, the girl also gave
way to a hysterical passion of weeping, which would not be checked,
and for which she could give no reason. She seemed not to have the
slightest recollection of the part she had just played. Old
Vandermeulen, still obsessed by his lust for the treasure, tried to
question her. She only stared at him dumbly—a vague fear coming
into her eyes, but giving no response. I silenced him with all the
authority of my professional position, and got the girl into her
stateroom, where we left her with her mother.
Throughout the next day neither of the two women appeared.
Pauline was utterly prostrated, and she remained in bed. Her mother
stayed with her, under strict injunctions to mention nothing of last
night’s terrible scene.
Meanwhile, of course, we were steadily drawing nearer to the
Nicaraguan coast and the island of Old Providence with its tiny and,
to us, fascinating satellite, Santa Katalina. Even I could not help
wondering what we should find there. The two Vandermeulens were
in a fever of excitement, cursing at every moment the slowness of
the yacht. We were, as a matter of fact, due to reach the island early
next morning.
Some time in the afternoon, the old man approached me
confidentially.
“Say, young know-all,” he said, “what d’you figure out was the
meaning of last night’s gaff? I guess Pauline ain’t got no natural
talent for play-acting like that.”
Rather foolishly, I amused myself with his credulity.
“Of course,” I said, concealing a smile, “it may be that in a previous
existence your daughter’s name was Lucia—the Spanish lady friend
of some of the buccaneers and particularly of a certain John
Dawson, who is now directing her to the treasure they buried
together a few hundred years ago.” I regretted my words the
moment they were uttered. The man’s infatuation needed no
fanning from me.
“By God, you’ve hit it!” he exclaimed. “And she’s just remembering!
—I guess she can lead us straight to it!”
“Don’t be absurd!” I said, pettishly. “I was only joking!”
He glared at me in savage disappointment.
“You’re joking with the wrong man!” he said harshly. “Besides, it
sure ain’t impossible!—You don’t know what happens to us when
we’re dead, though you do think you know everything!”
“No—it’s not impossible,” I conceded. “But it’s improbable.”
“That’s your opinion,” he sneered. “You know nothing about it!—I’ve
had them feelings myself—feelings that I’ve been to a place before
when I sure know I haven’t. By God, that’s it!—Pauline’s just
remembering—coming back to these old places—and she’ll take us a
bee-line to the cache!”
He strode off to impart this illuminating theory to his son, and I saw
no more of them until supper time. They were, I was sure,
concerting some plan for cutting me out of a share in the treasure.
They had the furtive look of a couple of conspirators as we three,
Pauline and her mother still absent, sat that night at table. Both
forced themselves to exhibit a strained politeness to me, which
obviously concealed some treacherous design. I didn’t like the
atmosphere at all and was impelled to clear it.
“By the way,” I remarked, casually, “I don’t want a share in that
treasure—I prefer to work for my living.” As I had not the slightest
faith in its existence, this renunciation was not difficult. “Supposing
your theory to be true, it belongs to Miss Vandermeulen if it belongs
to any one.”