Their status as contributory etiologic agents should be determined.

Predisposing Factors in the Etiology of Chronic Inflammatory Periodontal Disease

Static Occlusal Relationships

12

Data accumulated up to 1966 indicated some cor­ relation between periodontal disease and malocclusion. To be of etiologic significance, malocclusion or the altered anatomic relationships seen in malocclusion, must change the oral environment in such a way that: (1) Plaque accumulation or growth is favored; (2) M e ­ chanical injuries to the gingival unit are promoted; (3) A n inadequacy of periodontal tissue is created; or (4) Occlusal forces in excess of those which the periodon­ tium can accomodate are transmitted. Multiple factors which might be expected to affect the periodontal status are implicit in the term "maloc­ clusion." A b n o r m a l interarach cuspid and molar rela­ tionships, crossbite, increased overbite, increased overjet, and open bite are seen in malocclusion, while crowding, root approximation, suboptimal contact re­ lationships, suboptimal embrasure forms, uneven mar­ ginal ridges, rotation, drifting, inclination, spacing, fa­ cial and lingual displacement, and food impaction are seen in both maloccluded and nonmaloccluded mouths. Crossbite was positively correlated with severity of gingivitis in one study, while another reported no correlation. N o correlation has been found between open bite and the severity of periodontal disease. Interarch cuspid and molar relationships could not be correlated with gingivitis and no relationship between class of occlusion and periodontal destruction has been found. One author found no consistent relationship between overbite and overjet on the one hand and inflammation or periodontal destruction on the other. However, different i n v e s t i g a t o r s have reported significant correlations between both overbite and overjet and gingival health. G o u l d and P i c t o n found no correlation between periodontal disease and rotated, facially or lingually displaced or mesially or distally tilted teeth. They also reported that in the young, malrelationships of teeth appear to be related to poor gingival health while in older persons periodontal disease is not associated with poorly positioned, poorly occluded or crowded teeth. Tooth irregularities in dried skulls had no significant relationship to bone loss seen about them. A positive correlation was found between tooth drift and severity of periodontal disease but several years later the same author found no association between spacing and gin­ gival inflammation.

by BILLY

M .

PENNEL*

JAMES

G.

K E A G L E *

W I T H F E W EXCEPTIONS

1

—Malocclusion

13

investigators regard microor­

ganisms and their metabolic products as the primary cause of chronic inflammatory periodontal disease. However, bacterial accumulations and host responses to them will be considered elsewhere in this issue. The present report deals with adjunctive environmental fac­ tors which favor the accumulation of bacterial plaque and calculus near or apical to gingival margins, and with general factors which may alter the host's response to local irritants.

14

A N A T O M I C FACTORS

15

16

Distopalatal Groove of Maxillary

Incisors

14

Etiologic importance has been ascribed to an anom­ aly of maxillary lateral incisors and less frequently of maxillary central incisors, the distopalatal groove. Sometimes only the crown is involved but usually the groove extends apically along the root for varying dis­ tances. This groove is considered an ideal place for plaque to accumulate and cause a narrow but rapidly deepening destruction of periodontium.

17

18

14,15,19

2-5

15

Enamel

Projections

Masters and Hoskins noted that 9 0 % of isolated periodontal involvements in mandibular bifurcation areas were associated with enamel projections. A posi­ tive correlation also has been reported between the presence of enamel projections and loss of attachment apical to the level of furcation but another group found no such correlation. Two r e p o r t s on the prevalence and location of enamel projections mentioned possible predisposing roles in the etiology of destructive peri­ odontal disease. Loss of hemidesmosomal epithelial attachment to an enamel projection is likely to leave a cul de sac sulcus configuration favoring undisturbed plaque accumulation. After combining data from sev­ eral authors, A n d r e w s reported that about 7 0 % of all enamel projections are graded I or minimal. Therefore about 6 . 5 % of all molars have significant projections. 6

7

8

20

9,10

21

22

Food Impaction and Associated

Factors

Food impaction has been defined as "the forceful wedging of food against the gum through occlusal pres­ sure," the implication being that direct injury is in­ flicted on the gingiva causing a "physical break in the tooth-tissue attachment." F o o d debris retained near gingival margins may also act as a reservoir of nutri-

11

12

* Department of Periodontics, Medical College of Georgia, School of Dentistry, Augusta, Ga. 517

518

Fennel,

J. Periodontol. September, 1977

Keagle

ments for microorganisms, altering the local environ­ ment to favor the development of plaque. The possibil­ ity of lateral food impaction caused by pressures from lips, cheeks and tongue on facial and lingual gingiva and into enlarged subcontact embrasures also has been cited. However, reports of studies on the effects of food impaction or on the anatomic relationships re­ puted to promote it are scarce. Only 1 8 % of intrabony lesions on 121 human skulls were associated with such food impaction conditions as could be determined —plunger cusps on opposing teeth, open and deficient contacts, abnormal or defec­ tive marginal ridge relationships, and malalignment of teeth. Others found that spaced teeth and teeth with poorly shaped contacts had increased periodontal scores. O'Leary et a l . studied interproximal contact and marginal ridge relationships in three groups of periodontally healthy males. From 6 1 . 7 % to 7 6 % of the proximal contact were defective and 33.5 % of adjacent marginal ridges were unven. For these subjects defec­ tive interproximal contacts and uneven marginal ridges were apparently not incompatible with good periodon­ tal health. There is little hard evidence that factors presumed to promote food impaction have a causative relationship to periodontal disease. 1 3 , 2 3

24

15

25

Mouthbreathing

35,36

Frenulae, Vestibular Depth and Inadequate Gingiva Frenulae and muscle attachments which encroach upon gingival margins allegedly pull the margin from the tooth, fostering the accumulation of plaque and irritants, leading to gingivitis and pocket formation. Placek et a l . found a high percentage of papilla dis­ placement when frenulae were inserted into gingiva, directly into the papillae, or into both gingiva and papilla, especially in the mandible. A low incidence of displacement was found when the frenulum was in­ serted into mucosa apical to gingiva. In a companion study some types of labial frenulum attachment were found to influence periodontal conditions but only in those subjects who had a low ''periodontal resistance," i.e. a low Oral Hygierre Index to Periodontal Index ratio. It appears that where a frenulum is inserted into gingiva or papilla and pathologic change persists in an atmosphere of good plaque control, the frenulum can be considered an etiologic factor. Adequate vestibular depth has been presumed nec­ essary to provide space for unimpared food excursion, to reduce food retention at gingival margins, and to facilitate toothbrushing. However, the principal reason for deepening of the vestibule has been to create space for a broadened zone of gingiva or relocation of frenu­ lum attachments. Bergenholtz and H u g o s o n con­ cluded that the hygienic condition is unchanged by vestibular extension and that there is no justification for performing the operation simply because the vesti­ bule is considered too shallow for efficient oral hygiene measures. More recently W a r d studied the vestibular fornix in 100 healthy mandibular anterior areas and found that: (1) The minimum vestibular depth was variable and in most instances was associated with fren­ ulum or muscle attachments; (2) Even shallow vestibu­ lar fornices (2.5 mm) were compatible with gingival health, provided at least 1 mm of attached gingiva was present. O n the premise that a minimum width of attached gingiva is required to support the gingival fibers which brace the marginal gingiva and prevent it from being deflected from the tooth during mastication and lip and 23

37

38

O n the basis of clinical observation, writers of the 1930's felt strongly that mouthbreathing always led to gingivitis. The drying effect and frictional action of the continuous passage of air over the tissues were considered significant factors, a view recently sup­ ported. However, experimental air drying of rat gin­ giva did not cause it to become inflamed. Alexander reported that mouthbreathing had no ef­ fect on prevalence or extent of gingivitis except in patients with considerable calculus. Another study found crowding to be associated with gingivitis only in mouthbreathers. Jacobson concluded that mouthbreathers have more severe gingivitis than non-mouthbreathers with similar plaque scores. Sutcliffe reported no relationship between mouthbreathing and prevalance of gingivitis although it was associated with a slight increase in severity. H e considered mouthbreathing unimportant in the etiology of gingivitis. While there is some indication that mouthbreathing is associated with increased gingival inflammation the evidence is not entirely clear or without conflict. 26,27

28

29

30

16

31

29

32

Crowding and Root

Approximation

Opinion is widespread that crowding creates difficult or impossible situations for adequate daily plaque re­ m o v a l . Several a r t i c l e s have reported positive relationships between crowding and increased gingivitis or periodontitis. Other studies could find no positive association between crowding and periodontal destruc­ tion or gingival i n f l a m m a t i o n . Stahl has stated 13

that malposition may make plaque control more diffi­ cult but specific measures should be able to overcome this. Crowded, overlapping teeth may or may not exhibit root approximation. Root approximation has been as­ sociated with the long contact point or reduced proxi­ mal crown contours. A t least two a u t h o r s have commented on the grave prognosis of one of two roots in close approximation. The implication is that destruc­ tion of attachment apparatus will proceed rapidly in the absence or near-absence of bone between two roots, particularly since the approximating supra gingival con­ tours are apt to be difficult to keep plaque-free. No reports of studies of the root approximation problem were found, however.

1 4 , 3 2 , 3 3

15,22

34

23

39

40

Volume 48 Number 9

Chronic Inflammatory

cheek movements, operations to broaden the zone of attached gingiva have been commonplace. Lang and L o e found that even on plaque free surfaces, inflam­ mation as indicated by crevicular fluid flow persisted in areas of less than 2 mm of keratinized gingiva, 1 mm of which was attached. Maynard and Ochsenbein re­ ported that 19 of 100 children examined had mucogingival problems on the facial aspect of the mandibular incisor region. However, when photographs of the same patients were reviewed by others, as few as 12 of the 100 were recognized as having problems. The au­ thors recommended free grafts prophylactically in all cases when width of keratinized gingiva was 1 mm or less. 41

42

Position of Teeth in the Alveolus 43

Hirschfeld reported an association between facial inclination of teeth and thinned or absent alveolar plate on their roots. In a study of 108 skulls 7.5% of all teeth had fenestrations or dehiscences, and more than 9 0 % of these had prominent roots in relation to the rest of the arch. O n the other hand, another skull study reported no significant relationship between periodon­ tal disease and facial or lingual malposition or inclina­ t i o n . G o u l d and P i c t o n found no correlation be­ tween periodontal disease and facially or lingually malposed teeth. Novaes et al. proposed a scheme for the pathogen­ esis of dehiscences and gingival clefts. Such gingiva as overlies a prominent root surface is thin with decreased amounts of connective tissue and collagen sandwiched between sulcular-junctional and oral epithelia. Thin gingiva and alveolar mucosa are subject to retraction which leads to submarginal plaque and irritant accumu­ lation. In the presence of irritation, connective tissues are destroyed and proliferation of sulcular-junctional epithelium results in union with the oral epithelium, leading to necrosis and clefting due to lack of interven­ ing supporting connective tissue. It has been noted that alveolar bone over promi­ nent roots is thin and frequently consists only of cortical bone which is extremely vulnerable to both inflamma­ tory and traumatic resorption. The implication is that this can lead to rapid development of a dehiscence, which can in turn be followed by rapid destruction of overlying soft tissue. In attempts to create bony dehis­ cences and gingival recession by active orthodontic movement, Batenhorst et a l . found 10 times more bone loss on facially moved and extruded lower incisors than on unmoved control incisors in Rhesus monkeys. Wingard and B o w e r s , however, using a modification of Batenhorst's method produced no dehiscences or fenestrations. A t this point the evidence regarding root prominence as an etiologic factor is conflicting. There is a strong clinical impression that teeth in prominent positions in the alveolus are likely to have dehiscences and gingival recession. 44

20

15

45

45

46

47

Periodontal

Disease

519

It appears that several anatomic factors which con­ tribute to the etiology of chronic inflammatory peri­ dental disease do so by favoring the accumulation of bacterial plaque. Others such as inadequate gingival width, frenulae, and prominent teeth tend to make the periodontium more vulnerable to mechanical and bac­ terial insults. Etiologic contributions of still other fac­ tors are based largely on clinical impressions with little evidence to support them. RESTORATIVE A N D PROSTHETIC DENTISTRY

A very important and close relationship exists be­ tween periodontal health and restorative dentistry. In­ adequate dental restorations can contribute signifi­ cantly to the onset and progress of periodontal disease and will be discussed under the topics of crown con­ tour, margin location and fit, pontics, materials and removable partial dentures. Crown

Contour

Clinicians have long been concerned about the rela­ tionship between crown contour and gingival health. Explanations for this association have emphasized the protective function of the cervical convexity of the facial and lingual crown surfaces. Insufficient contour is considered to be a predisposing factor for food im­ paction or direct trauma to the gingival m a r g i n , and excessive contour is considered to interfere with the stimulating effect of food passing over the surface of the gingiva during mastication and to encourage the accumulation and retention of bacterial plaque adja­ cent to the gingival margin. Overcontoured restora­ tions could also interfere with plaque control proce­ dures and possible benefits from the rubbing activity of the adjacent cheeks, lips, and t o n g u e . The concept of food deflection and protection of the facial and lingual marginal gingiva and sulcus by cervi­ cal crown convexities has not been accepted by some authors and in one animal study removing the cer­ vical crown contours produced no detrimental effects on the marginal gingiva. Evidence for a positive associ­ ation between overcontoured crowns and periodontal disease is more abundant. Studies have shown overcon­ toured axial surfaces to be associated with an increase in gingival i n f l a m m a t i o n and alterations in mor­ phology. In 6 4 . 3 % of test sites where facial crown surfaces were experimentally overcontoured, the in­ creased inflammation of the subjacent periodontal tis­ sue was considered to be the result of inaccessibility to cleaning. These findings support the contentions of clinicians that excessive axial contour favors plaque accumulation and hinders efforts in plaque con­ trol The enlarged and inflamed interdental papilla in as­ sociation with a crowded interproximal area represents one of the most common and challenging periodontalrestorative problems. Overcontoured proximal crown surfaces invade the interdental space intended for the 48

48,49

50

4 8 , 5 0 , 5 1

51-53

54,55

55

5 1 , 5 3 , 5 6

520

J. Periodontol. September, 1977

Fennel, Keagle

gingival papilla. This not only causes pressure on the papilla, but also prevents or inhibits effective plaque control because of inadequate access. Following the surgical elimination of periodontal pockets, the reestablishment of interproximal papillae lags behind the marginal gingiva in terms of reaching a stable position. Although studies designed to provide information about the average time required for full papillae rebound are lacking, undertaking restorative procedures involving the interproximal'surfaces earlier than 3 or 4 months after surgery may result in inade­ quate interproximal spaces and strangulated papillae. Variations in the normal anatomy of the marginal and interproximal periodontium must also be considered in establishing crown contours. Margins

tion, microporosity and rough edges of restorations and cement were considered to be factors which promote bacterial growth. A sizeable area of exposed zinc phosphate cement between crown margins and the ad­ joining tooth surface has been demonstrated micro­ scopically and bacterial plaque has regularly covered the cement and penetrated into its porosites. Other human studies have reported a positive associ­ ation between subgingival margins and gingivi­ tis, and pocket depths. One investigation dem­ onstrated a more intense gingival inflammation the nearer the subgingival margin approached the base of the gingival crevice. Similar conclusions were re­ vealed by a study in which crowns were fitted on dogs and monkeys, and another animal study showed that the most severe inflammatory reactions occurred in association with subgingival margins. In opposition to the above findings, the gingival tissue adjacent to resto­ rations which were designed so that half of the buccal margin was located subgingivally and half supragingivally appeared uniformly healthy. The roughness of restorative materials adjacent to gingival tissues has promoted gingival inflam­ mation. Evidence has been provided that this oc­ curs because of a favorable environment for the accu­ mulation of bacteria rather than from mechanical irrita­ tion. The significance of subgingival margins was further shown in a study of the gingival reaction to well adapted restorations. Gingival inflammation was greater adjacent to subgingival margins, even though identical plaque scores were recorded for restorations with supragingival and subgingival locations. In an­ other study, the mean gingival fluid flow rate was significantly higher adjacent to rough and polished well-fitted gold inlay surfaces than it was when the proximal surfaces were without restorations. This oc­ curred even though no significant difference in plaque scores between filled and sound proximal surfaces were noted. Restorations with defective subgingival mar­ gins and even those of high quality encourage the growth of bacteria and the inaccessible margins prevent optimum plaque control measures. 68

72a

7 2 b , 7 3 , 7 5

72b

76

65

The relationship between periodontal health and the margins of restorations has been examined in terms of fit, location, smoothness, and materials. The quality of margins, particularly those with subgingival locations, is a recognized factor in peri­ odontal health. Clinical investigations concerned with posterior dental restorations with definite overhangs have shown a positive relationship to the severity of periodontal d i s e a s e . Defects in crown margins in the form of overhangs and the amount of excess filling material have been shown to bear a positive relation­ ship to a reduction in the interproximal bone height. The investigation involving full crowns found a high frequency of defective crown margins, with the major­ ity exceeding 0.2 m m . A defect of this magnitude provides a sizeable shelter for the accumulation and growth of bacteria.Locations recommended for the placement of crown margins include the base of the gingiva crevice, half the distance between the crevice base and gingival margin, 0.5 to 1 m m , or slightly below the gingival margin, the crest of the gingival m a r g i n , and a supragingival l o c a t i o n . Examples of clinically healthy periodontal tissues have been demonstated by the proponents of each margin location where the qual­ ity of the restoration was excellent and patients demon­ strated a high level of plaque control. Gingival inflam­ mation in association with full coverage crowns, how­ ever, is a common finding and considerable interest has been generated concerning the optimum location of crown margins. A series of investigations were performed to deter­ mine the effects of full and partial crowns, margin location, bridges with double abutment splints and pontics on the periodontal health of the involved teeth. The level of periodontal health was more closely associated with the location of the crown margins than any of the other periodontally related restorative fac­ tors. Subgingival margins were consistently associated with more severe gingival inflammation. A n in­ crease in the amount of soft deposits was a coexisting finding, and rough surfaces produced by tooth prepara­ 57,58

59

60

59

61

62

6 3 , 6 4

51

65,66

56,67

68

67

69

70

67-71

77

78,79

79,81

82

83

Pontics Pontics for fixed partial dentures can be predisposing factors in periodontal disease. In an evaluation of the periodontal status of proximal abutment tooth surfaces adjacent to pontics, the combination of pontics and supragingival crown retainers caused an increase in plaque and gingivitis but had little effect on pocket depth. Pontics in combination with abutment retainers which had subgingival margins were associated with a marked increase in plaque and gingival inflammation and some increase in pocket depth. The increase in pocket depth was considered to be related to the subgingival retainers. The response of adjacent alveolar ridge mucosa to the contacting pontic has been studied in relation to 70

Volume 48 Number 9

Chronic Inflammatory

pontic design and the materials employed. A n increase in ridge coverage intensified subpontic tissue changes and the amount of pressure exerted by the pontic on the edentulous ridge was found to be proportional to the amount of unfavorable tissue change. Investigations of the influence of pontic materials upon periodontal health have produced conflicting re­ sults. Some studies have rated glazed porcelain as supe­ rior and others have pointed to the inferiority of acrylic, with gold occupying an intermediate posi­ t i o n . Still other investigators have found no differ­ ences among the various materials evaluated. Studies of the relationship between pontics and peri­ odontal health have often failed to evaluate the quan­ tity of bacterial plaque on the pontic and adjacent crown surfaces. The studies which did measure or consider this aspect have reported plaque variations to be closely associated with variations in tissue inflam­ mation. Lack of access to the proximal and apical surfaces of pontics for plaque removal and ineffective oral hygiene by the patient are the major factors related to adjacent tissue irritation. Pressure on the alveolar ridge, concave ridge lap pontics and inadequate embra­ sure spaces inhibit plaque removal and act as predis­ posing etiologic factors.

Periodontal

Disease

521

Removable Partial Dentures

84

85

8 5 - 8 7

85,87

87

88-90

70

91

Materials

Unfavorable periodontal changes following the in­ sertion of removable partial dentures have been re­ ported by several investigators and observed by clini­ cians over the y e a r s . Longitudinal studies with evaluation periods from 1 to 4 years showed an in­ crease in mobility, gingival inflammation and pocket depth of the abutment t e e t h . Except for pocket depth, these changes started during the first year, progressed during the second and then either increased at a slower rate or remained approximately constant during the third and fourth years. Pocket depth decreased during the first year but increased during the second. The radiographic portion of the study revealed deterioration of about one-fourth of the bone supporting the abutment teeth among the den­ ture-wearers, while little change was noted among pa­ tients who did not wear dentures. The periodontal pathology strongly correlated with poor oral hygiene. In a 1-year study, gingival health was adversely af­ fected by removable partial dentures. The authors at­ tributed the increase in gingival inflammation and pocket depth to the combination of mechanical pres­ sure and bacterial colonization adjacent to the gin­ giva. In other longitudinal studies, the periodontal evalua­ tion did not find the increase in m o b i l i t y and gingival i n f l a m m a t i o n that was reported in the previous investigations. In one 2-year study, the au­ thors pointed out that the partials were carefully de­ signed and regularly checked, and oral hygiene instruc­ tions were reinforced periodically. N o differences were reported in gingival index, or pocket depth, and a decrease in mobility of the abutment teeth was noted. A n analysis of the factors which relate periodontics to restorative dentistry clearly demonstrates the impor­ tance of the bacterial component and the necessity for designing and fabricating restorations which provide access to all surfaces for effective plaque removal. Shel­ tered areas which promote the accumulation and growth of bacteria must be avoided. Since only slight defects offer bacteria a favorable environment, the margin for error in restorative dentistry is small. 102,104

1 0 3 , 1 0 5 , 1 0 6

102

7 4 , 1 0 7 , 1 0 8

A number of investigations have been performed in an attempt to identify the role of restorative materials in the etiology of periodontal disease. A n i m a l studies of the compatibility of periodontal tissues to amalgam, silicate, acrylic and c e m e n t have supported obser­ vations which demonstrate chronic inflammation in the gingival tissues which approximate the restorative ma­ terials. Additional investigations have shown bacterial plaque on the surface of restorative materials to be a more important and potent source of irritation than the materials. G o l d has been well tolerated by approximating peri­ odontal t i s s u e s . A recent ultrastructural investi­ gation showed no inflammation of the junctional epi­ thelium and subjacent connective tissue adjacent to gold foil restorations in the absence of bacterial plaque. Even though restorative materials differ in relation to plaque accumulation and r e t e n t i o n , the materi­ als employed today can be satisfactorily cleaned and are compatible with the periodontal tissues if the num­ bers of microorganisms are minimal. If oral hygiene is inadequate, bacterial plaque will accumulate on all materials, though the rate of accumulation varies. Glazed porcelain, for example, has demonstrated a resistance to plaque formation when compared to other materials. Except for s i l i c a t e , restorative materials were shown to have no influence on the composition of plaque. Plaque formed at the margins of the various restorative materials was similar in composition to plaque on the adjacent tooth surface. 92,93

7 9 - 8 1 , 9 2 , 9 4 , 9 5

81,96,97

94

98,99

98

100,101

100

74,107

74

PERIODONTAL

TRAUMA FROM

OCCLUSION

Periodontal trauma from occlusion and its treatment are dealt with in another report in this issue. SYSTEMIC

FACTORS

Several systemic conditions have become identified as being associated with increased incidence or severity of gingivitis and periodontitis. Diabetes Mellitus There continues to be a widespread belief that peri­ odontal disease is more severe and progresses faster in diabetics than in nondiabetics, despite the fact that the evidence is inconsistent, even conflicting. Hove and Stallard found that periodontal disease increased 109

522

J. Periodontol. September, 1977

Pennel, Keagle

with age in both diabetics and nondiabetics and that this increase was attributable to local factors. Cohen et al., on the other hand, reported that diabetics had significantly more gingivitis and greater loss of attach­ ment than nondiabetics of similar ages. Tuckman et a l . found that in 54 nondiabetic subjects the 12 with the highest periodontal scores had significantly higher glucose tolerance scores than the 12 with the lowest periodontal scores. However, this statistical method does not test for a possible correlation between the two variables. Bernick et a l . concluded that the incidence of gin­ gival inflammation was greater in diabetic than in nondiabetic children with similar oral hygiene scores. Bay et a l . found that diabetics had as much capacity for gingival healing as healthy controls. Pathologic change in small vessels has been identified as a possible cause of the allegedly altered response to local irritants which is seen in the periodontal tissues of diabetics. A significant increase in basement membrane width in small gingival vessels of diabetics compared to nondiabetics has been noted in one report. In an­ other, gingival capillaries of diabetics were found to have both normal and altered morphology. Several other authors indicated that duration of diabetes has little effect on gingival vascular c h a n g e s . List­ garten et a l . could find only a marginally significant increase in basement lamina width and concluded that this feature could not be used to diagnose diabetes. Opinions differ as to whether periodontal status is affected by diabetes. 1 1 0

111

1 1 2

1 1 3

had the same number of vessels in the crevicular plexus as control dogs, although the vessels of the experimen­ tal animals were substantially wider and more tortuous. These findings suggest that the effect of progesterone is mainly on the function and permeability of the vessels of the crevicular plexus, and together with previous findings of Lindhe and various collaborators they support a hypothesis that aggravation of gingivitis dur­ ing pregnancy is caused mainly by a raised level of progesterone and its effect on the microvascular sys­ tems of the gingiva. Subsequent f i n d i n g s have further supported this hypothesis. Few reports have addressed the question of how pregnancy affects the periodontal attachment level. Cohen et a l . noted little or no loss of attachment during pregnancy. Knight and W a d e studied the ef­ fects of oral contraceptives on young women and found that those taking them for more than 1½ years had significantly greater loss of attachment than a compara­ ble group of women practicing some other means of birth control. 126

127,129

1 1 8

130

114

115

109,114,116

1 1 6

Pregnancy Pregnancy is accompanied by a gradual worsening of chronic gingivitis which improves following deliv­ ery, however, areas of healthy gingiva are not affected. It has been speculated that increased levels of circulating hormones may in some way be responsi­ ble . The reproductive organs are the primary targets of estrogen and progesterone but basic reactions may oc­ cur in other tissues as well. Sex hormones or their metabolites are found in gin­ giva. Their concentrations are elevated in in­ flamed gingiva and may be influential in the etiology of gingival exudation and inflammation but the significance of these findings is difficult to assess. Hugoson summarized a series of experiments done in collaboration with others. H i s observations included: (1) Gingivitis became more severe during pregnancy without any increase in bacterial plaque accumulation; (b) Injection of estrogen combined with progesterone increased the amount of exudate obtainable from either chronically inflamed or healing gingiva; (c) Progester­ one in some way made regenerating gingival tissues more sensitive to irritation; (d) Progesterone-treated dogs had a larger number of polymorphonuclear luekocytes within the sulcular epithelium than controls; (e) Healing gingival wounds in progesterone treated dogs 1 1 7 , 1 2 1

119

1 2 2 , 1 2 4

122, 1 2 3 , 1 2 5

119

Puberty Puberty is often accompanied by increased gingival inflammation which appears to be an exaggerated re­ sponse to local irritants. B a e r has said that puberty gingivitis and pregnancy gingivitis are probably due to similar systemic factors. Sutcliffe's data indicated that 127 circumpubertal youngsters had more inflamed gin­ gival sites than would be statistically expected consider­ ing the number who had dirty teeth. H e attributed the discrepancy to a heightened response to local irri­ tants and suggested that it was related to the concentra­ tion of circulating sex hormones. 12

131

132

Other Endocrine

Secretions

Studies on the relationship of other endocrine secre­ tions to the etiology of periodontal disease reveal: that an excess of cortisone leads to subdued inflammatory cell reactions in infections, gingivitis and periodontitis; areas of diminished or absent fibroplasia in the peri­ odontal ligament and osteoporosis of alveolar bone, vertebrae and appendages of marmosets. Hydrocor­ tisone acetate significantly decreased the gingival con­ centrations of hyaluronic acid, chondroitin sulfate and heparin in rats. High fluoride concentrations in the drinking water gave a measurable degree of protection against resorption induced by excessive parathyroid hormones in marmosets. Hypothyroidism created in rats was associated with a lack of continuity between collagen fibers of the periodontium which increased with t i m e . Thyrocalcitonin failed to protect the al­ veolar bone of hamsters in which periodontal disease had been i n d u c e d . 133

134

135

136

137

Stress Stress induced in rats was accompanied by reduced oxygen consumption of the gingiva. Eleven cases of 138

Volume 48 Number 9

Chronic Inflammatory

advanced periodontal disease in Viet N a m War vet­ erans aged 22 to 32 could not be accounted for by local factors. A l l had served under stressful conditions. The author suggested that emotional stress was a key etio­ logic factor and termed the condition "periodontal emotional stress syndrome." Haskell found significantly greater interdental bone loss among pilots subjected to high noise and vibration levels while flying piston engine aircraft than among jet aircraft pilots of similar age and logged flying time who were subjected to negligible in-flight noise levels. Unfortunately no oral hygiene data were se­ cured. 139

140

Aging Studies continue to show that the prevalance and severity of periodontal disease and the degree of tissue destruction and tooth loss increase with age. It is generally agreed that periodontitis is a cumulative process and progressive destruction of the periodontal tissues with age is related to the length of time the tissues are exposed to bacterial plaque. Age changes in the periodontal tissue of humans and laboratory animals continue to be r e p o r t e d . Some of these changes may affect the disease experience of the perio­ dontium; however, there has been little documentation regarding their significance and contribution to the initiation and progression of periodontal disease. It has been found that gingivitis developed faster and was more severe in the elderly than in the y o u n g . N o differences were observed in percentage distribution of various plaque bacteria. The authors suggested that aging alters the immune response to plaque organisms. A study in aging rats found thicker cementum, wider periodontal ligament and decreased alveolar bone height in the interradicular area of multirooted teeth. These alterations may affect the initiation and progres­ sion of periodontal disease. O n the other hand, age could not be significantly correlated with the presence of gingivitis, the amount of accumulated debris and calculus or the depth of periodontal pockets. A n increase in width of at­ tached gingiva with increasing age was reported. The mucogingival junction apparently remains at its geneti­ cally predetermined location while healthy marginal gingiva accompanies the teeth as they move occlusally throughout l i f e . This might offer some protection against gingivitis associated with inadequate gingiva. Apical migration of the dentogingival junction (passive eruption) had been regarded as a physiologic concomi­ tant of aging. However, more recent reports indicate that such exposure is a consequence of pathol141

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ogy

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A variety of genetic disorders is accompanied by periodontal involvement. A c a t a l a s i a and PapillonLefvre S y n d r o m e show extensive destruction of 157

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periodontal support. H y p o p h o s p h a t a s i a leads to premature loss of the deciduous dentition. Additional evidence for periodontosis as a genetic disorder re­ cently has been published. However, the mecha­ nisms of periodontal involvement in these entities do not appear to be related closely to those of gingivitis or periodontitis. Chediak-Higashi syndrome occurs in humans, cattle, mink and mice. It is characterized by defective polymorphonuclear luekocytes and increased suscepti­ bility to infection. T e m p l e described four cases in humans. Two youngsters had severe gingivitis, tooth mobility, periodontal pockets and marked localized al­ veolar bone loss. The other two, brothers aged 19 and 20, had been edentulous for about 6 years because of "advanced pyorrhea." Lavine et a l . observed more severe and widespread gingival and periodontal disease in mink with Chediak-Higashi than in control animals. Animals with this syndrome may prove valuable in determining whether the role of the neutrophil is pro­ tective or destructive in the pathogenesis of periodonti­ tis. Persons afflicted with Down's syndrome react se­ verely to bacterial infections on their teeth and are more susceptible to periodontal disease than other indi­ viduals. This premise was supported by B r o w n who found that 3 5 % of mongoloids developed necro­ tizing ulcerative gingivitis compared to 4 % of nonmongloloid retardates in the same institution over a 10-year period. Down's syndrome patients treated with topical kanomycin sulfate paste developed less plaque and less gingivitis than a similar group treated with a placebo paste. Cutress concluded that an institutional envi­ ronment increased the susceptibility of mongoloids to periodontal disease. Gorlin et a l . pointed out the difficulty in studying the effect of multifactorial inheritance upon periodon­ tal disease. However, some attempts have been made. The periodontal index was distinctly higher among chil­ dren of Hawaiian ancestry than in other children living in Hawaii. A significant association between gingivitis and racial intermixture was shown even when the effect of oral hygiene and other environmental effects were accounted f o r . Recessive genes may be involved in gingivitis. A broad correlation was found between blood groups and periodontal disease which may also implicate genetic factors in the etiology of gingivitis and periodontitis. 164, 1 6 5

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Hematologic

Factors

Leukemias can be accompanied by enlargement, ul­ ceration, hemorrhage and varying degrees of inflam­ mation of the g i n g i v a . A positive correlation has been demonstrated between the gingival and plaque indices of 22 patients with various types of leukemia. Scaling and plaque control decreased their levels of gingivitis. Periodontal hard tissue alterations in leu­ kemia have not been as widely reported as the soft 1 7 7 ,1 7 8

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Pennely Keagle

tissue changes; however crestal alveolar bone destruc­ tion, loss of lamina dura and widening of periodontal ligament space caused by leukemic infiltrates have been observed. Severe periodontal destruction was reported in preleukemic syndrome, a clinical designation for hema­ tologic abnormalities which precede the development of overt leukemia. The authors suggested that neutro­ penia, impairment of phagocytic activity and decreased effectiveness of immune mechanisms, all of which are found in preleukemic syndrome, may be responsible for the periodontal destruction. Agranulocytosis (neutropenia, granulocytopenia) oc­ curs in several variations —acute, cyclic, recurrent, sub­ acute and chronic. Except for the cyclic type its etiology generally has been attributed to ingestion of certain drugs and chemicals, most of which are coal tar derivatives, gold or arsenic c o m p o u n d s . True cyclic neutropenia is idiopathic. Recently neutro­ penia in two siblings was termed hereditary and an­ other case designated as congenital. Periodontal findings are generally similar —severe gingival inflam­ mation with necrotic ulceration, recession and ad­ vanced alveolar bone d e s t r u c t i o n . It is possible that neutrophils which transmigrate the junctional epithelium of inflamed gingiva protect the periodontium from invasion by bacteria or their prod­ ucts, though no evidence for this protective role has been presented. Anemia. N o significant correlation between peri­ odontal index and hematocrit, hemoglobin and red blood count could be found in a study of 752 periodon­ tal patients. Infectious mononucleosis has been reported to be accompanied by swelling and redness of the marginal gingiva and interdental papilla. However, no gingival alterations were found in 15 patients with diagnosed infectious mononucleosis. Thirty-three patients with acute necrotizing ulcerative gingivitis were subjected to hematologic studies and the Monotest. While the symptoms of these patients were similar to those re­ ported characteristic of infectious mononucleosis, no lymphocytosis or atypical lymphocytes were found and all Monotests were negative. It is recognized that the response to bacterial plaque can be modified by systemic factors. The altered re­ sponse seen during pregnancy seems to have been at least partially explained. However, the mechanisms by which most systemic factors modify the response to local irritants are unknown, nor is it known whether any such factors by themselves can initiate inflamma­ tory periodontal disease. 180,181

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has been studied in animals but apparently not in hu­ mans. Although rodents developed more extensive periodontal lesions on a hard granular d i e t than a soft one, studies of dogs and ferrets indicated the benefits of a hard diet in the maintenance of periodon­ tal health. Cats maintained on a nutritionally adequate soft diet for 6 months to 2 years developed severe periodontal lesions and dogs fed a soft diet devel­ oped more bacterial plaque and gingivitis than dogs on a hard diet. 1 9 2 , 1 9 3

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Protein A variety of animals subjected to protein-deficient diets demonstrated similar alterations to the periodon­ tal tissues. Osteoporosis of the supporting bone, degen­ erative changes in the periodontal ligament and retar­ dation in deposition of cementum were common histo­ logic f i n d i n g s . Protein deficiency in animals without local marginal irritants caused changes in the attachment apparatus without affecting the level of the junctional epithelium. Protein deprivation and dental deposits in dogs caused gingival inflammation, periodontal pockets and rapid and advanced loss of the supporting bone. A more severe local lesion also occurred in response to gingival irritants in protein-deprived rats than in the controls. Advanced periodontal disease has been reported in rural Nigerians who eat protein-deficient diets and children with a severe protein deficiency have had more acute cases of necrotizing ulcerative gingivitis and sig­ nificantly higher PI and P M A values than a similar number of healthy children. A series of human studies demonstrated a reduction in sulcus depth, gingival i n f l a m m a t i o n and tooth mobility following protein supplementation. Other human studies compared local therapy to protein supplementation and to the combined procedures. The best results occurred when both protein supplementa­ tion and a prophylaxis were e m p l o y e d . 193,198-201

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Calcium A calcium-deficient diet in young rats caused osteo­ porosis of the alveolar b o n e , and a reduction in periodontal ligament fibers and secondary cemen­ t u m . Similar studies involving adult rats caused only slight alterations, if any, in the alveolar bone and sec­ ondary cementum. In a series of studies, nutritional secondary hyperpar­ athyroidism was induced in beagles by feeding them a low calcium, high phosphorus diet. This resulted in mobility of incisor teeth and pronounced loss of interradicular bone in the molar areas. Calcified deposits formed on teeth in both the calcium deficient animals and controls but loss of alveolar bone occurred only in the calcium-deficient animals. Repletion with added dietary calcium reversed the bone loss and resulted in a disappearance of clinical signs. 2 1 3 , 2 1 4

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NUTRITION A N D PERIODONTAL DISEASE

The role of nutrition in the etiology of periodontal disease will be discussed in relation to food consistency, protein, calcium and vitamins A , B complex, C and E . The effect of food consistency on periodontal health

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Chronic Inflammatory

In an investigation of humans with periodontal dis­ ease a supplemenation of 1000 mg of calcium per day reduced inflammation, pocket depths and tooth mobil­ ity and increased bone density. O n the basis of the animal and human studies, it has been hypothesized that dietary calcium deficiency causes osteoporosis of the alveolar process which represents the initial lesion in periodontal disease. This is progressively followed by bone resorption, recession of the alveolar bone crest, tooth mobility and secondary g i n g i v i t i s . In a recent study dogs developed nutritional hyper­ parathyroidism following a calcium-deficient phospho­ rus rich diet. This resulted in osteopenia in the alveolar process but in contrast to the previous studies did not cause an increase in tooth mobility or gingivitis in the absence of plaque. In the presence of plaque, patholog­ ical pockets developed but the degree of attachment loss did not exceed loss in control animals on a normal diet. A group of rats on a hypocalcemic diet without marginal irritation and inflammation developed varying degrees of interradicular alveolar osteoporosis with lit­ tle effect on the other periodontal structures. Local irritation created by interproximal stainless steel wires caused inflammation, apical migration of the epithelial attachment and marginal alveolar resorption to the same degree in rats on a normal and hypocalcemic diet. In the mature calcium-deficient rat no changes were noted in the collagen fibers of the periodontal ligament or to cemental resorption. In humans advanced periodontal disease has been reported in association with senile osteoporosis and an increase in alveolar bone resorption and loss of lamina dura has been reported in association with achlorhydria, a condition in which calcium absorption is defective. 219

218,220

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the g i n g i v a , periodontal f i b e r s , and alveolar bone. The gingival tissues of dogs with deficiencies in nia­ cin, riboflavin, pyridoxine, folic acid and panthothenic acid with and without local irritation were compared with each other and with controls and no differences were noted grossly or histologically. The severity of the involvement did parallel the degree of deficiency, and toothbrushing was effective in preventing gingivitis in all except two of the deficient dogs. In an extensive human survey, persons with clinical signs of Vitamin B complex deficiency showed, on an average, higher periodontal disease scores even when oral hygiene was constant. Other human studies, however, found no correlation between the status of periodontal health and urinary levels of thiamin and riboflavin. In a recent study involving humans, a supplementa­ tion of folic acid reduced the flow of gingival exudate approximately 5 0 % while the plaque levels for the supplemented and control groups were basically the same , 234

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2 3 6

Vitamin C Animals on an ascorbic acid free or deficient diet demonstrated tooth m o b i l i t y , hemorrhage and loss of fibers in the periodontal l i g a m e n t , osteoporosis of the alveolar process and gingival inflammation. Gingival inflammation in the ascorbic acid deficient animals is generally considered to be the result of an exaggerated reaction to local irritants rather than a deficiency in ascorbic a c i d . Human investigations of the relationship between the presence and severity of periodontal disease and plasma or serum ascorbic levels have not been in agree­ ment. The studies which failed to show a positive correlation are supported by observations of humans on ascorbic acid-deficient diets. These subjects developed signs and symptoms of scurvy, but either failed to show gingival changes or developed them late in the course of the deficiency state. The role of ascorbic acid in periodontal health also has been studied by human clinical trials. Ascorbic acid supplementation in combination with local therapy provided a greater reduction in gingivitis, sulcular depth, and tooth mobility than local therapy alone. A n improvement in gingivitis also was noted following the daily intake of orange and lemon j u i c e and with the combination of Vitamin C and water soluble bioflavin acids. In studies involving members of the Royal Canadian A i r Force, local therapy was employed initially to resolve gingivitis to the maximum level. A 75-mg daily supplement of ascorbic acid was noted to delay a recurrence of the signs of inflammation over that which occurred when only 10 mg or 25 mg of ascorbic acid was p r o v i d e d . In other investigations, however, ascorbic acid sup­ plementation has not improved the periodontal status 2373

237a

237b

2 3 7 3 , 2 3 8 , 2 3 9

240-242

229,243-246

Vitamin A Animals placed on a diet deficient in Vitamin A demonstrated alterations in the integrity of epithe­ lium, resorption of cementum and osseous changes. Rats with a Vitamin A deficiency plus local irritants developed deeper periodontal pockets than adequately nourished controls with local irritation of the same intensity. Human studies of the relationship between the inci­ dence and severity of periodontal disease and Vitamin A deficiency have reported either a slight correlation or no correlation. In the latter study, serum Vitamin A levels did not demonstrate an association with the patients' periodontal status. 225

225

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228

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B Complex

Vitamins

The role of Vitamin B complex deficiency in the etiology of periodontal disease was studied by depriv­ ing animals of the various subtances which constitute the B complex group of v i t a m i n s . The deficiency states caused destructive changes of varying degrees in 231-233

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of individuals. Ascorbic acid has been provided in syn­ thetic f o r m in conjunction with other vitamins and in the form of fruit and vegetables. Gingival inflammation did not improve with any of these meth­ ods of s u p p l e m e n t a t i o n nor did 300 mg daily for a 6-week period reduce tooth m o b i l i t y . Supple­ ments of 250 mg of ascorbic acid daily also failed to affect ascorbic acid levels of gingival tissue. 2 5 5 - 2 5 7

254

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Vitamin E The role of Vitamin E deficiency in the etiology of periodontal disease has been studied recently. Four­ teen patients with periodontal disease took 800 mg of Vitamin E daily and were compared with 12 controls who were provided with a placebo. After 21 days the sulcus fluid flow of the Vitamin E-treated patients ex­ hibited a significant decrease while the placebo-treated patients did not change. The authors hypothesized that Vitamin E inhibited the synthesis of prostaglandins which are associated with and perhaps contribute to inflammatory changes, besides serving as a possible cause of alveolar bone resorption. In another investigation, Vitamin E levels were mea­ sured in 24 patients, half of whom had periodontal disease. There was no significant difference in the levels of serum Vitamin E in the two groups. Certain factors must be considered in the studies of nutritionally deficient animals. The periodontal changes noted in the frequently used young animals do not accurately p o r t r a y changes in adult animals, and severe or total deprivation of the nutriment or nutri­ 260

261

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ments under study is not often applicable to clinical human problems.. Furthermore, the principal features of human periodontal disease, including periodontal pocket formation with loss of attachment and crestal bone, did not occur in deficient animals in the absence of local irritants. The results of animal studies, plus information pro­ vided by human surveys and clinical trials, suggest that nutrition plays a modifying rather than initiating role in the etiology of periodontal disease. The evidence that bacteria initiate gingival inflam­ mation and cause periodontal attachment loss is im­ pressive. Predisposing etiological factors which facili­ tate the accumulation of bacteria and interfere with its removal must receive the clinicians foremost attention. Although evidence that nutrition and systemic dis­ ease play a major role in the etiology of chronic inflam­ matory periodontal disease is far less convincing, clini­ cians should consider all possible etiological factors in the management of patients with periodontal disease. REFERENCES

1. D r u m , W . : A new concept of periodontal disease. J Periodontol. 46: 504, 1975. 2. Everett, F . , and Kramer, G . : The disto-lingual groove in the maxillary lateral incisor: A periodontal hazard. J Perio­ dontol 43: 352, 1972. 3. L e e , K . , L e e , E . , and Poon, K . : Palato-gingival grooves in maxillary incisors. Br Dent J 124: 14, 1968.

4. Prichard, J . : Advanced Periodontal Disease. Phila. 1965. 5. Simon, J . , G l i c k , D . , and Frank, A . : Predictable endo­ dontic and periodontic failures as a result of radicular abnor­ malities. Oral Surg 31: 823, 1971. 6. Masters, D . , and Hoskins, S.: Projection of cervical enamel into molar furcations. J Peridontol 35: 49, 1964. 7. Grewe, J . , Meskin, L . , and M i l l e r , T . : Cervical enamel projections: Prevalence, location and extent; with associated periodontal implications. J Periodontol 36: 460, 1965. 8. L i e b , A . , Berdon, J . , and Sabes, W . : Furcation involve­ ments correlated with enamel projections from the cemento enamel junction. J Periodontol 38: 330, 1967. 9. Risnes, S.: The prevalence and distribution of cervical enamel projections reaching into the bifurcation on human molars. Scand J Dent Res 87: 4 1 3 , 1974. 10. Tsatas, B . , M a n d i , F . and K e r a n i , S.: Cervical enamel projections in the molar teeth. J Periodontol 44: 312, 1973. 11. Andrews, N . : Periodontal significance of cervical en­ amel projections. J Can Dent Assoc 41: 50, 1975. 12. Ramfjord, S., K e r r , S., and A s h , M . : World Work­ shop in Periodontics. Univ. of Mich. A n n A r b o r , 1966. 13. Paunio, K . : The role of malocclusion and crowding in the development of periodontal disease. Int Dent J 23: 420, 1973. 14. M c C o m b i e , F . , and Stothard, D . : Relationship be­ tween gingivitis and other dental conditions. J Can Dent Assoc 30: 506, 1964. 15. G o u l d , M . , and Picton, D . : The relation between irregularities of the teeth and periodontal disease. Br Dent J 121: 20, 1966. 16. Alexander, A . G . : Habitual mouth breathing and its effect on gingival health. Parodontologie 24: 49, 1970. 17. Geiger, A . , Wasserman, B . , Thompson, R . , and Turgeon, L . : Relationship of occlusion and periodontal disease. Part V . Relation of classification of occlusion to periodontal status and gingival inflammatio'n. J Periodontol 43: 554, 1972. 18. Geiger, A . , Wasserman, B . , and Turgeon, L . : Rela­ tionship of occlusion and periodontal disease. Part V I . Rela­ tion to anterior overjet and overbite to periodontal destruc­ tion and gingival inflammation. J Periodontol 44: 150, 1973. 19. M i l l e r , J . , and H o b s o n , P . : The relationship between malocclusion, oral cleanliness, gingival conditions and dental caries in school children. Br Dent J 111: 4 3 , 1961. 20. Beagrie, G . , Thompson, G . , and Basu, M . : Tooth position and anterior bone loss in skulls. Br Dent J 129: 471, 1970. 2 1 . Geiger, A . : Occlusion in periodontal disease. J Perio­ dontol 36: 387, 1965. 22. Geiger, A . , Wasserman, B . , and Turgeon, L . : Rela­ tionship of occlusion and periodontal disease. Part VIII. Relationship of crowding and spacing to periodontal destruc­ tion and gingival inflammation. / Periodontol 45: 43, 1974. 23. G l i c k m a n , I.: Clinical Periodontology. Philadelphia, W . B . Saunders C o . , 1972. 24. Larato, D . : Relationship of food impaction to inter­ proximal intrabony lesions. J Periodontol 42: 237, 1971. 25. O ' L e a r y , T . , Badell, M . , and Bloomer, R . : Interprox­ imal contact and marginal ridge relationships in periodontally healthy young males classified as to orthodontic status. J Periodontol 46: 6, 1975. 26. Colzer, J . , and Sprawson, E . : Dental Surgery and Pathology, ed 6, New Y o r k , Longmans, Green and Co., 1938. 27. James, W . , and Hastings, S.: Discussion of mouth­ breathing and nasal obstruction. Proc Roy Soc Med 25:1343, 1932. 28. L i t e , T . , D i M a i o , D . and Beckman, L . : Gingival pathosis in mouthbreathers. Oral Surg 8: 382, 1955.

Volume 48 Number 9

29. Jacobson, L . : M o u t h breathing and gingivitis. J Perio­ dont Res 8: 269, 1973. 30. Klingsberg, J . Cancellaro, L . and Butcher, E . : Effect of air drying on rodent oral mucous membrane. A histologic study of simulated mouth breathing. J Periodontol 32: 38, 1961. 31. Jacobson, L . , and Linder-Aronson, S.: Crowding and gingivitis: A comparison between mouthbreathers and nonmouthbreathers. Scand J Dent Res 80: 500, 1972. 32. Sutcliffe, P . : Chronic anterior gingivitis an epidemio­ logical study in school children. Br Dent J 125: 47, 1968. 3 3 . Buckley, L . : The relationship between malocclusion and periodontal disease. J Periodontol 43: 415, 1972. 34. Stahl, S.: The need for orthodontic treatment: A per­ iodontist's point of view. Int Dent J 25: 242, 1975. 35. G o l d m a n , H . , and Cohen, D . : Periodontal Therapy. ed. 5, p. 8 3 2 - 3 , St. Louis, The C . V . Mosby C o . , 1973. 36. Prichard, J . : The effect of bicuspid extraction ortho­ dontics on the periodontium. J Periodontol 46: 534, 1975. 37. Placek, M . , Skach, M . , and Mrklas, L . : Significance of the labial frenum attachment in periodontal disease in man. Part I. Classification and epidemiology of the labial frenum attachment. J Periodontol 45: 891, 1974. 38. Placek, M . , Skach, M . , and Mrklas, L . : Significance of the labial frenum attachment in periodontal disease in man. Part II. A n attempt to determine the resistance of periodontium. J Periodontol 45: 895, 1974. 39. Bergenholtz, A . , and Hugoson, A . : Vestibular sulcus extension surgery in cases with periodontal disease. J Perio­ dont Res 2: 2 2 1 , 1967. 4 0 . W a r d , V . : The depth of the vestibular fornix in the mandibular anterior region in health. J Periodontol 47: 651, 1976. 4 1 . L a n g , M . , and Löe, H . : The relationship between the width of keratinized gingiva and gingival health. J Periodon­ tol 43: 623, 1972. 42. M a y n a r d , J . Jr., and Ochsenbein, C : Mucogingival problems prevalence and therapy in children. J Periodontol 46: 543, 1975. 4 3 . Hirschfeld, I.: A study of skulls in the American Museum of Natural History. J Dent Res 5: 241, 1923. 44. Larato, D . : Alveolar plate fenestrations and dehis­ cences of the human skull. Oral Surg 29: 816, 1970. 4 5 . Novaes, A . , Ruben, M . , K o n , S., Goldman, H . , and Novaes, A . Jr.: The development of the periodontal cleft. A clinical and histopathologic study. J Periodontol 46: 701, 1975. 46. Batenhorst, K . , Bowers, G . , and Williams, J . : Tissue changes resulting from facial tipping and extrusion of incisors in monkeys. J Periodontol 45: 660, 1974. 4 7 . Wingard, C , and Bowers, G . : The effects on facial bone from facial tipping of incisors in monkeys. J Periodontol 47: 450, 1976. 4 8 . Wheeler, R . C : Complete crown form and the perio­ dontium. J Prosthet Dent 11: 722, 1961. 49. Wagman, S. S.: The role of coronal contour in gingival health. J Prosthet Dent 37: 280, 1977. 50. Perel, M . L . : A x i a l crown contours. J Prosthet Dent 25: 642, 1971. 5 1 . Herlands, R . E . , Lucca, J . J . , and Morris, M . L . : Forms, contours and extensions of full coverage in occlusal reconstruction. Dent Clin North Am p. 147, March, 1962. 52. M o r r i s , M . L . : Artificial crown contours and gingival health. J Prosthet Dent 12: 1146, 1962. 53. Yuodelis, R . A . , Weaver, J . D . , and Sapkos, S.: Facial and lingual contours of artificial complete crown resto­ rations and their effects on the periodontium. J Prosthet Dent 29: 6 1 , 1973. 54. K o i v u m a a , K . K . , andWennstrom, A . : A histological investigation of the changes in gingival margins adjacent to

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gold crowns. Odontol Tids 68: 373, 1960. 55. Sackett, B . P . , and Gildenhuys, R . R . : The effect of axial crown over contour on adolescents. J Periodontol 47: 320, 1976. 56. Eissmann, H . F . , Radke, R . A . , and N o b l e , W . H . : Physiologic design criteria for fixed dental restorations. Dent Clin North Amer 15: 543, 1971. 57. G i l m o r e , N . , and Sheiham, A . : Overhanging dental restorations and periodontal disease. J Periodontol 42: 8, 1971. 58. Trott, J . R . , and Sherkat, A . : Effect of class II amal­ gam restorations on health of the gingiva: A clinical survey. J Can Dent Assoc 30: 766, 1964. 59. B j o r n , A . L . , B j o r n , H . , and G r k o v i c , B . : Marginal fit of restorations and its relation to periodontal bone level. Part II. Crowns. Odontol Revy 21: 337, 1970. 60. B j o r n , A . L . , B j o r n , H . , and G r k o v i c , B . : Marginal fit of restoration and its relation to periodontal bone level. Part I. Metal fillings. Odontol Revy 20: 311, 1969. 61. Stein, R . S., and G l i c k m a n , I.: Prosthetic considera­ tions essential for gingival health. Dent Clin North Am 4: 77, 1960. 62. T y l m a n , S. D . : The Theory and Practice of Crown and Fixed Partial Prosthodontics. ed. 6, p 94. St. Louis, The C . V . Mosby C o . , 1970. 63. Johnston, J . F . , Phillips, R . W . , and D y k e m a , R . W . : Modern Practice in Crown and Bridge Prosthodontics, ed 3, p 4 5 1 , Philadelphia, W . B . Saunders Company, 1971. 64. M i n k l e r , J . S.: Simplified full coverage preparations. Dent Clin North Am 9: 355, 1965. 65. M a r c u m , J . S.: The effect of crown margin depth on gingival tissues. J Prosthet Dent 17: 479, 1967. 66. Pini, C . E . : Co-report hygenie considerations in crown and bridge prosthesis. Int Dent J 8: 357, 1958. 67. Silness, J . : Periodontal condition in patients treated with dental bridges. III. The relationship between the loca­ tion of the crown margin and the periodontal condition. J Periodont Res 3: 225, 1970. 68. Silness, J . : Periodontal conditions in patients treated with dental bridges. II. The influence of full and partial crowns on plaque accumulation. Development of gingivitis and pocket formation. J Periodont Res 5: 218-224, 1970. 69. Silness, J . , and O h m , E . : Periodontal conditions in patients treated with dental bridges. V . Effects of splinting adjacent abutment teeth. J Periodont Res 9: 121, N o . 2 1974. 70. Silness, J . : Periodontal conditions in patients treated with dental bridges. I V . The relationship between the pontic and the periodontal condition of the abutment teeth. J Perio­ dont Res 9: 50, N o . 1, 1974. 71. Silness, J . : Periodontal conditions in patients treated with dental bridges. J Periodont Res 5: 60, 1970. 72a. Silness, J . , and T . Hegdahl: A r e a of the exposed zinc phosphate cement surfaces in fixed restorations. Scand J Dent Res 78: 163, 1970. 72b. Newcomb, G . M . : The relationship between the lo­ cation of subgingival crown margins and gingival inflamma­ tion . J Periodontol 45: 151, 1974. 73. Alexander, A . G . : Periodontal aspects of conservative dentistry. Br Dent J 125: 111, 1968. 74. Bergman, B . , Hugoson, A . , and Olsson, C : Periodontal and prosthetic conditions in patients treated with removable partial dentures and artificial crowns. Acta Odon­ tol Scand 29: 621, 1971. 75. Larato, D . C : Effects of artificial crown margin ex­ tension and tooth brushing frequency on gingival pocket depth. J Prosthet Dent 34: 640, D e c . 1975. 76. Karlsen, K . : Gingival reactions to dental restorations. Acta Odontol Scand 28: 895, 1970. 77. Richter, W . A . , and V e n o , H . : Relationship of crown margin placement to gingival inflammation. J Prosthet Dent

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30: 157, 1973. 78. B j o r b y , A . , and Löe, H . : The relative significance of different local factors in the initiation and development of periodontal inflammation. Abstract J Periodont Res 2: 76, 1967. 79. Waerhaug, J . : Effect of rough surfaces upon gingival tissue. J Dent Res 35: 323, 1956. 80. Sotres, L . S., Huysen, G . , and Gilmore, H . W . : A histologic study of gingival tissue response to amalgam, sili­ cate and resin restorations. J Periodontol 40: 543, 1969. 8 1 . Waerhaug, J . : Histological considerations with govern where the margins of restorations should be located in rela­ tion to the gingiva. Dent Clin North Am pp 161-176, March 1960. 82. Renggli, H . H . , and Regolati, B . : Gingival inflamma­ tion and plaque accumulation by well-adapted supragingival and subgingival proximal restorations. Helv Odontol Acta 16: 99,1972. 83. N o r m a n n , W . , Regaloti, B . , and Renggli, H . H . : Gingival reaction to well-fitted subgingival proximal gold inlays. J Clin Periodontol 1: 120-125, 1974. 84. Stein, R . S.: Pontic-residual ridge relationship: A re­ search report. J Prosthet Dent 16: 251, 1966. 85. Cavazos, E . : Tissue response to fixed partial denture pontics. J Prosthet Dent 20: 143, 1968. 86. A l l i s o n , J . R . , and Bhatia, H . L . : Tissue changes under acrylic and porcelain pontics., (abstr.). J Dent. Res 37: 66, 1958. 87. Pine, B . : Pontics for gold-acrylic resin fixed partial dentures. J Prosthet Dent 12: 347, 1962. 88. C l a y t o n , J . , and G r e e n , E . : Roughness of pontic ma­ terials and dental plaque. J Prosthet Dent 23: 407, 1970. 89. Henry, P . , Johnston, J . , and Mitchell, D . : Tissue changes beneath fixed partial dentures. J Prosthet Dent 16: 937-947, 1966. 90. Podshadley, A . G . : Gingival response to pontic. J Prosthet Dent 19: 5 1 - 5 7 , 1968. 91. Hirshberg, S. M . : The relationship of oral hygiene to embrasure and pontic design-A preliminary study. J Prosthet Dent 27: 26, 1972. 92. Waerhaug, J . , and Zander, H . A . : Reaction of gingi­ val tissues of self-curing acrylic restorations. J Am Dent Assoc. 54: 760, 1957. 93. Zander, H . A . : Effect of silicate cement and amalgam on the gingiva. J Am Dent Assoc 55: 1 1 , 1 9 5 7 . 94. Frank, R . M . ; B r i o n , M . , and DeRouffignac, M . : Ultrastrucutral gingival reactions to gold foil. J Periodontol 46: 6 1 4 , 1 9 7 5 . 95. Larato, D . C : Influence of silicate cement restora­ tions on gingiva. J Prosthet Dent 26: 186, 1971. 96. A p p , G . R . : Effect of silicate, amalgam and cast gold on the gingiva. J Prosthet Dent 11: 522, 1961. 97. Kawahara, H . , Yamagami, A . , and Nakamura, Jr., M . : Biological testing of dental material by means of tissue culture. Int Dent J 18: 443, 1968. 98. Kaqueler, J . C , and Weiss, M . B . : Plaque accumula­ tion on dental restorative materials. (Abstr.) 6 1 5 , 1 . A . D . R . Program and Abstr. of Papers. March 16-19, 1970. 99. Wise, M . D . , and D y k e m a , R . W . : The plaque retain­ ing capacity of four dental materials. J Prosthet Dent 33: 178, 1975. 100. N o r m a n , R . D . , M e h r a , R.. V . , Swartz, M . L . , and Phillips, R . W . : Effects of restorative materials on plaque composition. J Dent Res 51: 1576, 1972. 101. Skjarland, K . K . : Plaque accumulation on different dental filling materials. Scand J Dent Res 81: 538, 1973. 102. Bissada, M . F . , Ibrahim, S. I., and Barsoum, W . M . : Gingival response to various types of removable partial den­ t u r e s . / Periodontol 45: 651, 1974.

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103. Carlsson, G . E . , Hedegard, B . , and Koivumaa, K . K . : Studies in partial dental prosthesis. I V . Final results of a 4-year longitudinal investigations of dentogingivally sup­ ported partial dentures. Acta Odontol Scand 23: 443, 1965. 104. Seeman, S.: Study of the relationship between peri­ odontal disease and the wearing of partial dentures. Aust Dent J 8: 206, 1963. 105. Carlsson, G . E . , Hedegard, B . , and K o i v u m a a , K . K . : Studies in partial dental prosthesis. II. A n investigation of mandibular partial dentures with double extension saddles. Acta Odontol Scand 19: 215, 1961. 106. Carlsson, G . E . , Hedegard, B . , and K o i v u m a a , K . K . : Studies in partial dental prosthesis. III. A longitudinal study of mandibular partial dentures with double extension saddles. Acta Odontol Scand 20: 95, 1962. 107. D e r r y , A . , and Bertram, V . : A clinical survey of removable partial dentures after 2 years useage. Acta Odon­ tol Scand 28: 581, 1970. 108. O ' L e a r y , T . J . , and R u d d , K . D . : Stabilizing peri­ o d o n t a l ^ weakened teeth by using guide plane removable partial dentures. A preliminary report. J Prosthet Dent 16: 721, 1966. 109. H o v e , K . , and Stallard, R . : Diabetes and the peri­ odontal patient. J Periodontol 41: 713, 1970. 110. C o h e n , D . , Friedman, L . , Shapiro, J . , K y l e , G . , and Franklin, S.: Diabetus mellitus and periodontal disease: Two year longitudinal observations, Part I. J Periodontol 41: 709, 1970. 111. Tuckman, M . , Kaslick, R . , Shapiro, W . , and Chasens, A . : The relationship of glucose tolerance to periodontal status. J Periodontol 41: 513, 1970. 112. Bernick, S., C o h e n , D . , B a k e r , L . , and Laster, L . : Dental disease in children with diabetes millitis.7 Periodontol 46: 241, 1975. 113. B a y , I., A i n a m o , J . , and G a d , T . : The response of young diabetics to periodontal treatment. J Periodont 45: 806, 1974. 114. Campbell, M . : The effect of age and the duration of diabetes on the width of the basement membrane of small vessels. Aust Dent J 19: 414, 1974. 115. Frantzis, T . , Reeve, C , and B r o w n , A . : The ultrasturcture of capillary basement membranes in the attached gingiva of diabetic and nondiabetic patients with periodontal disease. J Periodontol 42: 406, 1971. 116. Listgarten, M . , Ricker, F . , Laster, L . , Shapiro, J., and C o h e n , D . : Vascular basement lamina thickness in the normal and inflamed gingiva of diabetics and non-diabetics./ Periodontol 45: 676, 1974. 117. C o h e n , D . , Shapiro, J . , Friedman, L . , K y l e , G . , and Franklin, S.: A longitudinal investigation of the periodontal changes during pregnancy and fifteen months post partium: Part II. J Periodontol 42: 653, 1971. 118. C o h e n , D . , Friedman, L . , Shapiro, J . , and K y o e , G . : A longitudinal investigation of the periodontal changes dur­ ing pregnancy. J Periodontol 40: 563, 1969. 119. Hugoson, A . : Gingival inflammation and female sex hormones. J Peridont Res (suppl.) 5, 1970. 120. Löe, H . : Periodontal changes in pregnancy. J Perio­ dontol 36: 2 0 9 , 1 9 6 5 . 121. N y m a n , S.: Studies on the influence of estradiol and progesterone on granulation tissue. J Periodont Res suppl. no. 7, 1971. 122. E l A t t a r , T . : Metabolism of progesterone 7-3H in vitro in human gingiva with periodontitis. J Periodontol 42: 721,1971. 123. E l A t t a r , T . , R o t h , G . , and Hugoson, A . : Compara­ tive metabolism of - 1 4 C progesterone in normal and chroni­ cally inflamed human gingival tissues. J Periodont Res 8: 79, 1973.

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124. Formicola, A . , Weatherford, T . I l l , and Grupe, H . : The uptake of H estradiol by the oral tissues of rats. J Periodont Res 5: 269, 1970. 125. E l A t t a r , T . , and Hugoson, A . : Comparative metab­ olism of female sex steroids in normal and chronically in­ flamed gingiva of the dog. J Periodont Res 9: 284, 1974. 126. L i n d h e , J . , and Branemark, P . : Experimental studies on the etiology of pregnancy gingivitis. Periodont Abstr 50, 1968. 127. Deasy, M . , G r o t a , L . , and Kennedy, J . : The effect of estrogen, progesterone and Cortisol on gingival inflammation. J Periodont Res 7:111, 1972. 128. L i n d h e , J . , Hellden, L . , and Lundgren, D . : Exuda­ tion and leukocyte emigration in progesterone and estrogen treated rats. Scand J Dent Res 80: 434, 1972. 129. M o h a m m e d , A . , Waterhouse, J . , and Friedman, H . : The microvasculature of the rabbit gingiva as affected by progesterone: an ultrastructural study. J Periodontol 45: 50, 1974. 130. Knight, G . and Wade, A . : The effects of hormonal contraceptives on the human periodontium. J Periodont Res 9: 18, 1974. 131. Baer, P . : Periodontal disease in children and adoles­ cents: A clinical study. J Am Dent Assoc 55: 629, 1957. 132. Sutcliffe, P . : A longitudinal study of gingivits and puberty. J Periodont Res 7: 52, 1972. 133. Dreizen, S., L e v y , B . , and Bernick, S.: Studies on the biology of the periodontium of marmosets. X . Cortisone produced periodontal and skeletal changes in adult cottontopped marmosets. J Periodontol 42: 217, 1971. 134. K f o e d , J . , and Bozzini, C : The effect of hydrocorti­ sone on the concentration and synthesis of acid mucopolysacharides in the rat gingiva. J Periodont Res 5: 259, 1970. 135. L e v y , B . , Dreizen, S., Bernick, S., and Hampton, I.: Studies on the biology of the periodontium of marmosets. I X . The effect of parathyroid hormone on the alveolar bone of marmosets pretreated with fluoridated and non-fluoridated drinking water. J Dent Res 49: 816, 1970. 136. Pinto, A . : Effect of hypothyroidism obtained experi­ mentally on the periodontium of rat. J Periodontol 45: 217, 1974. 137. El-Kafrawy, A . , and Mitchell, D . : Dental and peri­ odontal effects of calcitonin in hamsters. J Dent Res 55: 554, 1976. 138. M a n h o l d , J . , D o y l e , J . , and Weisinger, E . : Effects of social stress on oral and other bodily tissues. II. Results offering substances to a hypothesis for the mechanism of formation of periodontal pathology. J Periodontol 42: 109, 1971. 139. D e M a r c o , T . : Periodontal emotional stress syn­ drome. J Periodontol 47: 67, 1976. 140. Haskell, B . : Association of aircraft noise to peri­ odontal disease in air crewmembers. Aviat Space Environ Med 46: 141, 1975. 141. Hansen, G . : A n epidmiologic investigation of the effect of biologic aging on the breakdown of periodontal tissue. J Periodontol 44: 269, 1973. 142. Holm-Pederson, P . , Agerbaek, M . , and Theilade, E . : Experimental gingivitis in young and elderly individuals. J Clin Periodont 2: 14, 1975. 143. D o y l e , J . , Hollander, W . , G o l d m a n , H . , and Ruben, M . : Experimental atherosclerosis and the periodontium. J Periodontol 40: 350, 1969. 144. Grant, D . , and Bernick, S.: Arteriosclerosis in peri­ odontal vessels of aging humans. J Periodontol 41: 170, 1970. 145. Grant, D . , and Bernick, S.: The periodontium of aging humans. J Periodontol 43: 660, 1972. 146. L e v y , B . , Dreizen, S., and Bernick, S.: Effect of 3

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aging on the marmoset periodontium. J Oral Pathol 1: 6 1 , 1972. 147. R y a n , E . , Toto, P . , and Gargiulo, A . : A g i n g in human attached gingival epithelium. J Dent Res 53: 74, 1974. 148. Schneir, M . , Furuto, D . , and Berger, K . : Collagens of oral soft tissues. I. The influence of age on the synthesis and maturation of collagen in rat palatal mucosa as deter­ mined in vitro. J Periodont Res 11: 235, 1976. 149. Tonna, E . : Periodontal inflammation and aging in the laboratory mouse. J Periodontol 43: 4 0 3 , 1972. 150. Tonna, E . : Factors (aging) affecting bone and cementum.7 Periodontol 47: 267, 1976. 151. Tonna, E . , and Weiss, R . : The cell proliferative activity of periodontal tissues in aging mice. Arch Oral Biol 17: 969, 1972. 152. Demetriou, N . , Bazopoulou-Kyrkanidau, E . , and Sotriou, B . : Changes in the interradicular periodontium of rats correlated with age. J Dent Res 51: 1404, 1972. 153. Roper, R . , K n e r r , G . , G o c k a , E . , and Stahl, S.: Periodontal disease in aged individuals. J Periodontol 43: 304,1972. 154. A i n a m o , J . , and Talari, A . : The increase with age of the width of attached gingiva. J Periodont Res 11: 182, 1976. 155. L a n e , J . : Gingival fenestration. J Periodontol 48: 225,1977. 156. Manson, J . : Passive eruption. Dent Pract 14: 2, 1963. 157. Tiecke, R . E d . : Oral Pathology, pp. 826-827. New Y o r k , The Blakeston Division, M c G r a w H i l l B o o k C o m ­ pany, 1965. 158. Farzin, I., and Edalat, M . : Periodontosis with hyper­ keratosis palmaris et plantaris. (The Papillon-Lefevre syn­ drome) J Periodontol 45: 316, 1974. 159. Giansanti, J . , Hrabak, R . , and W a l d r o n , C : Palmarplantar hyperkeratosis and concomittant periodontal destruc­ tion. (Papillon-Lefevre syndrome) Oral Surg 36: 40, 1973. 160. Hickory, J . , Schell, J . , and R i c h a r d , G . : PapillonLefevre syndrome. J Oral Surg 33: 6 7 1 , 1975. 161. N a i k , D . , V e l o u , A . , Alavandar, G . , an and R a d hakrishna, B . : Papillon-Lefevre syndrome. Oral Surg 25: 19, 1968. 162. Beumer, J . , Trobridge, K . , Silverman, S., and E i senberg, E . : Childhood hypophosphatasia and the premature loss of teeth. Oral Surg 35: 631, 1973. 163. Brittain, J . , Oldenburg, T . , and Burkes, E . : Odontohypophosphatasia: Report of two cases. J Dent Child 43: 106,1976. 164. Jorgenson, R . , L e v i n , L . , Hutcherson, S., and Sali­ nas, C : Periodontosis in sibs. Oral Surg 39: 396, 1975. 165. Melnick, M . , Shields, E . , and Bixler, D . : Periodon­ tosis: A phenotypic and genetic analysis. Oral Surg 42: 32, 1976. 166. Lavine, W . , Page, R . , and Padgett, G . : Host re­ sponse in chronic periondontal disease. V . The dental and periodontal status of mink and mice affected by ChediakHigashi Syndrome. J Periodontol 47: 6 2 1 , 1976. 167. Temple, T . , K i m b a l l , H . , Kakehashi, S., and A m e n , C : Host factors in periodontal disease: Periodontal manifes­ tations of Chediak-Higashi syndrome. J Periodont Res Suppl 10: 26, 1972. 168. Kezes, P . , Bellack, S., and Jordan, H . : Studies on the pathogensis of destructive lesions of the gums and teeth in mentally retarded children. I. Dentobacterial plaque infec­ tion in children with Down's Syndrome. Clin Pediatrics 10: 711, 1971. 169. C o h e n , M . : Chromosomal disorders. Dent Clin North Am 19: 87, 1975. 170. B r o w n , R . : Necrotizing ulcerative gingivitis in mon­ goloid and non-mongoloid retarted individuals. J Periodont

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Res 8: 290, 1973. 171. Loesche, W . , and Nafe, D . : Reduction of supragin­ gival plaque accumulation in institutional Down's Syndrome patients by periodic treatment with topical Kanamycin. Arch Oral Biol 18: 1131, 1973. 172. Cutress, T . : Periodontal disease and oral hygiene in trisomy 2 1 . Archs Oral Biol 16: 1345, 1971. 173. G o r l i n , R . , Stallard, R . , and Shapiro, B . : Genetics and periodontal disease. J Periodontol 38: 5, 1967. 174. Chung, C , Runck, D . , Niswander, J . , Bilben, S., and K a u , M . : Genetic and epidemiologic study of oral char­ acteristics in Hawaiian school children: I'. Caries and peri­ odontal disease. J Dent Res 49: 1374, 1970. 175. Niswander, J . : Genetics of common dental disorders. Dent Clin North Am 19: 197, 1975. 176. Prodhan, A . , Chawla, T . , Samuel, K . , and Prodhan, S.: The relationship between periodontal disease and blood groups and secretor status. J Periodont Res 6: 294, 1971. 177. Keene, J . , Hussman, L . , and Brume, G . : Terminal oral manifestations of acute lymphoblastic leukemia. J Oral Med 27: 117, 1972. 178. Presant, G . , Safdor, S., and Cherrick, H . : Gingival leukemic infiltration in chronic lymphocytic leukemia. Oral Surg 36: 672, 1973. 179. L e v i n , S., and Kennedy, J . : Relationship of plaque and gingivitis in patients with leukemia. Va Dent J 50: 22, 1973. 180. Curtis, A . : Childhood leukemia: Osseous changes in jaws on panoramic dental radiographs. J Am Dent Assoc 83: 844, 1971. 181. Stern, M . , and Cole, W . : Radiographic changes in the mandible associated with leukemic cell infiltration in a case of acute myelogenous leukemia. Oral Surg 36: 343, 1973. 182. Deasy, M . , V o g e l , R . , A n n e s , I., and Simon, B . : Periodontal disease associated with the preleukemic syn­ drome. J Periodontol 47: 4 1 , 1976. 183. Davey, K . , and Konchak, P.: Agranulocytosis. Den­ tal case report. Oral Surg 28: 166, 1969. 184. V a n n , W . , and Oldenberg, T . : Atypical hereditary neutropenia: Case reports of two siblings. J Dent Child 43: 265, 1976. 185. B e i n o n , P . , and D y k m a , R . : Rehabilitative manage­ ment of cyclic neutropenia. J Prosthet Dent 31: 52, 1974. 186. A w b r e y , J . J . , and H i b b a r d , E . D . : Abbreviated case report. Congential agranulocytosis. Oral Surg 35: 526, 1973. 187. Lempert, T . , and Fessler, A . : Periodontal changes during chrojiic granulocytopenia in childhood. A case report. J Clin Periodontol 2: 105, 1975. 188. Rylander, H . , Attstrom, R . , and Lindhe, J . : Influ­ ence of experimental neutropenia in dogs with chronic gingiv­ i t i s . / Periodont Res 10: 315, 1975. 189. Lainson, P . , Brody, P . , and Fraleigh, C : A n e m i a , a systemic cause of periodontal disease? J Periodontol 39: 35, 1968. 190. Courant, R . , and Sobkov, T . : Oral manifestatory of infectious mononucleosis. J Periodontol 40: 279, 1969. 191. Cassingham, R . , O ' L e a r y , T . , Hansen, N . , Sevensen, H . , and Walker, F . : A possible relationship between acute necrotizing ulcerative gingivitis and infectious mononu­ cleosis. J Oral Med 26: 134, 1971. 192. Person, P.: Diet consistency and periodontal disease in old albino rats. J Periodontol 32: 308, 1961. 193. Stahl, S. S., M i l l e r , S. C , and Goldsmith, E . O . : Effects of various diets on the periodontal structures of ham­ sters. J Periodontol 29: 7, 1958. 194. Krasse, B . , and B r i l l , N . : Effect of consistency of diet on bacteria in gingival pockets in dogs. Odontol Revy 11: 152, 1960.

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195. K i n g , J . D . , and Glover, R . E . : The relative effects of dietary constituents and other factors upon calculus forma­ tion and gingival disease in the ferret. J Pathol Bac 57: 353, 1945. 196. Ferguson, H . W . : Effect of nutrition on the perio­ dontium. Melcher, A . H . and B o w m a n , W . H . (eds), Chapter in Biology of the Periodontium, p 424, L o n d o n , Academic Press, 1969. 197. Egelberg, J . E . : Local effect of diet on plaque forma­ tion and development of gingivitis in dogs. I. Effect of hard and soft diets. Odontol Revy 16: 3 1 - 4 1 , 1965. 198. Bavetta, L . A . , and Bernick, S.: The effect of trypto­ phan deficiency on the bones and teeth of rats. III. Effect of age. Oral Surg 9: 906, 1956. 199. Frandsen, A . M . , Becks, H . , Nelson, M . M . , and Evans, H . M . : The effects of various levels of dietary protein on the periodontal tissues of young rats. J Periodontol 24: 135, 1953. 200. G o l d m a n , H . M . : The effects of dietary protein dep­ rivations and of age on the periodontal tissues of the rat and spider monkey. J Periodontol 25: 87, 1954. 201. Stein, G . , and Z i s k i n , D . E . : The effect of a protein free diet on the teeth and periodontium of the albino rat. J Dent Res 28: 529, 1949. 202. Stahl, S. S., Sandler, H . C , and C a h n , L . R . : The effect of protein deprivation upon the oral tissues of the rat and particularly upon periodontal structures under irritation. Oral Surg 8: 760, 1955. 203. R u b e n , M . P . , M c C o y , J . , Person, P . , and Cohen, D . W . : Effects of soft dietary consistency and protein depri­ vation on the periodontium of the dog. Oral Surg 15: 1061, 1962. 204. Sheehan, H . : The prevalence and severity of peri­ odontal disease in rural nigerians. Dent Pract Res 17: 51, 1966. 205. Pindborg, M . B . , and Roed-Petersen, B . : Oral changes in South indian children with severe protein defi­ c i e n c y . / Periodontol 38: 40/218, 1967. 206. Lederman, N . J . , and Hazen, S. P.: Relationship between supplementary dietary protein and periodontal health (Abstr.) I.A.D.R. No. 66, 1965. 207. Ringsdorf, W . M . Jr., and Cheraskin, E . : Periodon­ tal pathosis in man: Effect of a relatively high protein low carbohydrate diet upon sulcus depth. J Periodontol 33: 341, 1962. 208. Ringsdorf, W . M . , and Cheraskin, E . : Periodontal pathosis in man. I V . Effect of protein versus placebo supple­ mentation upon gingivitis. J Dent Med 18: 9 2 - 9 4 , 1963. 209. Cheraskin, E . , and Ringsdorf, W . M . J . : Periodontal pathosis in man. V I I I . Effect of protein versus placebo supplemenation upon tooth mobility. Periodontics 2: 69, 1964. 210. Cheraskin, E . , and Ringsdorf, W . M . : Periodontal pathosis in man. X . Effect of combined versus animal protein supplementation upon sulcus depth. J Oral Ther Pharmacol 1: 497, 1965. 211. Cheraskin, E . , Ringsdorf, W . M . , Setyaadmadja, A . T . S. H . , and Ray, D . W . : A n ecologic analysis of tooth mobility: Effect of prophylaxis and protein supplementation. / Periodontol 38: 227, 1967. 212. Cheraskin, E . , Ringsdorf, W . M . , Setaadmadja, A . T . S. A . , and Barrett, R . A . : A n ecologic analysis of gingival state: Effect of prophylaxis and protein supplementations. J Periodontol 39: 316, 1968. 213. Ferguson, H . W . , and Hartles, R . L . : The effect of vitamin D on the alveolar bone of young rats maintained on diets deficient in calcium or phosphorus. A r c h . Oral Biol 9: 447-460, 1964. 214. Oliver, W . M . : The effect of deficiencies of calcium, vitamin D or calcium and vitamin D and of variation in the

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source of dietary protein on the supporting tissues of the rat molar. J Periodont Res 4: 56, 1969. 215. Ferguson, H . W . , and Hartles, R . L . : The effect of diets deficient in calcium or phorphorus in the presence or absence of supplements of vitamin D on the secondary cementum and alveolar bone of young rats. Arch Oral Biol 9: 647, 1964. 216. Ferguson, H . W . , and Hartles, R . L . : The effect of diets deficient in calcium or phorphorous in the presence and absence of supplements of vitamin D on the the incisor teeth and bone of adult rats. Arch Oral Biol 11: 1345, 1966. 217. K r o o k , L . , Lutwak, L . , H e r i k s o n , P . A . , Kallelz, F . , Hirsch, C , Romanus, B . , Belanger, L . E . , Marier, J . R . , and Sheffey, B . E . : Reversibility of nutritional osteoporosis: Physiochemical data in bone from an experimental study in dogs. J Nutr 101: 233, 1971. 218. H e n r i k s o n , P . A . : Periodontal disease and calcium deficiency. A n experimental study in the dog. A c t a Odont. Scand. 26 Suppl 50, 1968. 219. L u t w a k , L . , K r o o k , L . , Henrikson, P . A . , U r i s , R . , Whaler, J . P . , Coulston, A . , and Lesser, G . : Calcium defi­ ciency and human periodontal disease. Isr J Med Sci 7: 504, 1971. 220. L u t w a k , L . : Periodontal Disease. Curr Concepts Nut 4: 145, 1976. 221. Svanberg, G . , L i n d h e , J . , Hugoson, A . , and G r o n dahl, H . G . : Effect of nutritional hyperparathyroidism on experimental periodontitis in the dog. Scand J Dent Res 81: 155-162,1973. 222. Bissada, N . F . , and Demarco, J . T . : The effect of a hypocalcemic diet on the periodontal structure of the adult rat. J Periodontol 45: 739, 1974. 223. G r o e n , J . J . , Menczel, J . , and Shapiro, S.: Chronic destructive periodontal disease in patients with presenile os­ teoporosis. J Periodontol 39: 19, Jan. 1968. 224. Radusch, D . F . : Nutrition and dental health. The relationship of gastric acidity to periodontoclasia. J Periodon­ tol 18: 110, 1947. 225. M i g l a n i , D . C : The effect of vitamin A deficiency on the periodontal structures of rat molars, with emphasis on cementum resorption. Oral Surg 12: 1372-1386, 1954. 226. Frandsen, A . M . : Periodontal tissue changes in v i ­ tamin A deficient young rats. ,4eta Odontol Scand 21: 19-34, 1963. 227. Mellanby, H . : The effect of maternal dietary defi­ ciency of vitamin A on dental tissues in rats. J Dent Res 20: 4 8 9 - 5 0 9 , 1941. 228. G l i c k m a n , I., and Stoller, M . : The periodontal tis­ sues of the albino rat in vitamin A deficiency (Abstr.) J Dent Res 27: 758, 1948. 229. Russell, A . L . : International nutrition surveys, a summary of preliminary dental findings. J Dent Res 42: 233, 1963. 230. Russell, A . L . , Consolazio, C . F . , and White, C . C : Periodontal disease and nutrition in Eskimo scouts of the Alaska National G u a r d . J Dent Res 40: 604, 1961. 231. A f o n s k y , D . : Oral lesions in niacin, riboflavin, pyridoxine, folic acid, and pantothenic acid deficiencies in adult dogs. Oral Surg 8: 867, 1955. 232. Chapman, O . D . , and Harris, A . E . : Oral lesions associated with dietary deficiencies in monkeys. J Infect Dis 69: 7-17, 1941. 233. Shaw, J . H . , and Griffith: The relation of nutrition to periodontal disease. II. Systemic factors in periodontal dis­ ease. J Dent Res 41: 264, 1962. 234. Topping, N . H . , and Fraser, H . F . : O r a l pathology in monkeys in various experimental dietary deficiencies. Public Health Reports. 54: 4 1 6 - 4 3 , March 1939. 235. Waerhaug, J . A . : W o r l d Workshop in Periodontics,

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Chapter on Epidemiology of Periodontal Disease, p 197, 1966. 236. V o g e l , R . I., Fink R . A . , Schneider, L . C , Frank, O . , and B a k e r , H . : The effect of folic acid in gingival health. J Periodontol 47: 667, N o v . 1976. 237a. Dreizen, S., L e v y , B . M . , and Bernick, S.: Studies of the histology of the periodontium of marmosets. V I I . The effect of vitamin C deficiency on the marmoset periodontium. J Periodont Res 4: 274, 1969. 237b. Waerhaug, J . : Effect of C — avitaminosis on the supporting structures of the teeth. J Periodontol 29: 87, 1958. 238. G l i c k m a n , I.: Acute vitamin C deficiency and peri­ odontal disease. I. The periodontal tissues of the guinea pig in acute vitamin C deficiency. J Dent Res 27: 9, 1948. 239. G l i c k m a n , I.: Acute vitamin C deficiency and peri­ odontal disease. II. The effect of acute vitamin C deficiency upon the response of the periodontal tissues of the guinea pig to artificially induced inflammation. J Dent Res 27: 2 0 1 , 1948. 240. Brockley, C . H . , and Baenziger, P . E . : A n investiga­ tion into the connection between the vitamin C content of the blood and periodontal distrubances. Br Dent J 73: 57, 1942. 241. Shannon, I.: Significant correlations between gingi­ val scores and ascorbic acid status. J Dent Res 52: 394, 1973. 242. Weisberger, D . , Y o u n g , A . P . , and M o r s e , F . W . : Study of ascorbic acid blood levels in dental patients. J . Dent Res 77: 101, 1938. 243. B u r r i l , D . Y . : Relationship of blood plasma vitamin C level to gingival and periodontal disease. J Dent Res 21: 353, 1942. 244. Parfitt, G . J . , and H a n d , C D . : Reduced plasma ascorbic acid levels and gingival health. J Periodontol 34: 347, 1963. 245. Perlitsh, M . , Nielsen, A . G . , and Stanmeyer, W . R . : Ascorbic levels and gingival health in personnel wintering over in Antartica. J Dent Res 40: 784, 1961. 246. Russell, A . L . , Leatherhood, E . C , Consolazio, C . F . , and Vanreen, R . : Periodontal disease and nutrition in South V i e t n a m . J Dent Res 44: 775, 1965. 247. Crandon, J . H . , L u n d , C . C , and D i l l , D . B . : Exper­ imental human scurvy. N Engl J Med 223: 353, 1940. 248. Restarski, J . J . , and PiJoan, M . : Gingivitis and V i ­ tamin C . J Am Dent Assoc 31: 1323, 1944. 249. E l - A s h r y , G . M . , Ringsdorf, W . M . , and Cheraskin, E . : Local and systemic influence in periodontal disease. I I . Effect of prophylaxis and natural versus synthetic vitamin C upon gingivitis. J Periodontol 35: 250, 1964. 250. E l - A s h r y , G . M . , Ringsdorf, W . M . , andCheraskin, E . : Local and systemic influences in periodontal disease. III. Effect of prophylaxis and natural versus synthetic vitamin C upon sulcus depth. NY State Dent J 32: 254, 1964. 251. E l - A s h r y , G . M . , Ringsdorf, W . M . , and Cheraskin, E . : Local and systemic influences in periodontal disease. I V . Effect of prophylaxis and natural versus synthetic vitamin C upon clinical tooth mobility. Int J Vitamin Nutr Res 34: 202, 1964. 252. H a n k e , M . T . , Needles, M . J . , Marberg, C . M . , Tucker, W . H . , Ghent, C . L . , and Williams, J . M . : Nutri­ tional studies on children: The effects upon gingivitis of adding orange and lemon juice to the diet. Dent Cosmos 75: 570,1933. 253. Carvel, R . L . , and H a l p e r i n , V . : Therapeutic effect of water-soluble bioflavinoids in gingival inflammation condi­ tions. Oral Surg 14: 847, 1961. 254. Linghorne, W . J . , M c i n t o s h , W . G . , Tice, J . W . , and Tisdall, F . F . : The relation of ascorbic acid intake to gingivi­ tis. J Can Dent Assoc 12: 49, F e b . 1946. 255. C o v e n , E . M . : Effect of prophylaxis and vitamin

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supplementation upon periodontal index in children. J Perio­ dontol 36: 4 9 4 , 1965. 256. Kutscher, A . H . : Massive vitamin C therapy of chronic marginal gingivitis. NY State Dent J 19:422,1953. 257. O ' L e a r y , T . J . , R u d d , K . D . , C r u m p , P . P . , Krouse, R . E . : The effect of ascorbic acid supplementation on tooth mobility. J Periodontol 40: 284, 1969. 258. C u r s o n , I., and M a n s o n , J . D . : A study of a group of dental students including their diet and dental health. Br Dent J 119: 197, 1965. 259. G l i c k m a n , I., and Dines, M . M . : Effect of increased

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Announcements UNIVERSITY OF SOUTHERN CALIFORNIA SCHOOL OF DENTISTRY The University of Southern California, School of Dentistry an­ nounces the following graduate dentistry courses: Applications may be obtained for advanced training in Endodontics, Orthodontics, Pedodontics, Periodontics, Prosthodontics, Oral Path­ ology and Oral Surgery. Each program commences July 1. The Hospital residency programs are available in advanced Pedodontics and Oral Pathology which provide monthly stipends. For additional information, contact the University of Southern California, School of Dentistry, Office of Admissions, 925 West 34th Street, Los Angeles, California, 90007.

and Simplified Periodontal Procedures for General Practive) IRV­ ING B . STERN, D.D.S., Wednesday, May 10, 1978; $65. POSTGRADUATE EXTENSION PROGRAM (Off campus courses): Faculty members of the Postgraduate Dental Program, who are specialists in their fields, are available for short, intensive courses that can be given in various cities if a suficient number of practitioners evince interest. If clinical facilities are available, these courses can be a combination of lectures and demonstrations. For further information and application, write to: Dr. Irving Yud­ koff, Director, Postgraduate Dental Program, Albert Einstein Col­ lege of Medicine, 1165 Morris Park Avenue, Bronx, New York 10461. UNIVERSITY OF CONNECTICUT SCHOOL OF D E N T A L MEDICINE

P O S T G R A D U A T E D E N T A L P R O G R A M A L B E R T EINSTEIN C O L L E G E OF MEDICINE The following courses are available during the academic year, 1977-1978: PERIODONTICS FOR THE HYGIENIST, D P D 102 (A Participation Course) IRVING YUDKOFF, D . D . S . , MARVIN N . O K U N , D . D . S . , JOSEPH F. Puccio, D . D . S . , BERTRAM S. BILDNER, D.D.S., and EDMUND D . D'ONOFRIO, D . M . D . , Fridays, October 21 and 28, 1977; $130. PERIODONTIC REVIEW COURSE, D P D 67, MARVIN N . O K U N , D . D . S . , IRVING YUDKOF, D.D.S., JOSEPH F. Puccio, D.D.S., BERTRAM S. BILDNER, D.D.S., and EDMUND D . D'ONOFRIO, D . M . D . , Wednesday, Novemberr 16, 1977; $65. PERIODONTICS, D P D 66 (A 20 Session Periodontics Participating Course) MARVIN N . O K U N , D . D . S . , IRVING YUDKOFF, D.D.S., JOSEPH F. Puccio, D.D.S., BERTRAM S. BILDNER, D.D.S., E D ­ MUND D . D'ONOFRIO, D . M . D . , KALMEN D . EINBINDER, D.D.S., and DANIEL M . NACHMANOFF, D . D . S . , 20 Wednesdays com­ mencing January 4, 1978 through May 17,1978; $1950 (including manuals). PERIODONTICS, D P D 63 (Immunologic Aspects of Periodontal Dis­ ease), ROBERT J . GENCO, D.D.S., Ph.D., and DANIEL FINE, D . M . D . , Friday, January 20, 1978; $65. TEMPOROMANDIBULAR JOINT DISORDERS, D P D 99, JOHN R. VAROSCAK, D . D . S . , Friday, March 24, 1978; $65. PERIODONTICS, D P D 64 (Reconstruction Reparative Periodontal Therapy — A Rationale and Objectives) HENRY M . GOLDMAN, D . M . D . , Friday, April 28, 1978; $65. PERIODONTICS, D P D 65, EIGHTEENTH ANNIVERSARY ALUMNI LEC­ TURE, T H E DR. ZACHARY DEMBO MEMORIAL LECTURE (Effective

The University of Connecticut School of Dental Medicine an­ nounces the following courses: TITLE: Orthodontics as an adjunct to Periodontal Therapy DATES: September 14-15, 1977 FACULTY: DR. RAVINDRA NANDA, B . D . S . , Ph.D. Associate Profes­ sor of Orthodontics, University of Connecticut School of Dental Medicine. This course is designed to enhance the knowledge and skill of the periodontist in the treatment of minor orthodontia problems. TITLE: Temporization in Periodontal Prosthesis DATES: October 27-28, 1977 FACULTY: Jean Amara, D . D . S . Assistant Professor Restorative Den­ tistry University of Connecticut School of Dental Medi­ cine. TITLE: Periodontal Prosthesis DATES: November 18-19, 1977 FACULTY: MORTON AMSTERDAM, D . D . S . Professor of Periodontics and Periodontal Prosthesis, University of Pennsylvania School of Dental Medicine, Visiting Professor of Pros­ thetic Dentistry, Boston University of Graduate Den­ tistry. TITLE: Clinical Periodontology and Periodontal Prosthesis DATES: April 6 & 7, 1978 FACULTY: JAN LINDHE, D . D . S . , Professor and Chairman, Depart­ ment of Periodontology, University of Goteborg, Swe­ den For further information contact: Susan Duckworth, Administrative Assistant, Continuing Dental Education, University of Connecticut Health Center, Farmington, C T 06032.