The chemistry of calcification and its roentgenographic appearance

The chemistry of calcification and its roentgenographic appearance

The chem istry of calcification and its roentgenographic appearance L eR oy M . Ennis * D .D .S ., Philadelphia T h e physical properties of a cell ...

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The chem istry of calcification and its roentgenographic appearance

L eR oy M . Ennis * D .D .S ., Philadelphia

T h e physical properties of a cell modify

CALCIFICATION

its chemical processes and thus become the most important factor in the chemis­ try of many abnormal and pathologic lesions.

Pathologic

calcification

occurs

either as ( 1 ) a precipitation of calcium in secretions and excretions of the body, or as ( 2 ) the deposition of calcium salts in the tissues. A n understanding of calcifica­ tion permits one to interpret and explain the osseous changes revealed in roent­ genograms.

T h e cell is the structural unit o f the living organism. Its physical properties m odify the cell’ s chem ical processes and, there­ fore, the cell becomes the most im portant factor in the chemistry o f many abnorm al and pathologic lesions. Such lesions, as in the case o f those caused by ossification, calcification and concretion, all appear to be laid dow n according to definite law. It becomes necessary, therefore, to review and have a good understanding o f the chemistry o f the living cell, to interpret and explain m ore definitely the changes which take place in the tissue and which are revealed in the roentgenogram . O nly in this way can an intelligent diagnosis be reached.

T h e norm al calcium content o f b lood is 9 to 11 mg. per hundred cubic centi­ meters o f serum, and the quantity is not m odified by most diseases.1 T h e com posi­ tion o f the inorganic salts in calcified areas in the b od y seems to be similar, if not identical, whether the salts are laid dow n under norm al conditions (ossifica­ tion) or under pathological conditions.2 A study o f several specimens o f calcified tuberculous lesions, by M a ver and W ells,3 showed that the silica fou n d in calcified pulm onary and lym ph node lesions is not large in am ount; it ranges from 0.3 to 3.3 per cent o f the total inorganic m ate­ rial and is to be explained as inhaled dust. W ith b lood continually passing be­ tween the bones and the calcified areas, the com position o f the tw o must inevitably becom e similar or identical. T his can be shown by a table giving the proportion o f inorganic salts fou n d by analysis o f nor­ mal bone and o f calcified materials.4

RELATION OF CALCIFICATION TO OSSIFICATION

In normal ossification there is an accum u­ lation o f lime salts within the stroma or cells o f a tissue that has usually under­

ENN IS . . .V O LU M E 59, JULY 1959 • 57

gone certain preparatory changes in the way o f form ation o f a m ore or less h om og­ eneous ground substance, but has not suffered a total loss o f vitality, although the vitality is possibly decreased. Patho­ logic calcification is similar, insofar as there is a deposition o f quite the same salts in tissues that have undergone either a total or partial loss o f vitality and which very frequently are hyaline. T h e apparent essential differences, therefore, a r e :5 1. In calcification the lime salts always remain in clumps and masses, often fusing to a greater or less degree (Fig. 1 ), but they never display the diffuse, even permeation o f tissue seen in ossification ( F i g -

A com parison o f calcification with ossification is shown in chart form in Figure 3. PATHOLOGIC OSSIFICATION

In pathologic ossification, unlike simple calcification, there is form ation o f bone structures such as lamellae, lacunae, and sometimes marrow. Heteroplastic form a­ tion o f bon e m ay o ccu r in almost any tissue, such as kidneys, muscles, lungs, pleura and so forth. Myositis ossificans occurs in a localized form after trauma to a muscle and in a progressive, w ide­ spread form in which there is calcifica­ tion and ossification o f muscles, tendons, fasciae and ligaments6 (Fig. 4 ) .

2 ) '

2. T h e cells within a calcified region, if not dead at the beginning o f the p roc­ ess, eventually disappear fo r the most part, and sooner or later there is a per­ fectly inert mass, practically a foreign body, instead o f a specialized tissue as in ossification. 3. Ossification is accom plished only in types o f connective tissues; but calcifica­ tion may involve any sort o f cell or tissue provided it is sufficiently degenerated. Furthermore, any region o f calcification is likely to be replaced by bone, no matter what tissue may be in volved; apparently, the presence o f calcium salt deposits in any part o f the bod y can stimulate the connective tissues to form bone, but in the absence o f calcium salts, even the cells w hich are norm ally osteogenic will not form bone.

PATHOLOGIC CALCIFICATION

Pathologic calcification occurs in two form s: one is a precipitation o f calcium in secretions and excretions o f the body (Fig. 5 ) ; the other is the deposition o f calcium salts in the tissues themselves (Fig. 6 ) . A ll calcium deposits appear to contain calcium phosphate, calcium car­ bonate and variable small traces of other substances. As far as is known, calcifica­ tion seldom occurs in normal tissue except in the form ation o f bone. O ften the in­ filtrated tissue .is com pletely dead, as in the case o f infarcts, organic foreign bodies, caseous regions and, particularly, in old inspissated collections o f pus6 (Fig. 7 ). A ny region o f dead tissue that is not in­ fected and is so large or so situated that

Tab le • Proportion of inorganic salts found by analysis of normal bone and of calcified materials Tri-magnesium phosphate

Calcium carbonate

Tri-calcium phosphate

M g g lP O ^

CaCC>3

C a 3(P 0 4ï 2

Norm al ossification Human bone

1.57

10.1

87.4

Pathologic calcification In tuberculosis In human beings

0.85

10.2

87.8

1.1

13.4

85.4

Calcified nodules in thyroid tissue

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Fig. ! • Calcification of a periapical fibroma appearing as small masses but having a tendency to fuse into one large mass

Fig. 2 • Small osteoma in region of maxillary cuspid and bicuspids illustrates diffuse, even permeation of tissue seen in ossification

it cannot be absorbed, probably will be­ come infiltrated with lime salts (Fig. 8 ). Pathologic calcification is commonly classified as ( 1) dystrophic calcification, (2) metastatic calcification, and (3) cal­ cinosis, but it is not possible to make a clear distinction in all instances. Dystrophic calcification is the deposi­ tion of calcium in dead or degenerating tissues.6 This is the most frequent type of pathologic calcification, and, as any devitalized tissue tends to have calcium salt deposition in it, dystrophic calcifica­ tion occurs in extremely varied locations. The common sites are in regions of tuber­ culous necrosis (Fig. 9 ), in blood vessels (Fig. 10), in regions of fatty degeneration and necrosis, in degenerating thyroid

tissue (Fig. 11), in degenerating tumors and many others. Dystrophic calcification is not dependent on an increase in the amount of calcium in the blood but ap­ pears to be dependent on a change in the local condition of the tissues. Local alkalinity appears to be an important fac­ tor in initiating the precipitation of cal­ cium in degenerating and dead tissues. Metastatic calcification is the precipita­ tion of calcium salts in previously un­ damaged tissue because of an excess of salts in the circulating blood. It occurs particularly when there is an excess of parathyroid hormone, which depletes the bones of calcium and causes a high cal­ cium level in the blood.7 It is also promi­ nent in instances of associated damage to the kidneys which are then unable to ex­ crete phosphate adequately, so that the phosphate level in the blood is raised. Metastatic calcification also may result from hypervitaminosis D and from de­ structive bone lesions, particularly tumors (Fig. 12, right). In metastatic calcification, the calcium deposits tend to occur mainly in the kid­ neys, lungs, gastric mucosa, and in the media of blood vessels8 (Fig. 6 ). Elastic

E N NIS . . .V O L U M E 5?. JULY 1959 • 59

tissue seems prone to early calcification, and it is not uncom m on to see the elastic laminae o f the small arteries calcified in an apparently selective manner (Fig. 1 3 ). Degenerated or necrotic tissue tends to becom e infiltrated by calcium when the circulating calcium level is increased, the factor o f dystrophic calcification thus being present also in many circumstances. Figure 14 summarizes the distinction between dystrophic and metastatic ca l­ cification. Calcinosis is a condition o f calcifica­ tion in o r under the skin.6

CHEMISTRY OF THE PROCESS OF CALCIFICATION

In analyzing the etiological factors in the production o f pathologic calcifica­ tion fo r the purpose o f determining the chem ical changes that occur in the process, there are the follow ing facts on which to base con sideration:9 1. T h e calcium salts must com e from the blood, where they are normally held in suspension by the proteins, either as the carbonate and phosphate or as cal-

N orm al Conditions O S S IF IC A T IO N

Pathological Conditions C A L C IF IC A T IO N

Accumulation o f calcium salts within the stroma of cells of tissue that has undergone certain preparatory changes in the w ay o f formation of more or less homogeneous ground substances, in tissues that have not suffered total loss o f vitality, a l­ though vitality is possibly decreased

Deposition of. calcium salts similar to that in ossification

Calcium salts invade with a diffuse, even permeation of the tissue

Frequently hyaline

the

tissues

become

In lymph nodes— pulmonary and peritonsillar Silica ranges from 0.3 to 3.3 per cent of the total inorganic salts

Sites are specialized tissue Accomplished only in varieties of connective tissue

Absence of calcium salts in cells normally osteogenic will not form bone

Calcium salts alw ays remain in clumps and masses, often fusing to a greater or lesser degree, but never with the diffuse, even per­ meation seen in ossification

All cells within calcified region, if not dead at beginning o f process, essentially disappear and sooner or later there is an inert mass, prac­ tically a foreign body instead of specialized tissue as in ossification Involves any sort o f cell or tissue provided it is degenerated suffi­ ciently. Any region of calcification is likely to be replaced by bone, no matter what tissue is involved. Calcium salt deposits in any part o f the body can stimulate connec­ tive tissue to form bone

Fig. 3 • Comparison of ossification and calcification

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cium-ion-protein compounds, or per­ 3. In the regions that are to become haps both. calcified, the circulation is very feeble, 2. Retrogressive changes in the tis­ the blood plasma seeping through the sues are essential except in metastatic tissue, as through any dead foreign sub­ calcification. Hyaline degeneration, the stance of similar structure, without the chemical nature of which is not under­ presence of red corpuscles to permit stood, is a very favorable condition, oxidative changes. along with necrosis, when absorption is It may be supposed, therefore, that deficient. the deposition of calcium salts in such

Fig. 4 • Left: Myositis ossificans of long styloid process and stylomandibular ligament, illustrated between arrows. Right: Myositis ossificans of stylohyoid muscle and stylohyoid ligament, illustrated between arrows

Fig. 6 (Below) • Pathologic calcification of branch of facial artery caused by deposition of calcium salts in the body

Fig. 5 (Above) • Pathologic calcifica­ tion caused by precipitation of calcium in submaxillary (W harton's) duct as a result of secretions of submaxillary gland

E N NIS . . . VO LUM E 59, JULY 1959 • 61

Fig. 7 • Left: Pathologic calcification in inspissated area in region of mandibular first and second molars. Marginal areas of calcified regions have slightly diffused appearance because of blending of calcified area with normal trabeculated structure. Right: Same condition as in view at left except that area is much larger and calcification extends to alveolar border. In each instance patient had history of severe infection in region shown

Fig. 8 • Fibrous dysplasia, fibro-osseous lesion of obscure pathogenesis. Tumor of connective tissue with active osseous metaplasia illustrates one of three types of ossi­ fication. Lesion shown is one of ground glass type

regions of tissue degeneration depends on one or more of the following condi­ tions : 9 1. Increased alkalinity or decreased carbon dioxide in the degenerating tis­ sues, causing precipitation of the in­ organic salts in the fluids seeping through those tissues. 2. Utilization of the protein of the fluids by the starved tissues so com­ pletely because of its slow passage that the calcium can no longer be held in solution. 3. The formation within the degen­ erated region of a substance or sub­ stances having a special affinity for calcium. 4. Production of a physical condition favoring the local absorption of salts,

the least soluble salts accumulating in excess (Fig. 15). The first of these conditions seems to come into operation especially in meta­ static calcification. A decrease in the carbon dioxide content in calcifying tissues, especially when combined with other changes, may be important. Emphasis has been placed on the possible part played by changes in the proteins in inducing calcification. The theory gains credence that precipitation of colloids in the degenerated region, as in caseation, decreases the amount of crystalloids which can be held in solu­ tion, and the least soluble salts, those of calcium, are precipitated.10 However, the possibility of the formation of calcium-binding substances within the de­ generated area has received most atten­ tion by more recent investigators. These present the theory that of the special substances that might be present in such regions and would have a high affinity for calcium, phosphoric acid usually receives first consideration since it is as phosphate that most of the calcium is bound and since the possible sources of

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Fig. 9 • Dystrophic calcification of lymph nodes on left side of 23 year old man with history of tuberculosis. Lungs and lymph nodes are common sites of calcification during or after tuberculosis

Fig. 10 • Dystrophic calcification of branch of facial artery. Left: Patient with cheek in relaxed position. Right: Same patient with cheek extended laterally, showing calcified artery extended in same proportion

Fig. I I • Dystrophic calcification of lymph nodes. Left: Oblique angle projection showing calcifica­ tion close to angle of mandible. Center: Right angle projection showing calcification in its proper relation to vertebrae, mandible and hyoid bone. Right: Posteroanterior view showing lateral relation of calcification to vertebrae

ENNIS . . . VO LUM E 59, JULY 1959 • 63

Fig. 12 (Right) • Fibrous dysplasia (oste­ itis fibrosa cystica). This type of fibrous dysplasia contains characterized formations of fibrous connective tissues within spongiosa of affected bone and often associated with expansion of bone to cause deformity

Fig. 12 (Above) of metaplasia

• Ossification of nasal cartilage, an example

Fig. 13 • Metastatic calcification of small divisions of facial artery

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D Y ST R O P H IC C A L C IF IC A T IO N Frequent Type

M E T A S T A T IC C A L C IF IC A T IO N

Deposition o f calcium in dead or degenerating tissue

Frequent Sites o f Occurrence

Sites of Occurrence

Lymph nodes Tuberculous necrosis Blood vessels Fatty degeneration and necrosis Degenerating thyroid tissue Degenerating tumors Infiltrated tissues (necrotic) such as C aseo u s necrosis Infarcts (coagulation necrosis) Inspissated regions O rgan ic foreign bodies Large area o f dead, noninfected tissue, so large or so situated that it cannot be absorbed

N o t dependent on calcium in the blood

increase

Precipitation of calcium salts in previously undamaged tissues, due to excess calcium in circulating blood

of

Lymph n o d e s ' Kidneys Lungs G astric mucosa M e d ia of blood vessels

Cause 1. Excessive parathyroid hormone depletes bones of calcium caus­ ing high level in blood 2. Hypervitaminosis (D) 3. Inability of kidneys to excrete phosphate adequately. Phosphate level is raised in blood 4. Destructive bone lesions such as tumors

Dependent on local condition

a

change

in the

IM P O R T A N T F A C T O R — local a l­ kalinity o f region in comparison with surrounding undamaged tissue initiates precipitation o f calcium in degenerating tissues and dead tissues

Fig. 14 • Pathologic çalcificatîon

N orm al ossification and pathologic calcification depend more on physicochemical factors and variations in carbon dioxide concentrations than on the presence o f chemical précipitants in the tissues Deposition o f calcium salts in areas of degeneration depends on: Increased alkalinity or decreased carbon diox­ ide causing precipitation o f inorganic salts in fluid seeping through tissue

Utilization o f the protein of fluids by starved tissues so.com pletely that ca l­ cium cannot be held in solution

Formation of substances having a special affinity for calcium in degener­ ated tissues

Production of a physi­ cal condition favoring local absorption of salts, the least soluble salts accumulating in excess

If carbon dioxide tension is low because o f inactive or dead tissue, a favorable site fo r precipitation is present C a rtilage and trabecula normally have a lo w carbon dioxide supply and thus becom e very favorable sites fo r precipitation

Fig. 15 • Factors on which deposition of calcium salts in areas of degeneration depends

ENN IS . . . VO LUM E 59, JULY 1959 • 65

phosphoric acid in decreased nucleoproteins and lecithin are so obvious. Fatty acids offer another possibility, espe­ cially in view o f the fatty degeneration that so frequently precedes calcification.10 In calcification at all stages the p ropor­ tion o f calcium carbonate and phosphate is fou n d to be constant and exactly the same as fou n d in normal bone. It has been conclusively shown that for bone form ation the blood must contain a proper am ount o f both calcium and phos­ phate, indicating that the calcium is de­ posited as phosphates and not bound to some other binding substance. CALCIFICATION AS A SIMPLE PRECIPITATION

T h e deposition o f calcium in bone and pathologic calcification does not depend on the existence o f a special calcium binding substance in the tissues that are to be calcified, but on the saturated condi­ tion o f the calcium salts in the blood. H ow lan d11 and his associates fou n d that calcium , phosphoric acid and carbon dioxide exist together in the b lood in a well-balanced condition aided by the protective action o f the plasma colloids. H ow land further stated that calcification may be visualized in the follow ing way. Serum contains calcium and inorganic phosphorus in solution in m uch higher concentration than is possible in water because o f the high carbon dioxide ten­ sion. T here is evidence that part o f the calcium is bound in protein. It is assumed that this calcium -protein com pou n d is poorly ionized and this w ould be equiva­ lent to reducing the total calcium concen­ tration. Intercellular fluid o f the tissues contains roughly the same am ount o f cal­ cium and phosphorus as the serum, but the protein content is m uch lower, ap­ parently about 1 per cent, as contrasted with the 7 to 9 per cent in the serum. T h e carbon dioxide tension is relatively high on account o f cellular activity. H o w ­ ever, if the carbon dioxide tension is low

because the tissue is inactive o r dead, then conditions are favorable for precipi­ tation. Cartilage and the trabeculae o f the bone are both inactive tissues. It is in them that the carbon dioxide tension w ou ld be expected to be low and it is in them that precipitation takes place (Fig. 12, a b o v e ). This chem ical activity ex­ plains calcification in dead or inactive tissues such as tuberculous lesions. CONCRETIONS

T h e concretions that are discussed are: solidified or hardened masses com posed o f foreign material or produ ced by inspissation o f matter normal to the part; a cal­ culus. A ll pathologic concretions appear to be laid dow n according to a definite law. T here must first be a nucleus o f some substance different from the substance that is to be deposited. This is most fre­ quently a mass o f desquamated cells but m ay consist o f clum ped bacteria, a mass o f mucus, precipitated proteins, or a fo r­ eign body o f almost any sort. T h e structure o f a concretion depends on two factors: the crystals tend to be deposited at right angles to the surface, and thus give a radiating structure. T h e rate o f deposition is usually irregular. D uring periods o f quiescence, the surface tends to be covered with m ucin o r other organic substances, hence a laminated structure is fou n d (Fig. 16). Concretions in the Lung (L ung Stones)

• L un g stones may be form ed in the bronchi, through accretion about an in­ organic nucleus, similar to the form ation o f calculi in other epithelial-lined pas­ sages. T hey m ay also consist o f calcified areas o f lung tissue or peribronchial glands, w hich have been sequestrated through suppuration and have entered the bronchi. In the latter instance, the calculi have the usual com position of pathologic calcified regions. T hat the ex­

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Fig. 16 • Left: Large concretion in maxillary gland. Center: Concretion after removal showing laminated structure. Right: View revealing laminated structure developed around nucleus in concretion in submaxillary duct

pectorated stones frequently represent calcified tubercles was shown by Stern12 and Burgi13 who demonstrated tubercle bacilli in decalcified lung stones many years ago. Maver and Wells4 also found that these concretions have much the same composition as calcified lesions gen­ erally, that is, calcium phosphate and carbonate are present in about the same ratio as in bone; silica, when present, represents inhaled dust. Calcium Reaction in Tuberculosis • Tubercle bacilli in tissue result in local­ ized nodules of reaction called tubercles. The characteristic features are a core of coagulative caseous necrosis, surrounded by a cluster of peculiar mononuclear (epithelioid) cells, some of which fuse to form giant cells with multiple pe­ ripheral nuclei, and an outer border of lymphocytes. Near the central part of the cluster of epithelioid cells, there may be one or more giant cells. These are formed by fusion of epithelioid cells about a small amount of necrotic material, or possibly by amitotic division of nuclei without cellular division. A coagulative caseous necrosis de­ velops in the center of the tubercle. This

is caused by destructive action of bacterial products and contributes to the avascularity of the tubercle. No blood vessels are present within the tubercle itself.4 If the tubercle is very small, healing may result in its disappearance or replace­ ment by a fibrous scar. A considerable amount of caseous material may not be absorbed and may become calcified by the deposition of calcium salts. This tendency to calcification is comparable to calcium deposition in any devitalized tissues in the body (dystrophic calcification) and possibly depends on a localized increased alkalinity of the necrotic material. Calcification of Lymph Nodes9 • The lymph nodes are focal collections of lymphoid and reticuloendothelial cells. The main elements in lymph nodes are: (1) lymph follicles (germinal centers) supposedly the site of formation of lymphocytes; (2) lymph sinuses, lined by endothelium, and (3) the medulla, or pulp, consisting of lymphocytes and reticulum cells in delicate meshwork of reticulin fibers. The mucous membrane of the oro­ pharynx contains many scattered lymph­ oid follicles in its walls, especially on the sides, and above the level, of the tonsils.

ENNIS . . . VO LUM E 59, JULY 1959 • 67

Fig. 17 • Calcification of lymph nodes Above: Oblique lateral view Below: Posteroanterior view with symphysis of mandible on a level with external occipital protuberance allowing clear view of submaxillary region

The lymph nodes are an integral part of the reticuloendothelial system and are involved in its diseases. The main lesions of the nodes are inflammations (lympha­ denitis), tumors (primary and metastat­ ic), and calcification (Fig. 17). An important function of the lymph nodes is the removal of various substances from the lymph as it filters through them. Particulate matter (that is, coal dust, hemosiderin, tattoo pigments), cells (tumor cells) and bacteria are the most readily observed, but invisible toxic sub­ stances of various types also pass through the nodes and may effect morphologic changes. Tuberculous involvement of lymph nodes is commonly found as a result of drainage from a focus of tuberculosis. Tuberculosis of the bronchial lymph

Fig. 18 • Left: Four clusters of calcified lymph nodes. Arrows A point to calcified nodes; arrow B points to calcification of stylohyoid muscle and ligament. Right: Direct lateral view of same patient as in view at left. Arrows A point to calcified lymph nodes. Arrows B point to calcified stylohyoid muscle and ligament. BR is right side, BL is calcified ligament left side

68 • THE JO U R N A L O F THE A M E R IC A N DENTAL A SSO C IA T IO N

Fig. 19 • Left: Tonsillith shown on intraoral film posterior to angle of mandible. Right: Another view of tonsillith

nodes almost always arises from a primary infection in the lung parenchyma. This often results in the calcification of the lymph nodes affected. Single nodes or nodes in groups may be affected (Fig. 18), or there may be widespread involve­ ment of lymph nodes as part of dissemi­ nated tuberculosis (Fig. 9 ). When the practitioner is dealing with the bronchial

lymph nodes, he must realize that in calcareous degeneration, calcium salts tend to precipitate in degenerating, dying, or dead tissue. Although frequently termed calcareous degeneration, this is really not a separate type of degenerative change. Tonsillar concretions consist chiefly of calcium carbonate and calcium phos­

5

Fig. 20 • Left: Three arrows point to salivary calculus in parotid gland. Right: Salivary calculus in parotid duct. View taken on small intraoral film placed in vestibule of mouth

ENN IS . . . VO LUM E 59, JULY 1959 • 69

phate deposited upon inspissated secre­ tions and desquamated cells o f the tonsil­ lar crypts.14 This condition is known as tonsillith, w hich may be defined as a calcareous concretion in a distended ton ­ sillar crypt, a tonsillar calculus (Fig. 19). In structure, the tonsil is a mass o f adenoid tissue enclosed in a fibrous ca p ­ sule w hich is crossed on both the deep and free surfaces by a thin layer o f mus­ cular fibers. T h e closely adherent m ucous m em brane covers the free surface, which is full o f pits varying from 1 mm. to 1 cm. in depth. T h e large ones expand below the orifice so that they may collect and retain secre­ tions. A small free space, the supratonsillar fossa, lies above the tonsil at the apex o f the niche containing it ; at the front of this, there is often a series o f crypts with detached adenoid tissue about them, bur­ row ing under the anterior pillar from behind and making a pouch beneath a fold , the plica triangularis. It is in these regions that tonsilliths are sometimes found, w hich are masses o f calcium d e­ posit fou n d in the crypts o f the tonsils (Fig. 19). Salivary stones (calculi) are fou n d in the ducts, in the glandular tissue, or both. T h e submaxillary gland is m ore often involved than the parotid (Fig. 20 and 21). T h e obstruction is initiated by a central collection o f desquamated epithe­ lial cells and colonies o f organisms around which calcium salts are deposited (Fig. 21 and 2 2 ). In a few instances, foreign bodies may form the core. Salivary cal­ culus shows a variable com position be­ cause o f the amount o f organic material present. Prinz15 gives as the average of five analyses o f human m aterial: calcium phosphate 63.42 per cen t; calcium car­ bonate 9.14 per cen t; magnesium phos­ phate 1.31 per cent; organic material 15.16 per cent. Presumably, the calculus is form ed by precipitation o f calcium in the secretions o f .the salivary glands be­ cause o f loss o f the carbon dioxide which keeps it in solution (Fig. 2 3 ).

Epulis is a term applied to various tumorous growths o f the gingiva. T hey m ay be fou n d in children, in young adults and in w om en during pregnancy. A l­ though the epulis tends to recur after sur­ gical removal, it is not a true neoplasm. It is either a simple hypertrophic inflam­ matory growth due to a local m echanical irritation or an exuberant reaction o f the gingiva to an inflammatory resorptive and regenerative process which started in the alveolar process. T h e m icroscopic picture o f an early classic epulis, the form ation o f w hich was stimulated by an inflammatory resorptive process in the m arrow o f the alveolar process, is dom inated by abundant multi­ nucleated giant cells fou n d in a vascular and cellular connective tissue associated with hemorrhages and hemosiderin. This type is called giant-cell epulis. T h e giant­ cell epulis m ay undergo a slow transfor­ m ation into a fibrous lesion with few giant cells and newly form ed bone trabeculae (Fig. 24 and 2 5 ). Hyperparathyroidism • T h e parathyroid

glands produce a horm one concerned with the metabolism of calcium and phos­ phorus and the maintenance o f normal levels o f these elements in the blood. Excessive parathyroid function6 may be due to a benign or malignant neoplasm o f parathyroid tissue, to a benign hyper­ trophy o f all the parathyroid glands (ra rely ), or to a diffuse hyperplasia of parathyroid tissue secondary to a dis­ turbance o f calcium and phosphorus metabolism originating elsewhere in the body. T h e increased parathyroid horm one mobilizes excess calcium from the bones, bringing about the skeletal changes de­ scribed as osteitis fibrosa cystica (Fig. 12, r ig h t). T h e blood has an increased con ­ centration o f calcium and alkaline phos­ phatase, but a low level o f phosphorus. T h e excess serum calcium tends to be precipitated in soft tissue, and m ay cause severe damage in such tissues as blood vessel walls and kidneys.

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Fig. 21 • Left: Large salivary calculus filling entire duct. Right: Calculus after removal showing projection at distal end where it was descending into gland

Fig. 22 • Left: Three small circular calculi in submaxillary duct. Right: Calculus in submaxillary gland causing considerable swelling and infection in submaxillary region shown by arrow E

Fig. 23 • Left: Salivary calculus deposited on coronal third of root. Right: Vertical loss of supporting alveolar structure and lingual tis­ sue of mandibular cuspid with large mass of salivary calculus in apical region lingually

ENNIS . . . VO LUM E 59, JULY 1959 • 71

Fig. 24 • Left: Calcified giant cell tumor (epulis) in mouth of woman aged 52. Patient complained only of first incisor being loose and was oblivious to tumor. Center: View of same patient showing large calcified mass extending into mucobuccal fold. Right: View of same patient with slightly different angulation showing process of calcification affecting maxillary bone to depth indicated by arrows. Condition of first incisor had no connection with tumor

Fig. 25 • Left: Calcified giant cell tumor (epulis) in mandibular first molar region in woman aged 54. Above right: View of same patient showing large calcified mass surrounded with soft tissue extending above alveolar border in mandibular molar region. Below right: Tumor after removal showing calcified structure surrounded by fibrous tissue

SUMMARY

It has been shown how and why the physical properties of the cell modify the cell’s chemical processes and, therefore, become the most important factor in the chemistry of many abnormal and patho­ logic lesions. It is this knowledge that gives us a good understanding of why calcification takes place in the various areas of the body. Understanding makes it possible to interpret more accurately and to explain intelligently the osseous

changes which take place in the tissues and which are revealed in the roentgeno­ gram. *P ro fe sso r of oral roe n tg e n o lo g y, Sch oo l o f Dentistry an d G ra d u a te Sch oo l of M e d icin e , University of Penn­ sylvania. 1. Koechig, Irene. C a lc iu m content o f the b lo o d in p a th o lo g ic con ditio ns. J. Lab. & C lin . M e d . 9:679 Ju ly 1924. 2. H alve rson, Joh n; M ohler, H enry, and > Bergeim , O la f. C a lc iu m content of the b lo o d serum in certain p a th o lo g ica l con dition s. J. Biol. C he m . 32:171 N o v . 1917. 3. M a v e r, M . E., a n d W e lls, H . G . Studie s on the biochem istry an d ch e m o th e rapy o f tuberculosis. X X IV . A lim e n ta ry a b so rp tio n o f calcium and its de p o sition in the tissues in experim ental tuberculosis. A m . Rev. Tuberc. 7:1 M a rch 1923.

72 • THE JO U R N A L OF THE A M E R IC A N DENTAL A SSO C IA T IO N

4. Maver, M. E., and Wells, H. G . Studies on the biochemistry and chemotherapy of tuberculosis. X X III. Chemical composition of calcified tuberculous lesions. Am. Rev. Tuberc. 6:649 Oct. 1922. 5. Radasch, H. E. Determination of the percentage of the organic content of compact bone. Anat. Record 21:153 May 1921.

9. Wells, H. G. Chemical pathology, ed. 5. Phila­ delphia, W . B. Saunders Co., 1925, p. 486-493. JO. Lichtwitz, L. Über die Bedeutung der Koloide für die Konkrementbilding und die Verkalkung. Deut, med. Wschr. 36:704, 1910. 11. Howland, John. Etioloqy and pathogenesis of rickets. Medicine 2:349 Nov. 1923. 12. Stern, R. Über Lungensteine. Deut. med. Wschr. 6. Disturbances of mineral metabolism. InPathology, 30:1414, 1904. Anderson, W . A. D., editor. St. Louis, C. V. Mosey Co., 1948, p. 85-87. 13. BLirgi, Emil, über Lungensteine. Deut. med. Wschr. 32:798, 1906. 7. Wells, H. G . Metastatic calcification. Arch. Int. Med. 15:574, 1915. 14. McCarthy, Justin. Case of tonsillar calculus. Brit. M. J. 2:1062 Oct. 28, 1911. 3. Meyer, A. W., and Cajon, F. A. Anatomic and chemical report on a unique case of myeloma. Arch. 15. Prinz, Hermann. Oriqin of salivary calculus. D. Int. Med. 33:581 May 1924. Cosmos 63:231 March 1921.

Com parative evaluation of newer devices and technics fo r the rem oval of tooth structure: vibration characteristics and patient reaction

Jack L . Hartley * D .D .S .; Donald C. H udson,f D .D .S ., and Francis A . Brogan, B.A.,% Randolph Air Force Base, Texas

N ewer devices for removing tooth struc­ ture were compared and evaluated with respect to annoyance and discomfort to the patient. T h e number 10 was assigned to the conventional low-speed m ethod of cutting. T h e annoyance factor was deter­ mined to be 2 for the ultrasonic hand­ p iece; 3 for the air turbine handpiece with diamond cylinder; 4 for the air tur­ bine handpiece with no. 5 5 8 carbide bur, and so forth. Audiometric tests indicated no significant temporary loss in hearing in patients as a result of cutting with any of the handpieces studied.

Comprehensive studies o f the newer m e­ chanical instruments for the removal o f tooth structure which have recently been m ade available to the dental profes­ sion indicate that these devices are indeed

very effective. Increase in cutting effi­ ciency, ease o f operation, better control and reduction in pressure and heat p ro­ duction, however, should be considered as approaching the ultimate only when accom plished with an absolute m inimum o f patient annoyance and discom fort. Studies o f effectiveness, therefore, should include the factor o f patient response. A recent study1 has indicated that there is an unquestionable decrease in patient annoyance and discom fort when tooth structure is rem oved by any o f the newer instruments as com pared to the low speed handpieces. T h ere is, however, a significant variation in the degree o f an­ noyance produced by cutting with the newer devices, and some instruments ap­ pear to introduce new factors o f discom ­ fort. It is therefore desirable to evaluate the instruments com paratively with re­