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The effect of strontium cobalt and fluoride on rat incisor enamel formation.

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The Effect of Strontium, Cobalt and Fluoride on
R a t Incisor Enamel Formation '
B R A H A M NEIMAN AND DALE R. EISENMANN
The Department of Histology, University of Illinois at the Medical Center,
Chicago, Illinois 60680
This investigation examined ultrastructurally the entire period
of development of alterations in formative ameloblasts and the enamel which
they produce following injection with fluoride, strontium, and cobalt ions. Rats
injected with these ions were sacrificed at intervals of 1, 2, 4, 8, 16,24 and 48
hours to elucidate the sequence and detail of cytologic and cell product alterations which occur. Undecalcified sections of rat incisor teeth were studied using
electron microscopy and microradiography. All three ions initially produced disturbances in cell morphology and enamel formation consisting of dark globules,
vacuoles, and pooling of stippled material on the enamel surface. While a period
of decreased crystal formation occurred after injection with all three ions, only
cobalt responses included a period of apparently complete absence of crystd
formation. The hypermineralized layers occurring in the altered enamel are attributed to changes in the rate of enamel matrix formation and duration of its
exposure to tissue fluids. Morphologic changes in Tomes' process were observed
at the time of formation of abnormal enamel following injection of all three
ions. These observations are compared with previous studies of altered enamel
formation and analyzed with the goal of learning more about the mechanisms
of amelogenesis.
ABSTRACT
Schour and Smith, '34, '35) showed that
subcutaneous injections of sodium fluoride
caused disturbances in enamel formation
as layers of hypomineralized and hypermineralized enamel. They observed large
darkly stained globules in the ameloblast
a few hours following injection. Several
light and electron microscopic studies since
then have also reported morphological
changes in the formative ameloblast induced by fluoride (Bhussry, '59; Kruger,
'67, '68, '70; Walton and Eisenmann, '72).
These changes consistently include large,
darkly stained globules and large vesicles
in the distal region of the cell body.
Weinmann ('43) reported that injected
strontium caused enamel hypoplasia and
hypomineralization. The ameloblasts were
seen to undergo degenerative changes and
detachment from the enamel matrix. Recent electron microprobe studies of the
effect of dietary strontium on forming
enamel revealed a n increased uptake of
strontium and decreased uptake of calcium
and phosphate (Johnson and Singer, '67).
ANAT.REc., 183: 303-322.
Microradiography has been used to assess mineralization disturbances induced
by fluoride, strontium, and cobalt (Allen,
'63; Weber and Yaeger, '64; Yaeger, '66;
Eisenmann and Yaeger, '69; Kruger, '71).
Fluoride produced a double response i n
rat enamel consisting of a n inner (first
formed ) hypermineralized layer followed
by a n outer layer. Cobalt produced first a
hypomineralized layer and then a hypermineralized layer, the inverse sequence of
fluoride. Strontium produced a hypermineralized enamel followed by a diffuse continuous hypomineralized area.
Cell damage has been suggested as being
responsible for all developmental mineralization lesions except those caused by
amdogenesis imperfecta (Nylen et al.,
'72). Through electron microscopy, disturbances in rat enamel induced by injections of tetracycline were shown to result
from a change in rate of matrix secretion
Received Aug. 22, '74. Accepted Apr. 3, '75.
1This study was supported in part by grant PHS
DE03312 from the National Institute for Dental Research.
303
304
ABRAHAM NEIMAN AND DALE R. EISENMANN
and disturbances in nucleation. The inner
hypermineralized layer was thought to be
caused by uninterrupted ion transport to
previously nucleated crystals during the
period when the hypomineralized layer was
formed. Disturbances in crystal growth
were attributed to the inability of the injured secretory ameloblast to fully recover
and function normally during its maturative phase.
Previously cited studies have examined
alterations in enamel and changes in morphology of cells following various inducing
agents. These studies were limited in that
they usually considered these disturbances
only after they were completed. Investigators have usually studied either the alterations of cellular morphology or variations
in enamel density, but with little correlation of these two aspects. This study examines the ameloblasts and their product
during the entire period of apposition of
altered enamel, utilizing parenteral dosages of strontium, cobalt, and fluoride
known to induce disturbances in enamel
formation (Eisenmann and Yaeger, '69).
Its purpose is to gain further insight into
some of the mechanisms of amelogenesis.
MATERIALS AND METHODS
Electron microscopy
Male Sprague-Dawley rats weighing
175-250 g were given a single subcutaneous injection of either 5 m g sodium fluoride, 125 mg strontium chloride
(Yaeger and Eisenmann, '63), or 100 m g
cobalt chloride/100 g body weight (Eisenmann and Yaeger, '69) and sacrificed at
intervals of 1, 2, 4, 8, 16, 24 and 48 hours.
A minimum of two animals was utilized
for each time interval. This time period
covers the development of the altered
enamel produced by the secretory ameloblasts. Control animals were given identical dosages of sodium chloride and were
sacrificed at 1, 2 and 4 hours. Our control
animals plus controls done in a previous
study (Eisenmann and Yaeger, '69) at
longer time intervals confirm that the
enamel response is not a result of the injection procedure itself. The rats were
anesthetized with ether and fixed by vital
perfusion through the aorta with 4%
gluteraldehyde in 0.04 M cacodylate buffer
at pH 7.2. The maxillary incisors were reremoved along with the surrounding alveolar bone keeping the enamel organ intact.
[ncisors were mounted on a Gillings-Hamco
sectioning machine and longitudinal sections of 150-300
were cut through the
middle third using normal saline solution
as a coolant. These sections were returned
to cold gluteraldehyde for one hour, rinsed
in cacodylate buffer for one hour, and
post-fixed in veronal buffered 1% osmium
tetraoxide for one hour. Specimens were
then dehydrated in a graded series of alcohols and flat-embedded in araldite for
cross-sectioning. Sectioning was one with
a Porter-Blum microtome equipped with a
diamond knife. The sections were taken
from the region where inner enamel had
reached a thickness of 20-50 pm. Thick
sections (0.5 pm) were examined in the
light microscope to assist in achieving the
proper location and orientation. Ultra-thin
sections were floated on a saturated solution of dibasic calcium phosphate (Boothroyd, '64), collected on parloidin and carbon-coated grids and stained with uranyl
magnesium acetate and lead citrate. The
specimens were examined with a Hitachi
7-S electron microscope at 50 kv.
Microradiography
Forty-eight hour specimens of cobalt,
strontium, and fluoride were embedded in
methyl methacrylate. Two week specimens
of strontium were similarly processed.
Longitudinal sections of 80-100 pm in
thickness were cut from the middle third
of the tooth with a Gillings-Hamco sectioning machine. Microradiographs were obtained on Kodak 649-0 spectroscopic plates
using a nickel filter in a Siemens x-ray
generator operated at 19 kV.
OBSERVATIONS
Electron microscopy
The typical morphology of a tall columnar ameloblast equipped with abundant
organelles for protein synthesis and secretion were observed i n all control specimens (fig. 1).
1. Fluoride
The morphology of the ameloblast maintains a normal appearance one hour after
ION INDUCED DISTURBANCES IN AMELOGENESIS
injection with fluoride. After two hours
numerous large vacuoles and dark globules
appear to be stacked-up in the distal half
of the cell body (fig. 2). These spherical
bodies vary in size and density and are
often large enough to span nearly the
entire width of the cell, displacing profiles
of endoplasmic reticulum. The bodies are
membrane-bound and do not appear to
communicate with each other or with any
other organelle. The organelles of the cell
body are of a normal appearance and the
quantity of secretion granules is similar to
that of the control cells. No alterations appear in Tomes’ process or the adjacent
enamel crystals a t this stage of the response to fluoride.
After four hours, the dark globules and
vacuoles increase in number and in some
cases extend to the nuclear region. Small
pools of stippled material accumulate just
outside of the distal end of Tomes’ process.
Other than the large bodies, the general
appearance of the components of the cell
body and Tomes’ process appear unaltered
four hours after fluoride.
At eight hours, larger lakes of stippled
material form a t the distal ends of Tomes’
processes (fig. 3). There is a decrease in
enamel formation between the processes.
The large bodies seen earlier in the cell
body have decreased in number and size.
At 16 hours the cells appear to have
nearly recovered from the effects of fluoride. The dark globules and vacuoles seen
i n the central region of the ameloblasts are
similar in size and amount to those seen
i n the control cells. No alterations are present in any of the organelles, but the morphology and size of Tomes’ process has
been altered. Enamel formation has resumed between the Tomes’ processes and
a t the distal end of each process leaving
behind large lakes of noncrystallized or
sparsely crystallized stippled material.
At 24 and 48 hours after the injection
the ultrastructure of the ameloblast shows
no unique features other than a continued
alteration after 24 hours in Tomes’ process (fig. 4 ) . Normal enamel is being laid
down over the hypomineralized band. The
layer of altered enamel consists of areas
containing scattered disoriented crystals in
a homogeneous osmiophilic background
and spaces devoid of mineral but contain-
305
ing a loosely arranged granular material
(fig. 5).
2. Ctjbalt
The ameloblast maintains a normal appearance two hours after injection with
cobalt. Small pools of stippled material
lacking crystals accumulate just outside of
the distal and mid-proximal regions of
Tomes’ process. At four hours after injection, numerous large vacuoles and dark
globules varying in size and density appear
in the distal third of the cell body (fig. 6).
The quantity and size of the spherical
bodies are similar to those seen after injection of fluoride.
After eight hours the large spherical
bodies seem to have decreased in size and
number. The morphology and size of
Tomes’ process is altered. Lakes of stippled
materisl accumulate a t the distal end of
Tomes’ process (fig. 7).
At 24 and 48 hours after the injection,
the ultrastructure of the ameloblast appears normal. Crystal formation occurs
after 24 hours over the altered hypomineralized regions leaving behind lakes of
non-crystalline stippled material (fig. 8).
A resumption of normal enamel formation occurs overlying the hypomineralized
region (fig. 9 ) . The thickness of enamel
formed over the hypomineralized region is
less than the amount formed after the
fluoride response (fig. 5).
Strontium
One and two hours after injection with
strontium, the ultrastructure of the ameloblast reflects no morphological differences
from control cells. After four and eight
hours, large vacuoles and dark globules
accumulate in the distal half of the cell
body (fig. 10). Small lakes of stippled
material pool at the distal end of Tomes’
process and along the enamel spikes. At
eight hours, the enamel front exhibits a
disorganization of crystals and a lack of
prism morphology.
At 16 hours, the spherical bodies decrease in size and amount. Observations
of the organelles reveal nothing abnormal.
Pools of stippled material accumulate in
the intercellular spaces between the processes along with a decrease in the formation of interprismatic enamel in these
3.
306
ABRAHAM NEIMAN AND DALE R. EISENMANN
areas, A broad spectrum of alteration is
noted in the size and morphology of the
Tomes’ process of some cells. The normal
prismatic pattern of enamel is not evident
in such areas.
At 24 hours, large lakes of stippled material accumulate on the enamel surface
and more proximally between the Tomes’
processes. Large vacuoles and dense globules again appear in the distal cytoplasm.
Tomes’ processes are severely altered in
size and morphology and the adjacent
enamel contains scattered, disorganized
crystals.
At 48 hours after injection, numerous
large vacuoles and dark globules varying
in size and density persist in the distal half
of the cells (fig. 11). The distal end shows
a reduction of Tomes’ process into thin
finger-like structures of varied shapes.
Huge lakes of non-crystalline, dense homogeneous material accumulate in the intercellular spaces between ameloblasts on the
surface of the enamel (fig. 12). The
mineralizing front contains a decreased
concentration of crystals which are haphazardly organized (fig. 11). This area represents formation of a second hypomineralized layer. On either side of the first-formed
hypomineralized band, there is a lack of
prism morphology. The organic matrix observed in the first-formed hypomineralized
regions and that which is accumulating at
the enamel front consists of a n osmiophilic material containing a few scattered
crystals.
Microradiograp hy
Following are microradiographic descriptions of the response to each ion at 48
hours after injections in the formative
stage of amelogenesis :
Fluoride. The response to fluoride consists of two components: a n inner (firstformed) hypermineralized band, and a n
outer hypomineralized component covered
with a thin layer of newly formed normal
enamel (fig. 13).
Cobalt. The response to cobalt consists of a n inner hypomineralized region
which precedes a n outer hypermineralized
layer (fig. 4). On the surface is a layer of
newly formed normal enamel.
Strontium. The response seen in the
microradiograph consists of up to four
components in some regions. Proceeding
from the inner (first-formed) layer outward they are : 1. a n inner hypennineralized layer; 2. a hypomineralized layer; 3.
a hypermineralized layer; 4. a n outer hypomineralized region, Little, if any, normal
enamel is formed external to the outer
hypomineralized layer (fig. 15).
An additional %week follow-up examination of the strontium response revealed a
complete lack of resumption of normal
enamel secretion in the affected region
with normal enamel formation by ameloblasts developing later (fig. 16).
DISCUSSION
Electron microscopic investigation of
amelogenesis disturbed by strontium, fluoride, and cobalt has revealed alterations i n
both cell morphology and enamel formation. Early changes following injection
with all three ions consist of accumulations of dark globules and vacuoles in the
cell and pooling of stippled material on the
enamel surface. Permanent recovery of
enamel formation occurs after cobalt and
fluoride, but the brief recovery by the
ameloblasts after injection with strontium
is followed by another severe response in
the cell and enamel after 48 hours and a
lack of subsequent recovery in the affected
area. Johnson et al. (’68) have demonstrated that strontium incorporated in the
bone of rats is subsequently translocated
to the incisor teeth during the remodeling
process of bone. This process may be responsible for the second wave of disturbance following strontium injection.
The orientation of enamel crystals and
the resultant formation of a highly ordered
prismatic structure has been attributed to
the organizing properties of the Tomes’
process cell membrane (Boyde, ’64). Variations in Tomes’ process were observed in
ameloblasts at the time of formation of
abnormal enamel following injection of all
three ions. The severest alteration of
Tomes’ process was seen after injection
with strontium which also produced the
most extreme changes in enamel structure.
The least severe disturbance of Tomes’
process was produced by cobalt which induced the mildest defect insofar as prism
morphology is concerned. Variations in
enamel structure are also seen during nor-
ION INDUCED DISTURBANCES I N AMELOGENESIS
ma1 development when formation has first
begun at the dentino-enamel junction and
when it is nearly completed producing layers of prismless enamel. At both of these
stages of enamel formation Tomes' processes are undergoing marked changes in
morphology : either developing as cell processes or being phased out. This information along with the currently observed
relationship between Tomes' process morphology and the quality of enamel structure, support an organizational function
for Tomes' process.
A number of factors must be considered
in analyzing mechanisms of interference
with enamel formation. Among these are
quality of matrix, crystal nucleation and
growth, transfer of mineral ions to the
matrix and systems acting as regulators of
mineralization. Although it has been demonstrated autoradiographically (Kruger,
'70) that some variation in enamel matrix
occurs following fluoride injection, poorly
mineralized areas OE dentin induced by
strontium and fluoride were found capable
of accumulating mineral in vitro (Eisenmann and Yaeger, '72). This indicates that
the organic matrix, if it was altered, was
at least not permanently resistant to mineralization. The pools of unmineralized
stippled material observed in the present
study as well as the regions of sparsely
mineralized matrix are present at times
when mineral is being deposited in adjacent hypermineralized zones of the strontium and fluoride responses. The resistance
to mineralization by specific regions may
be due to localized interference with certain of the other factors involved in the
mineralization process and known to be
susceptible to interference by at least some
of the ions injected. For example, enzyme
systems essential for proper cell function
are inhibited by fluoride (Frajola, '59;
Yoshida et al., '68); and cobalt, fluoride
and strontium are reported to have various
inhibitory effects on crystal nucleation and
growth (Bird and Thomas, '63). In addition, it has been suggested by Russell and
Fleisch ('70) that fluoride may exert its
effect on mineralization indirectly by inhibiting phosphatase and permitting a
greater action by pyrophosphate, a known
inhibitor of mineralization.
307
Recent evidence points toward the active
involvement of formative cells in transferring mineral ions from the circulating fluids to various mineralizing tissues
(Kashiwa and Mukai, '71; Martin and
Matthews, '70; Kuhar, '74). If the ameloblast is a mineral transporting cell, it is
conceivable that the injected ions could
interfere with this process by enzyme disturbances, membrane alterations, or by
calcium and phosphate binding within the
cell.
Fluoride-induced enamel changes appear
to consist of localized interference with
mineralization of newly formed matrix
with concurrent accumulation of available
calcium and phosphate ions in the preresponse enamel. This pattern of formation of hypermineralized enamel has been
proposed by previous authors (Weber and
Yaeger, '64; Nylen et al., '72). Only isolated areas of matrix in the hypomineralized layer of some specimens appear to be
so severely altered morphologically as to
prevent mineralization completely. Those
areas of matrix which do contain crystals
but of a deficient number appear otherwise
similar to normal enamel matrix. Thus it
is likely that mineral ion flow has continued and a brief localized alteration in
mineralization of newly forming matrix
has occurred. This may be a result of inhibition of enzymes such as phosphatase
and/or interference by fluoride with the
processes of crystal nucleation and growth.
Complete recovery of the ameloblast is indicated by the substantial thickness of normal enamel deposited over the hypomineralized layer.
The response to strontium may be considered as a double fluoride response. Both
ameloblastic and enamel alterations g o
through two cycles which, as mentioned
previously, may reflect a secondary wave
of strontium ions as they are released from
bone, Strontium eventually leads to a cessation of enamel formation which is evidenced by the lack of post-response enamel
observed microradiographically two weeks
after injection.
The matrix produced shortly after cobalt
injection remains almost completely devoid
of crystals. It is interesting to note that
the appearance of this unmineralized ma-
308
ABRAHAM NEIMAN AND DALE R. EISENMANN
trix is no different from that of normal
stippled material. Also it is significant that
no hypermineralization occurs in the preresponse enamel. These observations lend
support for speculation that a temporary
interruption in mineral ion flow may occur.
However, it seems unlikely that this alone
could be responsible for the hypomineralized layer, because when ion flow is resumed it would lead to crystal formation
in the older crystal deficient regions as well
as the newly formed matrix. As a known
inhibitor of nucleation (Bird and Thomas,
'63), cobalt may be present in the hypomineralized region and thus prevent its
mineralization even after ion flow resumes.
The formation of a subsequent hypermineralized layer may well be due to a period
of decreased rate of enamel matrix formation as evidenced by the lesser amount of
post-response enamel as compared to after
fluoride.
Ion induced disturbances i n amelogenesis lead to various combinations of cellular and enamel defects which have many
aspects in common along with certain
major variations. Nylen et al. ('72) have
proposed that most disturbances in ameloblast function follow a similar pattern one that is comparable to that observed
here for fluoride and strontium. However,
i t appears that the response to cobalt is
unique and may lend itself to further study
of some of the intricate mechanisms by
which normal enamel is formed.
ACKNOWLEDGMENTS
The authors wish to express their appreciation to Mrs. Elena Baltrusaitis for
her technical assistance and Mrs. Izabele
Stoncius for her photographic work.
LITERATURE CITED
Allan, J. H. 1963 Observations o n the development of dental enamel in acute experimental
fluorosis. In: Advances in Fluorine Research
and Dental Caries Prevention. J. L. Hardwick,
J . P. Destin and H. R. Held, eds. The Macmillan
Co., New York, pp. 41-51.
Bhussry, B. R. 1959 Effects of sodium fluoride
on the developing teeth of rats. J. Dent. Res.,
38: 653-654.
Bird, E. D., and W. C. Thomas, Jr. 1963 Effect
of various metals on mineralization in vitro.
Proc. SOC.Exp. Biol. Med., 112: 640-643.
Boothroyd, B. 1964 The problem of demineral-
ization in thin sections of fully calcified bone.
J. Cell Biol., 20: 165-175.
Boyde, A. 1964 The Structure and Development of Mammalian Enamel. Ph.D. Thesis,
London Hospital Medical College, London.
Eisenmann, D. R., and J. A. Yaeger 1969
Alterations in the formation of rat dentin and
enamel induced by various ions. Archs. Oral
Biol., 1 4 : 1045-1064.
1972 In vitro mineralization of hypomineralized dentin induced by strontium and
fluoride. Archs. Oral Biol., 27: 987-999.
Frajola, W. J. 1959 Fluoride and enzyme inhibition. In: Fluorine and Dental Health. The
Pharmacology and Toxicology of Fluorine.
J. C. Muhler and M. K. Hine, eds. Indiana University Press, Bloomington, pp. 68-69.
Johnson, A. R., W. D. Armstrong and L. Singer
1968 The incorporation and removal of large
amounts of strontium by physiologic mechanisms ni mineralized tissues of the rat. Calc.
Tiss. Res., 2: 242-252.
Johnson, A. R., and L. Singer 1967 A n electronmicroprobe study of rat incisor teeth with low
or high concentrations of strontium. Archs.
Oral Biol., 12: 389-399.
Kashiwa, H. K., and C. D. Muai 1971 Lipidcalcium-phosphate spherule i n chondrocytes of
developing long bones. Clin. Orth., 78: 223-229.
Kruger, B. J. 1967 Histologic effects of fluoride
and molybdenum on developing dental tissues.
Aust. Dent. J., 12: 54-60.
1968 Ultrastructural changes in ameloblasts from fluoride treated rats. Archs. Oral
Biol., 13: 969-977.
1970 An autoradiographic assessment
of the effect of fluoride on the uptake of
H3-proline by ameloblasts in the rat. Archs.
Oral Biol., 15: 103-108.
1970 The effect of different levels of
fluoride on the ultrastructure of ameloblasts in
rat. Archs. Oral Biol., 15: 109-114.
1971 Scanning electron microscopy of
sections of fluorosed rat enamel. J. Dent. Res.,
50: 1685.
Kuhar, K. J. 1974 Fluoride-induced Calcification within the Maturative Ameloblast of the
Rat. M. S. Thesis, University of Illinois,
Chicago.
Martin, J. H., and J. L. Matthews 1970 Mitochondrial granules in chondrocytes, osteoblasts
and osteocytes. Clin. Orth., 68: 273-278.
Nylen, M., K. Ommell and C. Lofgren
1972
A n electron microscopic study of tetracyclineinduced enamel defects in rat incisor enamel.
Scand. J. Dent. Res., 80: 384-409.
Russell, R. G., and H. Fleisch 1970 Inorganic
pyrophosphate and pyrophosphatases in calcification and calcium homeostasis. Clin. Orth.,
69: 101-117.
Schour, I., and M. C. Smith 1934 The histologic changes in the enamel and dentin of the
rat incisor i n acute and chronic experimental
fluorosis. Univ. Ariz. Coll. Agric., Agric. Exp.
Sta., Techn. Bull., 52: 67-91.
1935 Mottled teeth: An experimental
histologic analysis. J. Am. Dent. Assoc., 22:
796-8 13.
ION INDUCED DISTURBANCES IN AMELOGENESIS
Walton, R. E., and D. R. Eisenmann 1974
Ultrastructural examination of various stages
of amelogenesis in the rat following parental
fluoride administration. Archs. Oral Biol., 19:
171-183.
Weber, D. F., and J. A. Yaeger 1964 A microradiographic interpretation of abnormal enamel
formation induced by subcutaneous sodium
fluoride. J. Dent. Res., 43: 50-56.
Weinmann, J. P. 1943 Recovery of ameloblasts.
J. Amer. Dent. Assoc., 30: 874-888.
Yaeger, J. A. 1966 The effects of high fluoride
309
diets on developing enamel and dentin in the
incisors of rats. Am. J. Anat., 18: 665-683.
Yaeger, J. A,, and D. R. Eisenmann 1963 Response in rat incisor dentin to injected strontium, fluoride, and parathyroid extract. J. Dent.
Res., 42: 1208-1216.
Yoshida, H.,D. Nagai, M. Kamei and Y. Nakagawa 1968 Irreversible inactivation of (Naf
- K+)-dependent ATPase and K+-dependent
phosphatase by fluoride. Biochem. Biophys.
Acta, 150: 162-168.
PLATE 1
EXPLANATION O F FIGURE
1
310
Control secretory ameloblasts. This electron micrograph is from inner
enamel. Note the axially oriented granular endoplasmic reticulum
( E ) , large dark and light granules ( G ) , mitochondria ( M ) , vacuoles
( V ) , terminal cell web ( W ) , and fibril (F). Magnification x 5,495.
ION INDUCED DISTURBANCES I N AMELOGENESIS
Abraham Neiman and Dale R. Eisenmann
PLATE 1
311
PLATE 2
EXPLANATION OF FIGURES
312
2
Ameloblasts two hours after injection with fluoride. This montage
shows numerous membrane-bound large vacuoles and dark globules.
Note the variety of sizes and densities of the spherical bodies. Some
endoplasmic reticulum is displaced by these bodies. V, vacuoles;
D, dark globules; E, endoplasmic reticulum. x 3,895.
3
Tomes’ process eight hours after injection with fluoride shows accumulation of larger lakes of stippled material. x 3,420.
4
Ameloblasts 24 hours after injection with fluoride. The cells appear
normal. Note alterations in size and morphology of Tomes’ process.
T, Tomes’ process. X 3,325.
5
Enamel formed 48 hours after fluoride injection. The hypomineralized band is overlaid by normal prism structure. 0, hypomineralized
band. Magnification X 3,040.
Inset: The hypomineralized band containing a few scattered
crystals. x 6,080.
ION INDUCED DISTURBANCES IN AMELOGENESIS
Abraham Neiman and Dale R. Eisenmann
PLATE 2
PLATE 3
EXPLANATION OF FIGURES
6
Ameloblast four hours after injection with cobalt. Note globules and
vacuoles are enclosed within membranes. Small dense bodies are
being formed in the Golgi zone. S, secretion granules; G, Golgi;
V, vacuoles; D, dark globules. x 5,400.
7 Tomes’ process eight hours after injection with cobalt. Stippled
material accumulates at tips of the enamel prongs and distal end
of the process (arrows). x 5,450.
8
Tomes’ process 24 hours after injection with cobalt. Note lakes of
non-crystalline stippled material forming a circumferential outline
around the prism (arrows). x 5,100.
9 Enamel structure formed 48 hours after cobalt injection. Normal
prism structure is formed over the hypomineralized region. Enamel
crystal formation is not observed in the hypomineralized region.
X 5,100.
314
ION INDUCED DISTURBANCES IN AMELOGENESIS
Abraham Neiman and Dale R. Eisenmann
PLATE 3
315
PLATE 4
EXPLANATION OF FIGURES
10
Montage of ameloblasts four hours after injections with strontium.
Large globules and vacuoles appear stacked up in the distal half
of the cell. G, globules; V, vacuoles; S, stippled material. x 4,590.
11 Ameloblasts from animal injected 48 hours previously with strontium.
Note the severe alterations in the morphology of Tomes’ process and
the accumulation of stippled material at the distal ends of the
process. Enamel on either side of the first hypomineralized region
shows some regions of increased electron density and a lack of
prism morphology. T, Tomes’ process; S, stippled material; 0, hypomineralized region. x 4,050.
316
ION INDUCED DISTURBANCES IN AMELOGENESIS
Abraham Neiman and Dale R. Eisenmann
PLATE 1
317
PLATE 5
EXPLANATION O F FIGURE
12 Higher magnification of enamel from area similar to figure 11. Huge
lakes of stippled material accumulate at the intercellular spaces.
S , stippled material. x 10,500.
318
ION INDUCED DISTURBANCES IN AMELOGENESIS
Abraham Neiman and Dale R. Eisenmann
PLATE 5
319
0
w
w
Microradiograph of enamel 48 hours after injection with fluoride. A n outer hypomineralized layer (dark) is formed above an inner hypermineralized layer ( b e
tween arrows). On the outermost surface is a layer of normal enamel. x 190.
16 Microradiograph of incisor two weeks after injection with strontium. Note the
lack of recovery in the affected area occupying most of the microradiograph and
the region of later-forming normal enamel ( n ) on the far right (dentino-enamel
junction, dark arrow). x 50.
15 Microradiograph of enamel 48 hours after injection with strontium. Note alternating rows of hyper- ( e r ) and hypomineralized ( 0 ) enamel (arrows). x 190.
14 Microradiograph of enamel response 48 hours after injection with cobalt. A n
outer hypermineralized layer (light) is formed above an inner hypomineralized
layer (dark). On the outermost surface is a layer of normal enamel. x 190.
13
PLATE 6
EXPLANATION O F FIGURES
ION INDUCED DISTURBANCES IN AMELOGENESIS
Abraham Neiman and Dale R. Eisenmann
PLATE 6
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effect, fluoride, formation, enamel, rat, strontium, cobalt, incisors
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