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TABLE I

REPORTED CAUSE.S OF ENAMEL HYPOPLASIA (-7)

1. Nutritional defects a. Rickets

b. Scurvy

i. Endocrine defects

a. Hypothyroidism

b. Abnormal calcium-phosphorus metabolism e.g.

hypoparathyroidism

3. Hereditary disease

a. Morquio’s syndrome

b. Amelogenesis imperfecta

4. Toxic

a. Keruicturus (from Rh+ incompatibility, ABO,

etc.)

b. Drugs (tetracycline)

5. Infectious disease

a. “Measles” b. Syphilis 6. Prematurity

7. Generalized metabolic defects (“nonspecific, severe

metabolic upset”)

S EASILY AS 1743 systemic disease was

reported to cause enamel defects.’

These defects, usually manifest as enamel

hypoplasia, have been associated with many

diseases. As collected from the literature,27

tile reported causes of enamel hypoplasia

may be divided into several broad

categor-ies (Table I). Among these no single

etio-logic factor is apparent. In only a few

in-stances, such as syphilis, has the

abnormal-ity

been reported in permanent teeth.

Recently, we recognized hypoplastic

enamel in permanent teeth of nephrotic

children. The absence of previous reports

of the association of the nephrotic syndrome

\Vitll dental defects prompted our interest.

REVIEW OF TOOTH DEVELOPMENT PERTINENT TO THIS STUDY

The enamel organ produces both dentin

and enamel, but only the latter can be easily

evaluated. When disturbed, the enamel

organ usually responds by production of

hypoplastic enamel. The resultant defective

teeth, in contrast to bone, provide a

perma-nent record of past disturbances, unique

in that enamel once formed cannot be

im-proved by later events.

Hypoplastic enamel is best understood

with reference to normal dental

develop-ment. Tile development of teeth follows an

orderly sequence. For each tooth, enamel

formation proceeds from the occlusal edge

toward the root. Tile enamel is laid down

in successively overlapping layers, as

illus-(Submitted February ; accepted for publicationApril 24, 1963.)

Assisted in part l)y grants from the Michigan Chapter of National Kidney Disease Foundation and

Na-tional Institute of Health (A-3796) and in part by Traineeship (2A-5278 C2) National Institute of Health

Grant.

Presented to the Midwest Society for Pediatric Research, Cincinnati, Ohio, October 25-28, 1962.

ADDRESS: (W.J.O.) University of Michigan hospital, 1405 E. Ann Street, Ann Arbor, Michigan.

PEDIATRICS, September 1963

399

HYPOPLASTIC

ENAMEL

ASSOCIATED

WITH

THE

NEPHROTIC

SYNDROME

William J. Oliver, M.D., Clyde L. Owings, M.D., William E. Brown, D.D.S.,

and Barry A. Shapiro, A.B.

1)eparlmc’nt of Pediatrics and Conununicable Diseases Gild School of Dentistry, University of Michigan

trated schematically for an incisor in Figure

1. Although this process is represented as

occurring in four stages, in reality it

con-sists of many small increments. Tile time

required for completion of enamel

forma-tion ranges from a few months for

decidu-ous teeth to 6 years for some permanent

teeth.8

If that process is disturbed temporarily,

hypoplasia of the developing layer occurs.

This is represented schematically in Figure

2 as occurring during the third phase of

enamel formation. If the insult is removed,

development then resumes the normal

(2)

re-4

of renal disease with development of faulty

enamel.

SUBJECTS AND METHODS

Forty children with a history of the

ne-phrotic syndrome were evaluated. Complete

records were available since most of these

patients have been treated exclusively for

their nephrotic syndrome at tile University

of Michigan Medical Center (UMMC).

Criteria for diagnosis follow those of

Met-coff.” Continuous steroid therapy was used

to induce remission, followed by

intermit-tent steroid therapy for periods of 1 to 2

years, as previously described.12 In some

patients prophylactic antibiotics were given

for periods as long as 2% years. No

supple-mentary calcium salts were given.

Examination, during the summer of 1962,

consisted of an attempt to demonstrate

ab-normal fluorescence by Wood’s light, and a

careful appraisal of the enamel of each

tooth. The findings were confirmed by a

pedodonist (W.E.B.), who estimated the

age at which the abnormality had occurred.

This estimate was accomplished without

knowledge of the clinical course and

treat-CHRONOLOCY OF ENAMEL FORMATION

2

lII I

I I

I _ I

I I

I I

I I

I 3 I

I I

II

I I

DEFECTIVE I

ENAMEL FORMATION

AT THIS STAGE

I I

I I

4

0 2 4 6

YEAR

8 0

400

FIG. 1. Normal enamel formation.

main as a chronological record of previous

illness.

The other important feature of dental

growth is tile orderly and precise sequence

by

which individual teeth undergo

devel-opment.9 This pattern for permanent teeth

is illustrated in Figure 3. The onset and

duration of enamel formation differs

be-tween teeth. Thus, the location of

hypo-plasia on a particular tooth allows an

esti-mate of the age at which the insult

oc-curred.

In this study the incidence and

loca-tion of enamel hypoplasia in our nephrotic

children were investigated. By using the

published tables of dental development,bO

an attempt was made to correlate the timing

1i-CsntvoI Incisors

t

Loterol Incisors

Cuspid

a‘ litBicuspid

2nd Bicuspid

c

st Motor

I 2nd Motor

MAXILLARY

Ic Csntrol Incisors

Lotsrol Incisors Cuspid st Bicuspid

1 2nd Bicuspid

.1 1, stMolar

2ndMolor

MANDIBULAR L

FIG. 3. Chronology of enamel formation. Each bar

represents the development of a single tooth,

plotted against age. The left margin of the bar

FIG. 2. Disturbed enamel formation. The residual represents the beginning of enamel formation,

(3)

(‘lassificalion

Condition of Enamel

Normal Ilypoplaslic Total

I. Patients with onset disease before 6 years; and no erupted

perma-itent teeth at time of study 8 0 8

II. Patients with onset disease after 6years; and with erupted

perina-nent teeth at time of study 10 0 10

III. Patients with onset disease before 6 years; and with erupted

per-manent teeth at time of study

14 (63.6%)

8 (36.4%)

2

Total (%)

3 (80%)

8 (o%)

40 401

TABLE II

SUMMARY OF DENTAL EVALUATION OF NEPUROTIC CHILDREN

ment of each patient’s disease. Where

avail-able, siblings were evaluated as controls.

RESULTS

Findings are summarized in Table II. No

enamel hypoplasia of deciduous teeth was

found in any patient in the study. Likewise,

abnormal fluorescence was not observed.

Siblings, used as controls, had no enamel

hypoplasia.

The subjects could be divided into three

groups. The first group consisted of those

patients who did not have erupted

perma-nent teeth at time of study. Since dental

roentgenograms were not routinely

ob-tamed, evaluation of this group is

incom-plete.

The second group consisted of 10 patients

with onset of their renal disease after

enamel formation was complete; there was

no enamel hypoplasia. This group may, in

a sense, serve as controls since their disease

and treatment could not affect dental

de-velopment.

In the remaining group of 22 patients,

who had onset of their renal disease before

6 years of age, 8 of the 22 patients had

enamel hypoplasia. The hypoplastic enamel

could be recognized easily because of its

distinct appearance. The

involved areas

were depressed and, in some patients,

ap-peared yellow in color. Normally, tooth

color is determined by the thick layer of

translucent enamel. The thin hypoplastic

enamel is more transparent and allows the

yellow dentin to be seen.

The following cases illustrate the

neph-rotic syndrome occurring during early,

middle or late stages of dental

develop-ment:

Case 1

DV., an 8-year-old girl, was the product of a

full-term pregnancy, with birth weight of 10 lb

3 oz (4,620 gm). The neonatal period was

un-eventful. She was apparently in good health until

7 months of age at which time she had onset of

the nephrotic syndrome (Fig. 4). Following 3

weeks of unsuccessful therapy, she was transferred

to UMMC. Tetracycline, 10 mg/lb/day, was begun

shortly after admission and continued for a total of

13 months. After 4 weeks of supportive treatment,

ACTH, 160 i.u./day, was given for 11 days.

Shortly thereafter diuresis occurred, and

albumin-uria disappeared. She was discharged on

inter-mittent cortisone therapy in a dosage of 100 mg

on 3 consecutive days of each week. Two months

after discharge, a relapse occurred which

re-sponded to intensive cortisone therapy over a

30-day period. Thereafter, she remained in

remis-sion and cortisone was later discontinued. The

total duration of cortisone therapy was five months.

Subsequently, she remained well without evidence

of the nephrotic syndrome.

Dental evaluation, at 8 years of age, revealed

severe hypoplastic enamel of the upper central

in-cisors, lower central and lateral incisors and all

first molars (Fig. 5). The involved areas were

de-pressed, yellow in color and sensitive to heat and

cold. The lingual surfaces of these teeth were also

(4)

AD. 750067 . , ‘I I’

Incisors

Incisors

MAXILLARY

Central Incisors

,,1’Lateral Incisors

T 1st Molar

MANDIBULAR

Central Incisors

,,‘LateraI IncIsors

,\

MANDIBULAR

_

Clinical Illness

Steroids

Tetracycline

0 2 4 6 8 lO

YEAR

YEAR plastic.

graph.

FIG. 5. Case 1. Teeth of Patient D.V. with

hypo-plastic enamel of incisors.

bicuspids, and second molars had not yet erupted.

Dental estimate of the age at which disturbance

of enamelization occurred was between 6 and 12

months.

DV. 806097

.-CenIroI Incisors

iiiir

‘ I

,,,f .- Lolerol Incisors

r “_t

_____

_______

-1st Molar

(i

::

MAXILLARY

:rArA

I

______

Clinical Illness Steroids #{149}

Tetrocychne

0 2 4 6 8

FIG. 4. Case 1. Clinical course and dental

develop-ment of Patient DV. The duration of clinical

ill-ness, steroid therapy and tetracycline therapy is

plotted against age. Dental development is plotted

against the same scale. The bars representing teeth

with hypoplastic enamel are diagonally striped as

are the involved teeth on the left portion of tile

Case 2

A.D., a 9-year-old white girl was the product of

a full-term pregnancy, with birth weight of 7 lb

73 oz (3,389 gm). Her course was uneventful until

onset of the nephrotic syndrome at 23 years of

age (Fig. 6). After 4 days of hospitalization with

only dietary treatment, she underwent a

spon-taneous remission. She remained well until 4

FIG. 6. Case 2. Clinical course and dental

develop-ment of Patient AD. Format is identical to that of

Figure 4. Only the gingival portion of the upper

i’o and lower central and lateral incisors was

hvpo-fllOnthS later when a recurrence of the nephrotic

syndrome followed an upper respiratory infection.

She was hospitalized and given tetracycline,

po-tassium chloride, and ACTHAR Gel, 100 its. daily,

for 10 days. Diuresis began on the fifth clay of

treatment. Subsequent to discharge, she was given

cortisone, 200 mg, on 3 consecutive days of each

week. After 5 months, she developed a relapse

which responded readily to 8 days of intensive

steroid therapy. Subsequently, three relapses.

which cleared with intensive therap\, occurred

during the next 18 months. Thereafter, she has

remained well. Steroids were given for a total

duration of 33 years, and tetracycline was

ad-ministered daily for a total of 2 years.

Dental evaluation at 9 years of age revealed

yellow areas of hvpoplastic enamel confined to the

gingival margin of all incisors (Fig. 7). The

af-fected areas were depressed, and clearly were not

Nasmyth’s membrane. All first molars were erupted

and completely normal. The remainder of her

permanent teeth were not erispted, bitt dental

roentgenograms appeared normal. Dental estimate

of age at which the disturbance of enamel

forma-tH)n occurred was between 3 and 4 ears I)f age.

Case 3

R.L.

,

a 12-year-old white l)o\, was the product

of a full-term pregnancy with birth weight of

8 lb 12 oz (:3,969 gm). Resuscitation was required

at birth, but the remainder of the neonatal course

was uneventful. His general health had been

(5)

R L 827810

Jj

r 2nd Bicuspid

2nd Molar

MAXILLARY

Clinical Illness $

Steroids $

Antibiotics

0 2 4 6 8 10

YEAR

l’ie. 7. Case 2 Teeth of Patient AD. with

hvpo-plastic enamel of gingival margin of incisors. The

narrow band of hypoplasia is most evident upon

tile tipper teeth, indicated by the arrows.

403

nephrotic syndrome (Fig. 8). He aS admitted to

his local hospital, and, despite therapy with

ACTI!, serum albumin, and oxvtetracycline, his

e(lema became worse. After 5 weeks he was

trans-ferred to UMMC. His disease 1)ersisted over the

next 2 months without response to numerous

tilerapeutic agents including nitrogen mustard and

dextran. Several paracenteses were required

be-cause of dvspnea, and pneumonia occurred once.

Finally, 3 months after onset of his disease, a

14-day course of cortisone resulted in diuresis and

(lecrease(l proteinuria. He received tetracycline in

therapeutic dosage for one month of his

hospitali-zation at U\IMC.

Dtsring the next 23 years there were eight

hos-l)it11izati11s for exacerbations of his neplirotic

syndrome. At no time during this interval was the

patient free of edema or proteinuria. Tetracycline,

10 mg/lb, was given daily for this 234-year period.

Corticosteroids were given 3 days of each week for

this interval. eXCeI)t during exacerbations when

daily therapy was used. Supplemental calcium salts

were not given.

Subsequently, the patient has done well except

for one short exacerbation at age 10 years which

readily responded to intensive steroid therapy.

Dental evalisation at age 113 years showed all

second l)iduspids and second molars to he small

and yellow and to have hypoplastic enamel (Figs.

9 & 10). All other permanent teeth, except third

molars which were not erupted, had normal

enamel. l)ental estimate of the age at which the

disturbance of enamel formation occurred was

4 to 6 years.

COMMENT

WTe are iml)ressed by tilecorrelation

be-tween the age of severe renal disease and

tue estimated age at which faulty enamel

was formed. This correlation was present in

#{231}_.__2nd Bicuspid

-2nd Molar

MANDIBULAR

FIG. 8. Case :3. Clinical course and dental

develop-ment of Patient R.L. Format is identical to that

of Figure 4. Hypoplastic enamel was limited to the

second bicuspids and second molars.

every patient examined and is clearly shown

on the graphs. In Patient D.V. (Fig. 4),

whose renal disease occurred during the

early phase of enamelization, the lesions are

located toward the occlusal or first formed

surface of the teeth. Tile enamel of these

teeth which formed later, after all signs of

renal disease had subsided, was normal.

This is contrasted with Patient AD. (Fig.

6), whose renal disease occurred late during

enaniel formation of the incisors. Her

le-sions are found near the gingival margin.

The enalilel formed prior to illness is

nor-mal. Likewise in Patient R.L. (Fig. 8) those

teeth, which had completed their enamel

formation prior to illness, were normal. His

defects were confined to the late

develop-ing teeth.

Four of the renlaining I)atiellts had

Pat-terns of involvelllent similar to that shown

in Figure 6. The remaining patient’s pattern

was almost identical to Figure 8.

The incidence of hypoplastic enamel in

OUr I)atiellts with the nephrotic syndrome

is far higher than estimates of incidence in

the general population (35%).13 Although

(6)

hypo-FIG. 9. Case 3. Teeth of Patient R.L. This view

of the upper left teeth shows hvpoplasia of the

secOfl(l bicuspid and second molar. The

interven-ing first molar is not hypoplastic, as shown by the

normal size and color. The black area of the

anterior portion of this tooth is amalgam

restora-tion, not related to enamel hypoplasia.

404

plastic enamel, there were no premature

births among our affected patients.

There are several other possible causes

for the enamel defects found in nephrotic

children. These include speeffic drugs, as

tetracycline and corticosteroids, as well as

changes secondary to the nephrotic

syn-drome. Disturbances in calcium and

phos-phorus metabolism consitute an example of

tile latter.

Schwachman et al.14 and Zegarelli et

al.’ observed brown to black staining of

deciduous and permanent teeth in

fibro-cystic patients treated with tetracycline.

More extensive studies by Davies et al.16

and Waliman and Hilton” showed that

many infants given tetracycline shortly

after birth had yellow deciduous teeth. In

such teeth, the drug could be demonstrated

in both dentin and enamel. They observed

an impressive yellow fluorescence of the

involved teeth when viewed in ultraviolet

light. Wallman and Hilton suggested the

enamel hypoplasia observed in their patients

was due to tetracycline. MillerlS considered

the enamel hypoplasia more likely due to

prematurity than to tetracycline. The fact

that ultraviolet light did not cause

fluores-cence of the involved teeth would appear

to be a strong point against tetracycline as

a cause of the hypoplastic enamel in our

patients. Evaluation of the effect of

tetra-cycline would require patients who were

otherwise similar but did not receive

tetra-cycline therapy. Unfortunately, all of our

subjects had long-term tetracycline therapy

during their illness.

Corticosteroid administration may be a

significant factor in formation of hypoplastic

enamel. Demineralization of bone

(osteo-porosis) frequently occurs during prolonged

steroid therapy. It has been postulatedl9

that the loss of calcium and phosphorus

from bones is due to inadequate formation

of protein matrix coincident to the catabolic

or antianabolic effects of adrenal hormones.

Although an association of steroid therapy

with enamel hypolasia has not been

re-ported, the adverse effects of such therapy

may include enamel defects.

To completely evaluate the effect of

steroid administration, the incidence of

enamel defects in nephrotic children not

receiving steroid therapy should be studied.

We were unable to obtain such a group of

patients since only one of the nephrotic

children followed in our clinic was treated

without steroid therapy. A comparison with

patients who developed the nephrotic

syn-drome before the era of steroid therapy

may not be valid because of differences in

supportive therapy. Further, the increased

attrition of teeth with hypoplastic enamel

complicates the comparison of the present

subjects with older patients.

,

‘r’

FIG. 10. Case 3. Patient R.L. View of defective

teeth illustrating the small size and defective

(7)

Disturbances of calcium and phosphorus

metabolism, not associated with drug

ther-apy, were reported by Calteux to cause

hypoplastic enamel.2#{176} In studies of

ne-phrotic children, Emerson and Beckman2l

demonstrated derangements of calcium and

phosphorus metabolism during periods of

active disease with edema. Phosphorus

bat-ance was negative while only 2% of ingested

calcium was retained. On roentgenograms,

they noted a diffuse rarefaction of shafts of

bones despite a normal rate of growth and

calcification at epiphyseal plates. The bone

changes were not those found in rickets.

Deficits of calcium were found to result

from excessive fecal losses of calcium. No

etiology was proposed for this finding, but

balances rapidly reverted to normal

follow-ing diuresis with loss of edema. Recently,

Stickler et al.22 emphasized the fecal loss

of calcium in many forms of renal disease,

including the nephrotic syndrome. The

con-tribution of these abnormalities of calcium

metabolism to enamel hypoplasia in the

nephrotic syndrome cannot be defined.

The nephrotic syndrome may have

im-portant adverse effects upon enamel

forma-tion which may be unrelated to any of the

previous factors. The problem is further

complicated by the observation that no

sig-nificant difference of severity, course or

treatment was found between patients with

enamel hypoptasia and those with normal

teeth.

SUMMARY

A high incidence of enamel hypoplasia

in permanent teeth was found in children

with the nephrotic syndrome. There was a

correlation between the time of severe renal

disease and the estimated time at which

faulty enamel was formed. The absence of

fluorescence of the defective teeth upon

exposure to ultraviolet light suggests that

tetracycline therapy was not a causative

factor. Other possible causes of the defect

include corticosteroid therapy and

meta-bolic disturbances associated with the

neph-rotic syndrome. Final identification of the

etiological factor remains uncertain.

REFERENCES

1. Quoted by Cavallaro, J.: Syphilis in its

rela-tion to dentition. D. Cosmos, 50: 1161, 1908.

2. Sarnat, B. D., and Schour, I.: Enamel

hypo-plasia (chronological enamel aplasia) in

re-lation to systemic disease: a chronologic,

morphologic and etiologic classification. J.

Amer. Dent. Ass., 28:1989, 1941; 49:67,

1942.

3. McMillan, R. S., and Kashgarian, M. : The

relation of human abnormalities of structure

and function to abnormalities of dentition

(in three parts), J. Amer. Dent. Ass., 63:38,

497, 1961.

4. Sheldon, M., Bibby, B., and Bales, M. : The

defects and infantile disabilities. J. Dent.

Res., 24: 109, 1945.

5. Kronfield, R., and Schour, I. : Neonatal dental

hypoplasia.

J.

Amer. Dent. Ass., 26: 18, 1939.

6. Teuscher, George W. : Systemic disease in

children of interest to the dentists. Dent. Clin.

N. Amer., pp. 481-488, July, 1958.

7. Via, Wm. F., and Churchill, J. A.:

Relation-ship of enamel hypopiasia to abnormal

events of gestation and birth. J. Amer. Dent.

Ass., 59:702, 1959.

8. Schour, I., and Massler, M. : The growth

pat-tern of human teeth. J. Amer. Dent. Ass.,

27:1778, 1940.

9. Logan, W. H. C., and Kronfeld, R. :

Develop-ment of the human jaws and surrounding

structures from birth to the age of fifteen

years. J. Amer. Dent. Ass., 20:379, 1933.

10. After Logan and Kronfeld (Slightly modified

by McCall and Schour) from Finn, S. B.

et al.: Clinical Pedodontics, Philadelphia,

Saunders, 1953.

11. Metcoff, J., and Janeway, C. A.: Studies on

the pathogenesis of nephrotic edema. J.

Pediat., 58:640, 1961.

12. Oliver, W. J., and Owings, C. L. : The

ne-phrotic syndrome in childhood : diagnosis

and treatment.

J.

Mich. State Med. Soc.,

61:1114, 1962.

13. Hartsook, J. T.: Personal conmiunication.

Oc-tober, 1962.

14. Shwachman, H., Fekete, E., Kulczycki, L. L.,

and Foley, C. E.: The effect of long-term

antibiotic therapy in patients with cystic

fibrosis of the pancreas; in Antibiotics

An-nual; edited by Welch and Marti-Ibanez,

New York, Medical Encyciopjedia, Inc.,

1958, p. 692.

15. Zegarelli, E. V., et a!.: Tooth discoloration in

cystic fibrosis. PEDIAnucs, 26: 1050, 1960.

16. Davies, P. A., Little, K., and Aherne, W.:

Tetracyclines and yellow teeth. Lancet, 1:

(8)

17. Wailman, I. S., and Hilton, H. B.: Teeth

pig-mented by tetracycline. Lancet, 1:827, 1962.

18. Miller, J.: Tetracycline in teeth and bone.

Lancet, 1:7238, 1962.

19. Albright, F.: The effect of hormones on

osteogenesis in man. Recent Progr.

Hor-mone Res., 1:293, 1947.

20. Calteux, J. P., Die Schmelzhypoplasie, Deutsch

Zahnheilk, 1934. (Leipzig, Georg Thieme)

21. Emerson, K., Jr., and Beckman, W. W.:

Cal-cium metabolism in nephrosis: I. A.

descrip-tion of an abnormality in calcium metabolism

in children with nephrosis. J. Clin. Invest.,

24:564, 1945.

22. Stickler, C. B., Burke, E. C., and Roseveal,

J. W.: Familial renal osteodystrophy with

review of calcium and phosphorus balances

in renal disease (abstract). Midwest Soc.

Pediat. Res., 25-26, 1962, Cincinnati, J.

(9)

1963;32;399

Pediatrics

William J. Oliver, Clyde L. Owings, William E. Brown and Barry A. Shapiro

HYPOPLASTIC ENAMEL ASSOCIATED WITH THE NEPHROTIC SYNDROME

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(10)

1963;32;399

Pediatrics

William J. Oliver, Clyde L. Owings, William E. Brown and Barry A. Shapiro

HYPOPLASTIC ENAMEL ASSOCIATED WITH THE NEPHROTIC SYNDROME

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