Roentgenographic manifestations of osseous changes in the jaws

ORAL .

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ROENTGENOLOGY .

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ROENTGENOGRAPHIC OSSEOUS CHANGES

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MANIFESTATIONS

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OF

IN THE JAWS

ISTRODIJCTION

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HE roentgenographic reflections of osseous changes are the direct result (that the degree of bone mincralization.l, 2 The amount of mineralization the concentration of calcium salts) present in bone tissue at any one moment a function of the simultaneous interplay of factors which are contributing Consequently, consideration must first bone formation and bone resorption. given to the conditions which produce normal bone tissue. SORMAL

01 is, is to be

BONE TISSIW

Under physiologic conditions, bone tissue is caonstantly being formed and tlestroyrd. llence, two mechanisms are operating in I)arallel (Fig. 1) Bone formation, also called osteogenesis, takes place in two phases. First? a.11organic matrix consisting of collagen and mucopolysaccharides is formed. Xext, this organic stroma is modified by molecular rearrangement and mineralization. From a chemical standpoint, the mucopolysaecharides are conjugated with calcium salts arranged in the form of hexagonal crystals.:‘, 4 Bone resorption, in the light of present information, is due to the action of highly differentiated cells, the so-called osteoclasts.“, G Unlike bone formation which occurs in two stages, bone destruction is an all-or-none process during which there is removal of both the organic and inorganic components of bone tissue. Hence, such terms as den~inerulixation and decalcification of bone are incorrect, since they imply the extraction of the calcium salts without removal of the organic matrix. Throughout the life of bone tissues in the adult human being there are constant, simultaneous, and more or less equal bone formation and bone reFrom a roentgenogra.phic standpoint, t,he bone tissue (Fig. 2) is sorption. tion,

From the Section on Oral Medicine, University of Alabama School of Dentistry. Presented at the ninety-ninth azmual scientific session of the American Dental Section on Roentgenology, Nov. 10-13, 1958, Dallas, Texas.

442

Associa-

OSSEOUS CHANGES IN JAWS

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443

represented by a series of blacks to whites. There are areas of relative roentgenolucency (for example, cancellous bone and periodontal membrane) and other regions of relative roentgenopacity (for example, lamina dura and alveolar crest).

Fig. I.-.Mechanism

of physiologic

bone formation

Fig. Z.-Roentgenogram P.ZTIIOLOGIC

of normal

and hone resorption.

bone

BONE TISSUE

It becomes readily apparent, even from this simple explanation of normal bone tissue, that disturbances in the osseous mechanism can occur in either the formation or the destruction of bone (Fig. 3). A. Underproduction

of bone (roedgenolucent) 1. Reduced bone formation a. Reduced matrix formation 1). Reduced matrix mineralizat~ion 2. Increased bone resorption 13. Overproduction of bone (rocn~tgenopnqm) 1. Increased bone formation a. Increased matrix formation 2. Decreased bone resorption

Fig. 8.-Roentgenographic

analysis

of jaw

pathosis.

All or part of a boric ma.y show evidence ot’ u~ierpxdut~t ion 01 overpwThe former will appear as a roentgenolucent shadow; the latter will duction. be roentgenopaque. Roentgenolucency, in turn, may 1~ the result of reduced bone formation or Finally, a reduction in the formation of hone ma! increased bone resorption. stem from impairment in one of two nleclianisms. There is the possibility of reduced development of the osteoid matris or a normal matrix may never become properly mineralized. Whatever the mechanism, the end result, is a ment,genolucent shadow. On the other hand, an overproduction of bone tissue may arise in one of two ways. First, there is a mechanism which leads to an increa.se in matrix The other possibility is a, decrease in which subsequently becomes mineralized. Whatever the mechanism, the end result is a roentgenopaquc bone resorption. shadow. ROENTGENOLUCENT

SHADOWS

Roentgenolucent shadows are always the result of (1) lscduced boric formation due to a decrease in mat,rix development or lack of matrix mineralization These arc the basic mechanisms. Howe\-er, or (2) increased bone resorption. the observed roentgenographic picture will be the result of modifications of these basic processes. For example, the picture will vary in accordance with whether the pattern is generalized or localized in one of the jawbones, whether the lesion is clearly delimited or ill defined, whether the mandible or the maxilla is implicated, and whether or not local irritating factors are operative.‘-l”

Fig.

I.-Mechanism

of osteoporosis

Roentgenolucent lesions due to a defect in matrix formation: Reduced matrix formation, in the presence of normal mineralization of the matrix which is being formed and in the presence of normal bone resorption, will produce roentgenolucent shadows (Fig. 4). The roentgenographic appearance is reOsteoporosis is due to one of three things (Fig. 5) : ferred to as osteoporosis. (1) a disturbance in the osteoblasts which form the osteoid matrix, (2) a matris defect itself, and (3) idiopathic causes.

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The normal stimuli to the osteoblasts are stresses and strains. Immobilization of a part of the skeleton for any reason (for example, plaster cast, intermaxillary jaw fixation, or neurologic or muscular disease) leads to decreased osteoblastic activity. Thus, with an inadequate osteoid matrix, total mineralizaThe tion of that area is reduced. The end result is a roentgenolucent picture. importance of disuse atrophy has been convincingly shown in a study of four healthy young men who were immobilized in bed by means of plaster casts for six weeks.lly I2 During this intell-al, these subjects lost 9 to 24 grams of calcium, which is equivalent to 1 to 2 per cent of t.otal body calcium. 1. Distzcrbance in the Osteoblasts a. Lack of stress and strain (disuse atrophy) b. Estrogen deficiency (climacteric, congenital hypoestrinism) c. Congenital osteoblastic defect (osteogenesis imperfecta) 2. Matrix

defect

a. Androgen deficiency (eunuchoidism, senile osteoporosis) b. Nutrition deficiency (protein, ascorbic acid, Gushing’s syndrome, hyperthyroidism, diabetes mellitus) 3. Unknown defect a. Acromegaly, idiopathic Fig.

5.-Causes

for

roentpenolucent

shadows

alarm syndrome,

osteoporosis due sis).

to a defect

in matrix

formation

(osteoporo-

Osteoporosis may be present in all of the skeleton, generalized in a particular bone, or occur only in a portion of a single bone. Osteoporosis of the entire mandible and/or maxilla without other bone involvement is rare except in isolated cases (e.g., intermaxillary jaw immobilization). However, osteoporosis of the jaws as part of a systemic skeletal problem is frequently encountered. CASE l.-Fig. of approximately

6 shows the markedly fourteen years’ duration.

atrophic hands of a patient with sclerodermal3 Fig. 7 demonstrates the marked osteoporosis

Fig.

of

6.-Immobile

hands

a patient

with

scleroderma.

14 of

446 Fig.

7.

Fig.

8.

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447

the phalanges and the carpal and metacarpal bones due, in part, to t.he disuse atrophy. Fig. S shows the rigid facial skin and points up the difhculty which the patient had opening snd closing her mouth. Finally, Fig. 9 demonstrates the obvious roentgenoluccnt rcflcctions It is germrally agreed that several factors operate to prcducc of osteoporosis of the jaws. I I nwewr, the pertineot lmint hero is that the oxtcoporosis in such stress disorders. osteoporosis is the result of a disturbance in matrix formation and that disuse atrophy is one of the important causes. Fig.

10.

Fig.

il.

Fig. lO.-Periapical roentgenogram of a patient who wears a partial denture. The denture is tooth borne on one side. The large trabecular spaces (indicating osb?OporOSiS) are probably due to lack of stimulation of the subjacent bone (disuse atrophy). Fig. ll.-Periapical roentgenograrn of a patient who wears a partial denture. The denture is tissue borne on one side. The small trabecular spaces should be compared with those in Fig. 10 from the same patient.

due to a lack of physiologic stresses and strains may be confined CASE 2.-Osteoporosis to a portion of a single bone. Fig. 10 shows a periapical projection of an area of the left mandible where a tooth-borne prosthesis is worn with little if any stress exerted to the underlying bone. The trabeculae are widely spaced and the dominant feature is relative roentgenolucency. In contrast, Fig. 11 shows a periapical view of the opposite side of the arch, taken under the very same roentgenographic standards, where a free-end saddle prosthetic appliance is worn. Here there are very obvious stresses and strains to the subjacent bone. The roentgenogram discloses a much more dense trabecular pattern with greater mineralization leading to greater roentgenopacity.

Time does not permit a detailed discussion of the many reasons for failure of the matrix to develop physiologically (Fig. 5). It is enough to say merely

I-.,)+I.-;::,) (-1 k-n.

fornlfio”

C’ia. 12.-Mcc~tlanism

< bone

rCIo:ptior

of osteomalxcia.

Osteomalacia may be due to one of The basic difficulty is one of mineralization. four reasons (Fig. 13) : (I ) lack of intake or failure of utilization of vitamin D 251ZG (2) renal acidosis,27, 28 (3) idiopathic loss of calcium in the urine, and (i) the transitional period of hyperparathyroidism after parathyroidectomy. 1. Vitamin D deficiency a. Dietary vitamin D lack b. Vitamin I) resistance c. Steatorrhea 2. Renal acidosis 3. Idiopathic hypercalciuria 4. Transitional period of I(~~~e~~~aratllyroidisrn after parathyroidect,omy Fig.

13.-Causes

for

rwntrenolucrnt

slmdows

due to 5 defect

lnalsciit ).

CASE 3.-Fig. 14 shows the rocnt,genogram of rickets. The characteristic cupping at the distal ends with the lack of cupping in the wrist of a nonrachitic relative roentgenolueency of the mandible due to a the presence of normal matris formation.

in matrix

mineralization

(osteo-

the wrist of a l3-year-old boy with of the radius and ulna20 are compared 13-year-old child. Fig. 15 depicts the lack of physiologic mineralization in

Roentgenolucent lesions due to increased bone resorption: Roentgenolucent shadows may also be due to accelerated bone resorption in the presence of normal bone formation (Fig. 3 j. This mcrhanism is depicted graphically in Fig. 16. The classical, but uncommon, example is prin1ar.v hyperparathyroidism, also called osteitis, fibrosa. cystica gencralisata, which is caused by a parathyroid

Volume 12 Number 4

Fig,

Fig.

I&-Roentgenographic

IS.-Pwiapical

OSSEOUS

comparison in

roentgenogram

CHANGES

of a normal two 13-year-old

of

IN

449

JAWS

wrist (Jeft) boys.

& 13-year-old

rachitic

and

child

tons formation < bone rcrorptban

Fig.

16.-Mechanism

of osteitis

fibrosa.

a rachitic

showing

wrist

(right)

osteomalacin.

450

CHERASKIN

sdenoma or hyperplasia of parathyroid tissue.3u, :‘I( Howevtlr, there are many other, more common disorders characterized by increased bone resorption. Some of these are systemic, while others are localized. Included in this group, for example, are multiple mye10nia,32~Z3:( mctastases of malignant neoplasms,:‘“, Q5and cvcn localized areas of infection3G, 37 encountered with periapical infect,ion. CASE 4.--A 3%year-old man kacl a “mole” removcil from his back five years previously. Biopsy proved it to be a mel:~noma.~% ~1 \\lcn the patient was last seen, five pears after removal of the lesion flont

the l~nck, 132 metastatic

lesions could he counted

in the skin alone

Fig. li.

Fig. 18. Fig. 17.-Patient Fig. 18.-Osteitis Fig. lg.-Osteitis

Fig. 19.

with melanon~a :tn(l I32 palpable nretastatic nodules. fibrosa secondary to melanoma metastasis causing loose teeth flbrosa secondary to mcl;rnoma me&static causing loose teeth.

OSSEOUS

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IN JAWS

451

(Fig. 17). However, he was referred to the dental clinic because of tenderness and looseness The roentgcnolucent shadows apparent in the periapical (Fig. of the lower anterior teeth. 18) aud occlusal projections (Fig. 39) reprexeut metastntic lesions. These roentgenolucent shadows are duo to accelerated Itone destruction in the prescucc: of normal boric fornmtion. CASE L-Fig. 20 sl~ows well-dclined roentg,renolricc~lIt shadows in tlro mandible. Fig. 21 simply underscores the fact that they are multiple. This type of roentgenolucent lesion can be due to a number of systemic and local causes. However, Fig. 22 shows a similar punched-out lesion in the skull, characteristic of multiple myeloma. Of importance to this discussion is the fact that such lesions are the result of invasion of tumorous tissue leading to increased bone resorption in the presence of normal bone formation. Fig.

20.

Fig. Fig. Fig.

20.-Osteitis 21.-Osteitis

flbrosa flbrosa

21.

secondary secondary

to multiple

myeloma.

to

myeloma.

multiple

All of the cases shown thus far have one common denominator. The roentgenolucent lesions are the result of (1) a decrease in the formation of osteoid matrix, (2) a reduction in the physiologic mineralization of normal matrix, or (3) increased bone resorption.

Roent,gcnopaqne lesions, like ~.otrl~t~~~t~olrlc~cttli OII~~S, i)I’c tturbancc ill either bone formation 01 hot~c~~*cw~~plio~~. \VllHt(?\.(‘l’ the rocntgcnographic pictwcx is t(li’m(Ld oslc~osc~lcrosis.

Fig.

?2.-‘l’ypiral

punchrd-out

skull

lesion

suggestive

of

multiple

III<>

rcsr~lt

01’

;I

tlis-

t IIC’ ltIN’llillliS11t,

myelorn:~.

Roentgenopaque lesiom due to increased bone formation: Mice t,reated with estrogens show evidence of a gcncralized overproduction of ostcoid matrix, probably the result. of osteoblastic stimulation. The exuberant rnat,rix is The end result, not due to hypermineralization but rather to mineralized. physiologic mineralization of overabundant matrix, is a generalized roentgenopaque skelet.on.40 There is no human count,erpart of such generalized roentgenopacity due to increased matrix formation. However, this very same mechanism can and does operate in man within a circumscribed segment of bone tissue. Thus, it is possible to observe in the human being an area of welldelimited roentgenopacit,y due to an overproduction of ost,coid matrix (Fig. 23).

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OSSEOUS

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CIIANGES

453

1N JAIVS

CASE 6.-Fig. 24 shows a typical roentgenographic picture of an osteoma4L 42 of the mandible. This pattern of a benign bone-forming neoplasm is dnc to an overprodurtion of osteoid matrix and the normal mineralization of this osteoid frame.

Fig.

23.-Mechanism

of

osteosclerosis

due to increased

matrix

formation.

Roentgenopaque lesions due to decreased bone resorption: Finally, roentgenopacity may be the result of decreased bone resorption in the presence of normal matrix formation and physiologic mineralization (Fig. 25). This is classically shown in osteopetrosis, also called Albers-SchGnberg or marble bone developmental disorder, osteoclastic activity is disease.43,4-1 In this particular reduced although normal bone formation is present.

Fig.

24.-Osteoma

demonstrating

osteosclerosis

This same mechanism may operate locally. A classic example of stomatologic import is the separation of a bone fragment from the neighboring bone and blood supply. The roentgenopaque area is called a sequestrum, which is a section of neerot.ic, highly mineralized bone associated with chronic suppurative osteonlyclitis.45T 4c

0 s., 0. \I.& 0. I’. .\,,,,I. I’,<‘2

The slor;\. 1.1111s fill' (Icscrilxxl discussion,

one

Ini&

giltllel':

that,

is sirtlljl(t oss(‘olls

iI1 I’avl. dMrl~c’:i

ii, is loo sillli)lo. ilL’C sinll3ly

tilt?

f!‘i*o111 tllis IYMllt


il

disturbance which OWIII’S in a sillpI<> Inr:chanism while the others continue ilt a physiologic fashion. ,\ctually, the patliopli~~siologic sequence of events in osseous disease is more complex. It follows that t,he roentgenographic pict,ure will also I)e more romplicatcd.

pk.

z(i.--1LIerhanism

of

roentprnolucrnt

(osteitis

fibrosa)--loentgenopaque

(osteosclerosis)

hone.

In many instances, the pattern observed in the roentgenogram is characterized by some areas which are roentgcnolucent and other regions which arc relatively Toentgenopaque. This type of roentgenographic pattern usually signifies a primary process of chronic bone destruction. It should be recalled that bone resorption per se is a stimulus to bone formation. >IIence, it is not unusual to find roentgenolucent areas indicative of increased bone resorption and, close to these, otheli’ roentgenopaque areas representing compensatory osteoid matrix formation and mineralizat,ion. This mechanism is graphically portra.yed in Fig. 26. CASE 7.-Fig. 27 show the characteristic roentgenographic of bone.47, 4s There are roentgenolucent areas intermingled with

lesions of Paget’s other roentgenopaque

disease areas.

12 4

OSSEOUS

CHANGES

Actually, increased bone resorption is the primary genolucent shadows. However, the irritant is of to increased osteoblastic action. The end result is and mineralization, represented in the rocntgenogram

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JaWS

455

process. This accounts for the roentlow-grade intensity. This is a stimulus compensatory osteoid matrix formation hy the roentgenopaque areas.

Fig. 27.

Fig. 28 Fig. 27.-F’aget’s Fig. 28:--Chronic

disease of bone. osteomyelitis.

CASE S.-The mechanism just described is a common one and occurs in many systemic This same sequence of events may be found in local disorders confined to a pordisorders. Usually, the basic process is a low-grade infection or mechanical t,ion of a single bone. trauma. This is the stimulus which sets off compensatory bone formation. Fig. 28 shows a typical example of intermingled roentgenolueent and roentgenopaque areas in a person with chronic suppurative osteomyelitis.

456 SUMMARY

I. Bone tissue, under physiologic condit,ions, is the result of an int,erplay of two mechanisms : (a) lmr~c?formation and (b) bone resorption. 2. Bone formation actually OCCI~Win two phases: (a) t,lre formation of an ostroid matrix and (b) matrix mineralization. :i. Boric resorption is an all-or-norlc phenomenon characterized by removal of both the organic and the irrorganiv c*omponents of bone. 1. l’athologic boncl tissue is thv r-c&t gf a disturbance in either hone formation or bone r’csorption. 5. Roentgenoluccnt shatlo~rs are due to (a) decreased osteoid mat,rix formation, (b) decreased mineralization of the osteoid frame, or (3) increased boric resorption. 6. Osteoporosis may be defined as a roengenolucent shadow due to a decrease in osteoid matrix formation. 7. Osteomalacia is defined as a rocntgenolucent shadow, the result of an interference with phr-siologic mineralization. 8. Osteitis fibrosa is defined as a rocntgenolucent shadow caused by an increase in bone resorption. 9. Roentgenopaque shadows, referred to as osteosclerosis, are caused by an increase in the formation of ostcoid matrix or a decrease in bone resorption. 10. Many disorders are characterized by a basic process of increased bonr resorption with superimposed secondary and compensatory bone formation. Il. Roent,genolucent, rocntgenopaquc, and roentgenolucent-roentgenopaquc shadows ma)- be part of gencralixcd skelet,al disease, confined to a single bent:, 01 rest.ricted to only a small poi-tion of one bone. REFERENCES 1. Weinmann, J. P.: Variations in the Structure of Bone and Bones and Their Rignificanee in Radiology, ORAL SURG., ORAL, MED. & ORAL PATII. 8: 988, 1955. 2. Swenson, P. C., and Jeffery, R. B.: Defective Skeletal Mineralization, GP 7: 34, 1<95:i. Chemical Nature of Salts From H., Dallemagne, M. I., and Melon, T.: 3. Brasseur, Bones and Teeth and of Triealcium Phosphate Precipitates, Nature (London) 157: 453, 1946. The Physiology of Supporting Tissue, Ann. Rev. Physiol. 12: 101, 4. Dallemagne, M. I.: 1950. Bone Formation and Bono Resorption, Oaar, SURF., 0~111. MEI). & 5. Weinmann, J. I’.: ORAL PATH. 8: 1074, 1955. An lntrodurtion to the Physiology of 6. McLean, F. C., and Urist, M. R.: Bone: Skeletal Tissue, Chicago, 1955, University of Chicago Press, p. 64. of Disease (to be published). 7. Cheraskin, E. : The Arithmetic Preventive Medical Case-Finding Opportunities and Responsibilities E.: 8. Cheraskin, of the Dentist, D. Clin. North America, p. 253, July, 1958. of Systemic Diseases, J. South (‘arolina M. A. 53: 9. Cheraskin, E.: Oral Manifestations 241, 1957. of H>,‘stemic Diseases, .I. Sat. 11. A. 50: 241, 1958. E.: Oral Manifestations 10. Cheraskin, Upon Various J. E., Whedon, G. D., and Shorr, 15.: Effects of Immobilization II. Deitrick, Metabolic and Physiologic Functions of Normal Men, Am. J. Med. 4:: 3, 1948. The Effects of Bed Rest and ImJ. E., Whedon, G. D., and Shorr, E.: 19-. Deitrick, mobilization Upon Various Chemiral and Physiological Functions of Normal Their Modification by the Use of the Oscillating Bed, Conference on Men: Transactions of the Twelfth Meeting, Feb. Metabolic Aspects of Convalescence, 4-5, 1946, New York, Josiah Macy, Jr. Foundation, pp. 44-61.

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13. Looby, J. P., and Burket, L. W.: Scleroderma of the Face With Involvement of the Alveolar Process, Am. J. Orthodontics & Oral Surg. 28: 493, 1942. 14. Taylor, D. V.: A Case of Atrophy of the Mandible Associated With Scleroderma, Brit. D. J. 87: 246, 1949. Osteoporosis, Tr. Am. F.. Bloomberg, E., and Smith. P. H.: Post-menopausal 15. Albright, Physici&ns 55: 298;‘194i). Osteoporosis: Its 16. Albright, F., Smith, P. H., and Richardson, A. M.: Post-Menopausal Clinical Features, J. A. M. A. 116: 2465, 1941. by Primary F., Smith, P. H., and Fraser, R. TV.: A Syndrome Characterized 17. Albright, Ovarian Insufhcienc~and Decreased Stature; Report of Eleven (‘ases n’ith a Digression on Hormonal Controls of Axillary and Pubic Hair, Am. .I. M. Se. 204: 625,

l!M".

Rimmond’s Disease or Panh~vpopituitarism 1’3. Fraser, R. IV., and Smith, I’. H.: (Anterior): Its Clinical Diannosis bv the C'oml)inecl r-se of Two Olbiective Tests. CJuart.

J. ked.

10: 297.

l!Ml.-

'

H., and Gould, B. Y.: Blood and Tissue Phosphatase in Espcrimental 19. Rhwarhman, SCWV!-, AIL .I. Dis. Child. 64: 949, 1942. “0. \Voll)ach, 8. H.: The Pathologic Changes Resulting From \‘itamin I)eliciency, ,I. .\. M. A. 108: i, 1RRi. H. J.: Thyrotoxic Osteoporosis, Internat. Clin. 2: 4S, 21. ~Villiaurs, R. H., and Morgan, 1940. *>o Kinsell, The Effect of Testosterone W. C., Jr.: --. L. \V., Hertz, S., and Reifenstein, Compounds Upon the Nitrogen Balance and Creatine Excretion in Patients With Thyrotoxicosis, J. Clin. Invest. 23: 880, 1944. Imperfecta (Odontogenesis Imperfecta), ORAL SURG., J. S.: Osteogenesis 23. Mittleman, ORAL MED. & ORAL PATH. 3: 1562. 1950. G. R., and Maiocco, P. D.: ’ Osteogenesis Imperfecta and Odontogenesis Im24. Winter, perfecta, ORAI, SURG., ORAL MED. & ORAL PATH. 2: 782, 1949. Hypovitaminosis of All Fat-Soluble Vitamins Due 25. Albright, F., and Stewart, J. D.: to Steatorrhea; Report of a Case, New England J. Med. 223: 239, 1940. Studies on the Mode of Action of Irradiated 26. Bauer W., Marble, A., and (Xaflin, I).: I. Its Effect on the Calcium, Phosphorus, and Nitrogen Metabolism Ergosterol. of Normal Individuals. J. (Ilin. Invest. 11: 1, 1942. Bone dhanges in the Jaw Caused 1)~ Renal Hyperparathyroidisrn, 27. Weinmann,, J. P.: .I. Perrodont. 16: 94, 1945. 2s. Lighterman, I.: Renal Osteodystrophy \Vith Oral hZanifestat,ions, .J. Oral Surg. 10: 2x3 lY5” . I -. Clinics on Bone Diseases, New York, 1949, Interscience Pub 29. Snapper: I. : Medical lishers. Inc.. D. 134. F: R., Jl., and Cook, E. N.: The Recognition of Primary- Hyperparathy-roitl30. Keating, ism; an Analysis of Twenty-four (laxer, J. A. M. A. 129: 994, 1945. (Generalized Osteitis Fibrosa), ORAL SURG., ORAL 31. Schneider, W.: Hyperparathyroidism MEL). & ORAL PATH. 6: 745. 1953. Multiple Myeloma Occurring in the Jaws; a Study 32. Bruce, K. W., and Royer, R. ‘Q.: of Seventeen Cases, ORAI, SURF., ORAI, Mm). R- ORAT, PATH. 6: 729, 1953. Mandibular Lesion as First Evidence 33. Meloy, T. M.,, Gunter, J. H., and Sampson, 1). A.: of Multiple Myeloma, Am. J. Orthodontics & Oral Burg. 31: 685, 1945. Metaatatie Tumors of the Oral Cavity, ORAL SURG., ORAL 34. Salman, I., and Langel, I.: MED. & ORAI, PATH. 7: 1141, 1954. Tumors That Have Metastasized to the Jaws, ORAL 35. Aisenberg, M. S., and Inman, C. L.: S~JRG.,ORAI, MED. & ORAL PATH. 9: 1219, 1956. 36. Thoma, K. H.: Oral Pathology, cd. 4, St. Louis, 1954, The C. V. Mosby Company, p. 424. 37. Shafer, W. G., Hine, M. K., and Levy, B. M.: A Textbook of Oral Pathology, Philadelphia, 1958, W. B. Saunders Company, p. 356. 38. Bluestonc, L. I.: Malignant Melanoma Metastatic to Mandible, ORAL SURG., ORAI, MEI). & ORAI, PATH. 5: 237, 1953. 39. Baxter, H. : A Review of Malignant Melanoma of the Mouth, Am. J. Surg. 51: 379, 1941. 40. Gardner, W. U., and Pfeiffer, C. A.: Influence of Estrogens and Androgens on the Skeletal System, Physiol. Rev. 23: 139, 1943. 41. Smith, A. G., and Zavaleta, A.: Osteoma, Ossifying Fibroma, and Fibrous Dysplasia of Face and Cranial Bones, Arch. Path. 64: 507, 1952. 42. Wilkinson, F. C., and Pollack, E.; Benign Bone-Forming Tumors of the .iaws, Brit. I). .I. 77: 341. 1944. 43. Seigman, E. L., and Kilby, W’. L.: Osteopetrosis, Am. J. Roentgenol. 63: 865, 1950. 44. Kneal, E.., and Sante, L. R.: Osteopetrosis (Marble Bones); Report of Case With Special Reference to Early Roentgenologic and Pathologic Findings, Am. J. Dis. Child. 81: 693, 1951.

45. Thoma, K. H., Howe, H. D., and Wenig, M.: Osteomyelitis, Am. J. Orthodontics & Oral Hurg. 31: 235, 7945. 46. IVilensky, A. 0.: Osteomyelitis; Its Pathogenesis, Symptomatology and Trwtnlent, New York, 1934, The Macmillan Company, p. 3811. 47. Stafne, E. C., and Austin,, I,. T.: A Stntly of Dent,al Roentgenograms in (21~s of Paget’s Disease (Osteltis l)eformans), Osteitis Fibrosa Cystica and Osteoma, .I. Am. I)ent. A. 26: 1202,,183S. 45. Albright, F., and Reifensteln, E. C., Jr.: The Parathyroid Glands ant1 Metabolic Bouts Disease, Baltimore, 1948, Williams L \Vilkinn Company, p. 284.