PEDIATRIC /Copyright © 1981 by The American Academyof Pedodontics/Vol. 3, No. 2 CAS

Periodontal changesassociated with chronic idiopathic

KennethL. Kalkwarf, DD$, MS DennisP. Gutz, DDS,MS

Abstract and respiratory tract. Severalcases 7-11,~,~.4~-57.4.s~have dis- cussed the response of the gingiva and periodontal This case report focuses on the periodontal status of a supporting apparatus during the disorder. youngpatient with chronic idiopathic neutropenia. A four- year clinical courseis presented.Chronic idiopatin’c Severe , oral ulcers and destruction of the neutropeniais a relatively rare dyscrasia alveolar crest have been consistently noted. characterized by a severe decrease in the numberof Suggested for children exhibiting this circulating . Youngindividuals exin’biting tins hematologic phenomena has included cysteine, ~ blood problemexperience rapid destruction of periodontal transfusions/ pyridoxine hydrochloride (vitamin B6), structures. A reviewof related literature reveals that the few ~.~ plasma transfusions, s transfusion with packed white discussions of dental symptomsavailable relate common cells, ~ non-specificu,~3 therapy/ splenectomy, findings: exaggeratedgingivitis, prematureexfoliation of the cortisone, 41,~.u testosterone, 5 and somatotropic hor- primary dentition and recurrent occurrence of aphthous- mone? Only therapy has had predictable type lesions. While some mechanismsexplaining the lack of success in control of the systemic sequela.’s,~a.4~ Newer circulating neutrophils have been postulated, the exact methods of transfusion appear to exhibit etiology of chronic idiopathic neutropeniais unknown. ~ Dentaltherapy for individuals exin’biting tins condition significant promise in future therapy regimes? shouMbe aimedat the reduction of local inflammationby The purpose of this paper is to present a case report careful and frequent removalof local irdtational factors. of a child exhibiting chronic neutropenia, discuss clas- Great care shouMbe employedduring dental therapy to sification of such neutropenias and review dental man- reducethe possibility of bacteremias. agement for children with such problems.

Introduction MedicalHistory Neutropenia is characterized by a severe decrease in the number of circulating neutrophils in the peri- The patient, a slight, well nourished 31/~-year-old pheral blood vessels. Classically, neutropenia occurs in caucasian female, in no apparent distress, was referred adults, typically middle-aged women,and is a result of to the Periodontics Department, College of Dentistry, specific drug injection, radiation or severe ; University of Nebraska Medical Center, for evaluation Several cases of and children exhibiting and treatment of her gingival condition. A medical severe neutropenias of questionable or idiopathic history revealed that initial problems were noted at origin have been reported in the literature. Due to age 21/~ weeks, when she developed an intense papular differences observed in onset, severity, symptomsand rash in the diaper area. A diagnosis of staphylococcal etiology, a number of names have been used to de- dermatitis was made and the patient was treated with scribe the clinical entities: infantile congenital agranu- ampicillin and oxacillin sodium. The rash cleared, but locytosis, ~ , TM chronic benign recurred two weeks following discontinuance of the neutropenia, m~ reticular dysgenesia, 1~,~ congenital . The patient also experienced numerous neutropenia,~*= infantile aneutrocytosis," chronic idio- early bouts of respiration difficulty and frequent ~ ~-s~ febrile episodes, with temperatures ranging from 101- pathic neutropenia and others. All children re- ° ported a history of persistent of the skin 103 F. Each illness was treated with antibiotic ther- apy. The clinical picture recurred with cessation of Accepted: December 2, 1980 each course of .

PEDIATRICDENTISTRY 189 Vo|. 3, No. 2 The patient was evaluated at age three months and a diagnosis of was made. She was treated with two injections of gammaglobu- lin. Multiple complete blood counts were completed during the course of her initial therapy. At no time was her granulocyte count above 3%. At age five months the patient was referred to the University of Nebraska Medical Center for a hema- tologic evaluation. Laboratory data obtained at that time was as follows: Hemaglobin: 11.5 : 552,000 WBC: 10,900 Urinalysis: normal Figure 1. Age three years, six months, mild plaque accumulation. A Differential: 76% Lymphocytes IgG: 630 granulomatous collar forms the gingival margin around each . 20% IgA: 45 Exaggerated gingival recession is evident, particularly in the ante- 3% IgM: 97 rior region. l% 9% Neutrophils A repeat blood count was comparable to the first. A examination was reported to be consist- ent with congenital neutropenia. A diagnosis of con- genital neutropenia, specifically of the congenital infantile form, was made. 3y,6m Following the diagnosis, the patient experienced numerous dermatologic infections that were treated with antibiotic therapy. At age two, severe re- quired lancing of the typanic membranes. Ampicillin therapy was initiated at that time and continued in multiple two week courses. 4y, 6m

Family History Outside of a family history of allergic disorders, no significant familiar characteristics could be identified. Hematologic evaluations of the patient's parents were within normal limits.

Dental Findings Intital periodontal examination revealed swollen, edematous gingiva. A distinct granulomatous collar was evident at the cervical region of the teeth. It was crimson red in and bled easily when manipulated 6y, 9m (Figure 1). No evidence of perioral or other lesions within the oral cavity or pharyngeal region was Figure 2: Serial bitewing radiographs. present. Gingival recession had occurred in the ante- The importance of plaque control was stressed to rior regions, resulting in exposed root surfaces. The the mother. She was instructed in disclosing and ginival tissue was very tender and the patient resisted cleaning her daughter's mouth with an extra soft attempts at gentle probing. No clinical evidence of ac- nylon brush, being careful to remove all traces of vis- tive carious lesions was detected. Moderate accumula- ible plaque. An emollient was prescribed to provide tions of plaque were present. The mother noted that pallative relief to local regions devoid of epithelium. A the patient frequently complained of a "sore mouth" thorough prophylaxis was performed and the patient and resisted attempts at toothbrushing. Radiographic was placed on a frequent maintenance regimen. The examination revealed exaggerated alveolar bone loss, patient's mother was told to call if any change in oral particularly in the anterior regions of the mouth (Fig- symptoms was noticed. ures 2 and 3). No radiographic evidence of active car- The patient was seen at one to three month inter- ies was found. vals over the next four years. At maintenance appoint-

CHRONIC IDIOPATHIC NEUTROPENIA 190 Kalkwarf and Gutz Figure 4: Age four years, moderate plaque, gingival edema and swelling. Gingival architecture in the anterior regions is becoming 5y, 0 m quite distorted. Granulomatous collar is not as evident.

6y, Om

Figure 5: Age four years, six months, moderate plaque accumula- tion. Recession is more pronounced in the anterior region. Drifting 6y ,9m of the mandibular anterior teeth is becoming noticeable.

Figure 3: Serial anterior radiographs. ments, plaque control was evaluated and discussed with the patient and her parents. Gingival contour, color and consistency were evaluated. Gentle debride- ment and polishing were accomplished as required. Kodachromes were obtained at six-month intervals for documentation. Bitewing and anterior radiographs were obtained yearly to evaluate osseous changes (Fig- ures 2 and 3). During the four years of observation, the patient's plaque control varied from fair to poor. From conver- sations with her mother it was determined that gin- Figure 6: Age five years, mild plaque accumulation. Recession and gival periodically progressed to a point staining are more prominent. The mandibular incisors are extremely mobile and exhibit evidence of drifting. where use of even a soft toothbrush was very uncom- fortable. During these periods, the parents would not insist that cleaning be performed and massive manent dentition (Figures 5, 6, and 7). Clinical evi- amounts of bacterial plaque would accumulate, result- dence of active caries was not identified at any exami- nation. Soft tissue lesions, appearing to be aphthous- ing in increased gingival swelling and edema (Figure type ulcerations were occasionally present in the oral 4). The granulomatous collar remained present at each observation period, being more evident during some and perioral regions (Figure 9). Radiographic evalua- periods than others (Figures 1, 5 and 8). tions revealed progressing destruction of the alveolar Progressive gingival recession eventually resulted in bone about the primary dentition. This was especially advanced root exposure throughout the primary den- evident about the anterior teeth and in the furcation tition. This was especially evident in the anterior re- regions of the primary molars (Figures 2 and 3). gions of the mouth (Figures 5 and 6). Instrinsic staining The mandibular primary incisors were exfoliated at became readily apparent in both the primary and per- 5 years, 7 months. Eruption of the permanent incisors

PEDIATRIC DENTISTRY 191 Vol. 3, No. 2 Figure 7: Age six years, plaque accumulation moder- ate. Maxillary incisors are mo- bile and show evidence of drifting. The deciduous mandi- bular incisors were exfoliated at age five years, seven months. followed a normal pattern, although chronologically advanced. Alveolar support about the permanent Figure 8: Age six years, three months, plaque accumulation moder- teeth is within the normal limits through age seven. ate. The deciduous, maxillary, incisors were exfoliated at age six years, '/2 month. Decalcification of the remaining is clinically visible, but there is no evidence of an active carious process. Discussion were similar to those reported for cyclic neutropenia Several systemic conditions in children can initiate by Telsey,10 and Wade,11 the persistence of the neutro- the oral manifestations of gingival inflammation, al- penia exhibited by our patient does not allow dupli- veolar bone loss and mucosal ulceration. A differential cate classification. diagnosis for a child presenting with these conditions Classifications such as infantile genetic agranulocy- must include such entities as juvenile periodonti- tosis2*43'44 as well as genetic, familial or hereditary tis,56-57 Papillon-Lefevre syndrome,58 X,59 neutropenias3742'4™9 were ruled out because of the appar- Chediak-Higashi syndrome,60'61 acatalasia,62 chronic ent lack of hereditary ties. The term reticular dys- granulomatous disease,63 hypophophatasia,64 diabetes,65 genesia161766 cannot be utilized because the patient ,65 and neutropenia. exhibits no evidence of an . The Juvenile periodontitis and Papillon-Lefevre syn- term chronic benign neutropenia131546 was not applied drome may be confirmed by the pattern of onset, because this patient shows no evidence of spontaneous clinical and radiographic features and lack of distin- remission. guishing laboratory features. Biopsy will confirm his- Several individuals19-20-31 •" have described cases of tiocytosis X. Chediak-Higashi syndrome exhibits neutropenia in children which they labeled as chronic identifying characteristics in peripheral leukocytes idiopathic neutropenia (granulocytopenia). The condi- and lymphocytes as well as peculiar eosinophila inclu- tion was so named because of the clinical course. A sion bodies in the myeloid cells of the marrow. Aca- persistent neutropenia was present from birth with no talasia may be identified by clinical or hemotologic apparent etiology; no familial tendencies were discov- evaluation for blood catalase activity. Chromic granu- ered. It differed from chronic benign neutropenia in lomatous disease can be positively diagnosed by the that the children were followed for several years with qualitative nitro blue tetrazolium test. Hypophospha- no documentation of self-limitation. Clinical tasia may be confirmed by measurement of serum al- symptoms consisted of persistent, recurrent infections, kaline phosphatase. Hematologic evaluation will posi- including gingivitis, throughout the patient's lifetime. tively identify diabetes, leukemia or neutropenia. Laboratory tests revealed severely depressed Neutropenic conditions in childhood are separated neutrophil counts with accompanying rises in the into various classifications based upon clinical number of monocytes, lymphocytes and eosinophils. symptoms, age at onset, duration, white cell counts, Bone marrow specimens revealed that immune function, familial tendencies and bone mar- was active and orderly to the level. Meta- row alterations. Cyclic neutropenia is the most , bands and segmented forms were rare. No common form of granulocyte alteration exhibiting per- decrease in immune functions was detectable. Ther- iodontal changes.711 In this disease, a predictably re- apy modalities other than antibiotics to control the current diminution of neutrophils occurs as a result of recurrent episodes of infection were not successful. suppression or maturation arrest. The phenomenon The condition apparently varied in severity from indi- occurs for five to seven days at regular 21-day inter- vidual to individual. Some of the patients may survive vals. The etiology of the process is unknown. In the into adolescence with suitable antibiotic therapy. This time periods between these suppressions, the white patient meets all those criteria and can be diagnosed blood cell counts increase, but neutrophil counts sel- as having chronic idiopathic neutropenia. dom exceed 50% of the total leukocyte population. Al- Her dental findings are similar to other reported though the clinical symptoms exhibited in this case neutropenia cases.1525464752 While periodontal destruc-

CHRONIC IDIOPATHIC NEUTROPENIA 192 Kalkwarf and Gutz the children to a later age, report eventual alveolar bone destruction about the permanent teeth as a com-

Figure 9: Age six years, six mon sequela. This patient has exhibited a normal months. An apthous-type le- eruption sequence of the permanent dentition. The sion present in the region of eruption schedule has been accelerated, probably due the right commissure. to the early loss of some primary teeth secondary to accentuated alveolar bone loss. It is expected that al- veolar destruction about her permanent teeth will occur with time. This patient, as well as others2547 exhibited several episodes of recurrent aphthous lesions (Figure 9). Such problems have been noted to occur frequently, but tion, marked gingival recession, there doesn't appear to be a clear relationship with and moderate to heavy accumulations of plaque were the circulating neutrophil count.77 present, there was never any evidence of carious activ- With the advent of more sophisticated antibiotic ity during the four years of follow-up. Tooth discolor- therapy, a greater number of children exhibiting ation was primarily a result of intrinsic staining, prob- hematologic disorders are surviving infections and re- ably due to antibiotic ingestion during formative peri- quiring dental therapy. While some children with ods and extrinsic staining due to plaque control at- neutropenic conditions require no special management tempts that were below acceptable levels. The lack of during dental therapy, many have an increased sus- carious activity in this patient and in others with ceptibility to all infections, including periodontal dis- neutropenic conditions"2545" is difficult to explain. It ease. It is imperative that practicing dentists have a may be that the relative lack of certain inflammatory thorough knowledge of the dental management regi- cells alter the microbial makeup to one incapable of mens required by these patients. initiating a carious process. Mishkin et al.,25 describe, in great detail, the biora- Infections in children with chronic neutropenic con- tionale for dental management of neutropenic pa- ditions are common.6"8 With the lack of polymorpho- tients. Although caries activity does not appear to be nuclear leukocytes in the circulation, it is assumed a major problem for individuals with chronic idio- that the increased susceptibility to infection is due to pathic neutropenia, daily stannous fluoride gel is rec- the diminished phagocytic clearing of . The ommended to retard the possibility of or patients commonly exhibit a compensatory increase in dental infection secondary to a carious lesion. Stan- eosinophils and monocytes in the bone marrow and nous fluoride application has also been shown to be peripheral blood. While these cells are also phagocytic, capable of reducing plaque formation and potentially it has been shown that they are inferior to neutrophils useful in the control of early .78 A 6970 71 in their ability to clear bacteria. ' Generally the strict oral hygiene program, complete with scaling and infections reported in the medical literature are of prophylaxis at short-term intervals, is suggested to dermal or upper respiratory origin. It stands to reason decrease the intensity of gingival inflammation and that the oral cavity, with its constant exposure to slow the rate of alveolar bone loss. Maximum precau- , would be a common site for infections tions, including irrigation and antibiotic to appear. coverage, prior to tissue manipulation is suggested to While the exact role of the neutrophil in the protec- reduce the possibility of bacteremias and postopera- tion of periodontal tissues has not been delineated, tive infections. several investigators have determined that the cell may pass through junctional epithelium and reside in 7273 the gingival sulcus in a viable state. Decreased num- Conclusion bers of neutrophils have also been associated with de- velopment of gingivitis.74 Recent work has related Chronic idiopathic neutropenia is characterized by decreased neutrophil function with increased suscepti- a severe decrease in the number of circulating bility to certain periodontal diseases.7576 It appears neutrophils. The condition is characterized by oral logical that the exaggerated periodontal destruction symptoms consisting of: oral ulceration, gingival seen in patients with chronic idiopathic neutropenia is inflammation and rapidly advancing alveolar bone a result of decreased protection by the neutrophil. destruction. Previous reports24'45 mention that the severe alveolar It is important that the practicing dentist be aware bone loss occurring around the primary teeth does not of the dental ramifications exhibited by individuals appear to interfere with the eruption pattern of the with this disorder and be knowledgeable concerning permanent teeth. Other observations,154750 that follow their management.

PEDIATRIC DENTISTRY 193 Vol. 3, No. 2 Dr. Kalkwarf is associate professor and director of graduate stimulating activity, Acts HaemJap, 40:52, 1977. studies in periodontics, and Dr. Gutz is associate professor and act- 29. Aarskog, D.: Infantile congenital aneutrocytosis, Arch l~’s ing chairman of pedodontics, University of Nebraska Medical Cen- Child, 36:522, 1961. ter, College of Dentistry, Lincoln, Nebraska 68583. Requests for 30. Browne, E. A. and Marcus, A. J.: Chronic idiopathic neutro- reprints should be sent to Dr. Kalkwarf. penia, NEngJMed, 262:795, 1960. 31. Krill, C. E. et al.: Chronic idiopathic granulocytopenia, N Eng J MePediatrics, 35:596, 1965. second year of life, Acts PaediatrScand, 38:590, 1949. 4. Rodin, A. E. et al.: Infantile genetic agranulocytosis, AmDis 36. Kniker, W. T. and Panos, T. C.: Idiopathic infantile agranulocy- Chi’Id, 16:18, 1976. tosis with hypergammaglobulinemia, Am J Dis Child, 94:552, 5. Kostman, R. R. 0.: Infantile genetic agranulocytosis, Acta 1957. PaediatrScand, 64:362, 1975. 37. Luhby, A. L. et al.: Congenital genetic agranulocytosis, AmJ 6. Olofeson, T. et al.: Granulopoiesis in infantile genetic agranulo- Dis Child, 94:552, 1957. cytosis, Scand JHaematol, 16:18, 1976. 38. McClean, M. M.: Chronic neutropenia, Arch Dis in Ctn’ld, 32: 7. Becker, F. T. et ah Recurrent oral and cutaneous infections asso- 431, 1957. ciated with cyclic neutropenia, Arch Dermatol, 80:731, 1959. 39. Hedenberg, F.: Infantile agranulocytosis of probably congenital 8. Gorlin, R. J. and Chandhry, A. P.: The oral manifestations of origin, Acts PadeiatrScand, 48:77, 1959. cyclic (periodic) neutropenia, Arch Dermatol, 82:344, 1960. 40. Gitlin, D., Vawter, G. and Craig, J. M.: Thymlc alymphoplasia" 9. Cohen, D. W. and Morris, A. L.: Periodontal manifestations of and congenital aleukocytosis, Pedlatdcs, 33:184, 1964. cyclic neutropenia, J Pedodontol, 32:159, 1961. 41. Zuelzer, W. W. and Bajoghli, M.: Chronic granulocytopenia in 10. Telsey, B. et al.: Oral manifestations of cyclic neutropenia asso- childhood, Blood, 23:359, 1964. ciated with hypergammaglobulinemia, OrMSurg, 15:540, 1962. 42. Cutting, H. O. and Lang, J. E.: Familial benign chronic neutro- 11. Wade, A. B. and Stafford, J. L.: Cyclic neutropenia, Oral Surg, penia, Ann Intern Med, 61:876, 1964. 16:1443, 1963. 43. Krill, E. E. and Mauer, A. M.: Congenital agranulocytosis, J 12. Smith, J. F.: Cyclic neutropenia, Oral Surg, 18:312, 1964. Pediatr, 68:361, 1966. 13. Strahlie, R. D.: Chronic benign neutropenia in infancy and early 44. Matsoniotis, N. et al.: Chromosomes in Kostman’s disease, childhood, J Pediatr, 48:710, 1956. Lancet, 2:104, 1966. 14. Andrews, R. G. et al.: Chronic benign neutropenia of childhood- 45. Aubrey, J. J. and Hibbard, E. D.: Congenital agranulocytosis, associated oral manifestations, Oral Surg, 20:719, 1965. OrMSurg, 35:526, 1973. 15. Reichart, P. A. and Dornow, H.: Gingivo-periodontal manifesta- 46. Lampert, F. and Feeseler, A.: Periodontal changes during tions in chronic benign neutropenia, J Clin Pen’odontol, 5:74, chronic benign granulocytopenia in childhood. A case report, 1978. J Clin Pe~odont, 2:105, 1975. 16.Devaal, O. H. and Seynhaeve, V.: Reticular dysgenesia, Lancet, 47. Vann, W. F. and Oldenburg, T. R.: Atypical hereditary neutro- 11:1123, 1959. penia. Case reports of two siblings, J Dent Child, 43:265, 1976. 17.Alonso, K. et al.: Thymic alymphoplasia and congenital aleuko- 48. Joyce, R. A. et al.: Neutrophil kinetics in hereditary and con- cytosis (reticular dysgenesia), Arch Pathol, 94:179, 1972. genital neutropenias, N Engl J Med, 295:1385, 1976. 18. Andrews, J. P. et al.: Lethal congenital neutropenia with 49. Levine, S.: Chronic familial neutropenia with marked perio- occurring in two siblings, AmJMed, 29:358, 1960. dontal lesions, Or~/Surg, 12:310, 1959. 19. MacGillivray, J. B. et al.: Congenital neutropenia: a report of 50. Davey, K. W. and Konchak, P. A.: Agranulocytosis, Oral Surg, five cases, Acts Paediatr Scand, 53:188, 1964. 28:166, 1969. 20. Miller, D. R. et al.: Congenital neutropenia, Am J Dis Child, 51. Gates, G. F.: Chronic neutropenia presenting with oral lesions, 115:337, 1968. Oral Surg, 27:563, 1969. 21. Wriedt, J. et al.: Defective in congenital neutro- 52. Deasy, M. J. et al.: Pamilial benign chronic neutropenia associ- penia, NEngl JMed, 283:1072, 1970. ated with periodontal disease, JPedodontol, 51:206, 1980. 22. Biggar, W. D. et al.: Metabolic and functional studies of mono- 53. Gilman, P. A. et al.: Congenital agranulocytosis: prolonged sur- cytes in congenital neutropenia, Bdt J Haematol, 28:233, 1974. vival and terminal leukemia, Blood, 36:576, 1970. 23. L’Esperance, P. et al.: Abnormalin vitro differentiation of four 54. Rossman, P. L. and Hummer, G. J.: Chronic neutropenia in patients with congenital neutropenia, Blood, 46:733, 1975. siblings: the effect of steroids, Ann Intern Med, 52:242, 1960. 24. Parmley, R. T. et al.: Congenital neutropenia: neutrophil prolif- 55. Berkman, E. M. et al.: Supportive granulocyte transfusion in the eration with abnormal maturation, Blood, 46:733, 1975. infected severely neutropenic patient, Transfusion, 18:643, 1978. 25. Mishkin, D. J. et al.: Congenital neutropenia, Oral Surg, 42:738, 56. Sonis, A. L.: Periodontosis of the primary dentition: a case 1976. report, Pediatr Dent, 2:53, 1980. 26. Rich, K. et al.: Abnormalin vitro granulopoisesis in phenotypi- 57. Mason, J. D. and Lehner, T.: Clinical features of juvenile perio- cally normal parents of some children with congenital neutro- dontitis (periodontosis), J Pe~odontol, 45:636, 1974. penia, PediatHcs, 59:396, 1977. 58. Ingle, J. I.: Papillon-LeFevre syndrome: precocious periodon- 27. Zucker-Franklin, D. et al.: Congenital neutropenia: an intrinsic tosis with associated epidermal lesions, J Pedodontol, 30:234, cell defect demonstrated by electron microscopy of soft agar 1959. colonies, Blood, 49:425, 1977. 59. Chase, D. C. et al.: Histiocytosis X with jaw involvement, J Oral 28. Nishihira, H. et al.: Congenital neutropenia with a decrease in Sung, 52:494, 1974. neutrophilic colony forming cells and with an abnormal colony 60. Temple, T. R. et al.: Host factors in periodontal disease: perio-

CHRONICIDIOPATHIC NEUTROPENIA I94 Kalkwarf and Gutz dontal manifestations of Chediak-Higashi syndrome, J Perio- 70. Baehner, R. L. and Johnston, R. B., Jr.: Metabolic and bacteri- dont Res, 10:26, 1972. cidal activity of humaneosinophils, Brit J Haemat, 20:277, 1971. 61. Gillig, J. L. and Caldwell, C. H.: The Chediak-Higashi syn- 71. Baehner, R. L. and Johnston, R. B., Jr.: function in drome: case report, JDent CbJld, 37:527, 1970. children with neutropenia and chronic infections, Blood, 40:31, 62. Delgado, W. and Calderon, R.: Acatalasia in two Peruvian 1972. siblings, J Oral Path, 8:358, 1979. 72. Skapski, H. and Lehner, T.: Subgingival microflora and perio- 63. Wolf, J. E. and Ebel, L. K.: Chronic granulomatous disease: dontitis, JPeriodont Res, 11:19, 1976. report of case and review of the literature, J Am Dent Assoc, 96: 73. Attstrom, R.: Studies on neutrophil polymorphonuclear leuko- 292, 1978. cytes at the dentogingival junction in gingival health and dis- 64. Baer, P. N. et al.: Hypophosphatasia: report of two cases with ease, J Periodont Res, (Suppl. 8), 1971. dental findings, Pedodonticz, 2:209, 1964. 74. Attstrom, R. and Schroeder, H. E.: Effect of experimental 65. Eversole, L. R.: Cllrdcal Outline of Oral : Philadel- neutropenia on initial gingivitis in dogs, Scand J Dent Res, 87:7, phia, Lea and Febiger, 1978. pp 192-197. 1979. 66. Haas, R. J. et al.: Congenital immunodeficiency and agranulocy- 75. Cianciola, L. J. et al.: Defective polymorphonuclear leukocytes tosis, Acta Paediatr Scand, 66:366, 1977. function in a humanperiodontal disease, Nature, 265:445, 1977. 67. Howard, M. W. et al.: Infections in patients with neutropenia, 76. Cianciola, L. J. et al.: A family study of neutrophil in Am J Dis Ctdld, 131:788, 1977. idiopathic juvenile periodontitis (periodontosis), AADR,Abstr 68. Kauder, E. and Mauer, M. A.: Neutropenias of childhood, J # 155, 1977. Pediatr, 69:147, 1966. 77. Dale, D. C. et al.: Chronic neutropenia, , 58:128, 1979. 69. Cline, M. J. et al.: by human eosinophils, Blood, 78. Tinanoff, N. et al.: Effect of stannous fluoride mouthrinse on 32:922, 1968. dental plaque formation, J Clin Periodont, 7:232, 1980.

Pin Oak, Iowa John B. Ferguson

[Editor’s Note: Beginning with this issue we will be publishing member’s photographs in Pediatdc Dentistry. Though any subject matter will be considered, general, scenic photographs (as above) will be favored. Submissions from all members are invited and will be used on a space-available basis.]

PEDIATRICDENTISTRY 195 Voh 3, No. 2