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Oral radiographic changes in patients with progressive systemic sclerosis (scleroderma)
Intraoral and panoramic radiographs were made of 35 patients with progressive systemic sclerosis. Of those patients, 13 (37%) were found to have abnormally thickened periodontal ligament spaces. Six of the 35 demonstrated mild to significant resorption of the posterior mandibular angle. Three patients, including two showing angle resorption also had some degree of coronoid process destruction. All patients with this disease should receive initial and follow-up panoramic radiographic examinations to determine any osseous changes.
Oral radiographic changes in patients with progressive systemic sclerosis (scleroderma) S tu a rt C. W h ite , N e a l W . F re y ,
DDS, PhD, Los Angeles
DDS, MS, Conneaut, Ohio
D o n a ld D. B la s c h k e , M ic h a e l D. R oss,
P h ilip J. C le m e n ts , D a n ie l E. Furst,
DDS
MD MD
MD
H a ro ld E. P a u lu s ,
MD, Los Angeles ■ ■ ■ ■ ■ ■ ■ ■ ■ ■ ■
Progressive systemic sclerosis (PSS) is a gener alized disease that causes sclerosis of the skin and connective tissues. In addition to the skin involvement, the disease may be manifested by abnormalities in the gastrointestinal tract, heart, lungs, and kidneys. It is this involvement of or gans other than the skin that usually results in more serious complications. For example, gas trointestinal involvement can lead to malabsorp tion and cachexia, cardiac involvement can re sult in heart failure, pulmonary involvement can give rise to severe respiratory insufficiency, and renal involvement can develop into uremia, with or without malignant hypertension. Since involvement of the skin is often very obvious, with prominent resultant cutaneous manifestations, several terms have been used to identify this condition. CRST syndrome indi cates the combined occurrence of calcinosis, Raynaud’s phenomenon, sclerodactyly, and telangiectasia; scleroderma denotes the thick1178 ■ JADA, V ol. 94, J u n e 1977
ened hidebound quality of the involved skin (the lack of mobility of the skin over the underlying tissues); acroscleroderma emphasizes cutaneous changes, particularly in the distal portions of the extremities; and Thibierge-Weissenbach syn drome is an eponymic term used to describe ex tensive subcutaneous tissue calcinosis. In these conditions, systemic involvement of organ sys tems other than the skin is extremely common and is often uncovered either concomitantly with the diagnosis of the cutaneous disorder, or on future evaluation. PSS is, therefore, the pre ferred term and should be distinguished from morphea and linear scleroderma, in which the changes are local and limited to the skin. It is a disease that affects about three times more wo men than men. The greatest incidence occurs during ages 30 through 50; the disease rarely be gins during infancy or after age 60. Each year 4.5 persons out of every million find out they have PSS.1 Although the etiologic factors are uncer-
Table 1 ■ Incidence of thickened periodontal ligament spaces in all patients. No. of patients with thickened P P M * spaces Full-m outh Panoram ic No.________________radiographs____________ radiographs Patients with P S S t Control patients
35 40
13 0
No. of teeth with thickened PP M spaces Full-m outh Panoram ic radiographs_________ radiographs
Ï1
0
52 0
37 0
*PPM : periodontal m em brane fP S S : progressive systemic sclerosis
tain at present, various infectious, biochemical, immunologic, and vascular hypotheses have been proposed.2 Oral manifestations of PSS were initially re ported in 1944 by Stafne and Austin,3 who de scribed an increase in the thickness of the per iodontal ligament space on dental radiographs. This finding was noted in about 7% of their pa tients; the increase in the periodontal ligament space was fairly uniform in width and surround ed the entire root of the involved tooth. The pos terior teeth were more commonly affected than the anterior teeth. Despite this widening of the periodontal ligament space, it was noted that the teeth were not mobile and that the gingival at tachment was intact. Clinical or radiographic evaluation of the involved teeth did not reveal evidence of supraocclusion or periodontal dis ease. Since that original report, many other in vestigators have reported the thickening of the periodontal ligament space in such patients.*6 In 1950, Krogh7 described a patient in whom thickening of the periodontal ligament space dis appeared after its earlier occurrence, thereby documenting reversibility of this lesion. Microscopic examination of thickened perio dontal ligament spaces by Gores8 revealed “loss of normal arrangement of collagenous fibers . . . , and thickening of the walls, with accompanying narrowing of the lumina of the blood vessels of the periodontal membrane.” Despite such defin itive radiographic and microscopic descriptions, as well as histochemical studies,9 the cause of these findings is unknown. Resorption of the posteroinferior angle of the mandible was first described in patients with PSS by Taveras10 in 1959. Seifert and co-work ers11 subsequently described 16 patients with PSS; 5 had resorption of the mandibular rami, and 1 had suffered bilateral fractures on trauma. These authors11 reported that their patients with mandibular resorptive changes had restricted oral apertures. Because fractures have been known to complicate this bone resorptive phe nomenon, this change can be of significant clin ical importance.12 In the present study of the oral radiographic changes in patients with PSS, such
mandibular changes are given particular atten tion, in addition to the better known changes of the periodontal ligament space.
Study design Thirty-five patients with PSS were referred to the Oral Radiology Clinic from the Division of Rheumatology. Criteria for diagnosis were the same as those used by Medsger and Masi.13 These patients ranged in age from 24 to 79 with a mean of 44; there were 30 women and 5 men, 1 black and the others white. Panoramic and fullmouth intraoral radiographs were taken on each patient. All patients had at least some teeth re maining. Forty adults of similar age and with a similar distribution by sex, who were seeking general dental care and who did not have PSS, were used as controls. Radiographs of all patients were examined blindly in random sequence simultaneously by two dental radiologists (S. W. and D. B.). Thick ening of the periodontal ligament space was scored when a uniformly thickened space around the entire tooth was observed, when a uniformly thickened space was seen to extend along one side of the root surface from the interdental al veolar crest to the root apex, or when a uniform ly thickened space around the apical third of a tooth was observed and there was no evidence of periodontal or pulpal pathologic conditions, and no reasonable evidence of traumatic occlusion. In all instances, the scored periodontal mem brane spaces were at least twice the width of normal spaces in the same patient. Teeth with uneven thickness of the periodontal ligament, especially near the alveolar crest, were not scored. Other osseous changes were noted as observed.
Results Table 1 shows that radiographs of 13 of 35 of the patients with PSS (37%) demonstrated thickenW h ite -o th e rs : PROGRESSIVE SYSTEMIC SCLEROSIS ■ 1179
Fig
1 ■ Abnormally thickened
periodontal
ligament spaces
are seen around all aspects of both bicuspids and first and sec
Fig 2 ■ Panoramic radiograph of W. K. demonstrating bilateral resorptive changes of posteroinferior angles of mandible.
ond molars.
ing of the periodontal ligament space, whereas radiographs for none of the 40 control patients demonstrated such a finding (Fig 1). The num ber of teeth involved ranged from 1 to 14, with an aver age of 4.5, a median of 3, and a mode of 1. Five patients with PSS had only 1 tooth in volved, six had 2 to 5 teeth involved, and the re maining two patients had 13 and 14 teeth in volved. It was easier to see the thickened perio dontal ligament spaces on the intraoral films than on the panoramic projections. For 16 of the 35 patients with PSS, two or more sets of intraoral radiographs were available, separated by up to two years. In radiographs of two patients, progressive thickening of the per iodontal ligament space was observed. Over time, in one patient, the number of involved teeth increased from 1 to 3; in another, the in crease was 0 to 1. Decrease in the number of affected periodontal ligament spaces was not ob served. Table 2 indicates the distribution of teeth with thickened periodontal ligament spaces as ob served on the intraoral radiographs. The fre quency of affected teeth was similar in the maxil la and the mandible. The lamina dura assoc iated with the thickened spaces around 52 teeth were intact and of normal thickness except around two teeth. There was a strong tendency for lesions to appear in posterior rather than an terior teeth. Forty-seven of the 52 lesions were found around the roots of posterior teeth. In addi tion, all patients with anterior lesions had con2 ■ Distribution of teeth with thickened periodontal ligament spaces in patients with progressive systemic sclerosis.
T a b le
Maxilla Mandible Total
Anterior
Premolar
Molar
Total
3 2 5
7 9 16
16 15 31
26 26 52
1 180 ■ JADA, V ol. 94, J u n e 1977
Fig 3 ■ Schematic drawing of panoramic appearance of man dible illustrating varying degrees of resorptive changes seen in our patients. (Each patient is identified by initials.) Crosshatched lines in region of coronoid process indicate areas of local bone resorption. In B. P. entire left coronoid process is absent.
comitant lesions in the posterior teeth; no in stances of isolated anterior lesions were ob served. Radiographs of 6 of the 35 patients with PSS demonstrated osseous resorption in the region of the mandibular angles. Figure 2 illustrates one of the five instances of bilateral angular resorption. These changes were not observed in radiographs of any of the control patients. The extent of the resorption in the six patients varied from mild to prominent. Figure 3 illustrates schematically the extent of the mandibular osseous defects. All angular lesions were bilaterally symmetrical except one; this lesion was minimal and unilater al. The angular lesions varied in appearance from erosion primarily along the inferior border of the mandibular body near the angle, to loss primarily on the posterior border of the ramus. For three of the six patients with resorption of
Fig 4 ■ Panoramic radiographs of P. M. 15 months apart illus trating interval resorptive changes. Remnants of cortical bone
Fig 5 ■ Portion of panoramic radiograph of B. P. illustrating com
are identified with arrows in bottom photo.
plete absence of left coronoid process.
the mandibular angle, follow-up films for up to two years were available for comparison. In ra diographs of all three, progression of the resorp tion was observed (Fig 4). No instances of path ologic fracture were observed in the current study. Partial or complete resorption of the coronoid process also was observed radiographically in two of the six patients with PSS who had resorp tion of the mandibular angle, and in another pa tient with PSS. The extent of this finding varied from mild resorption, to amputation with a free fragment, to complete resorption of the coronoid process (Fig 5). Bony changes correlated well with thickening of the periodontal ligament spaces, in that radio graphs of six of the seven patients with resorp tion of the mandibular angles and/or coronoid processes also demonstrated thickening of the spaces around one or more teeth (Table 3). Ra diographs of almost half (6 of 13) of the patients with thickened periodontal ligament spaces also demonstrated the osseous mandibular changes.
Discussion
We found thickened periodontal ligament spac es in radiographs of 37% of our patients with PSS. This figure is noticeably higher than the 7% reported by Stafne and Austin. Possible rea sons for this difference are: different criteria may have been used in evaluating the abnormal thick ening of the periodontal membrane, and the ex tent of the disease in our group of 35 patients with PSS may have been more severe than that stud ied by other authors. Radiographs published in articles by other investigators have generally shown noticeable thickening of the periodontal ligament around all surfaces of involved roots. While such lesions were frequendy scored in our sample, radiographs of many patients also demonstrated thickening of the periodontal membrane around only the apical third of a tooth or along one root surface. Inclusion of such less prominent occurrences in our data may account, in part, for the higher incidence of lesions ob
■ Mandibular osseous and periodontal membrane changes in patients with progressive systemic sclerosis.
T a b le 3
Patient W. K. P. M. I. P. B. P. D. R. D. S. Z. U.
Angular resorption Bilateral Unilateral X X X
Coronoid resorption X X
X X X
X
Thickened periodontal spaces 1 1 14 4 3 0 5
W h ite — o th e rs : PR O G R ESSIVE S Y S TE M IC S C LE R O S IS ■
1181
served in this study. In all our patients, how ever, scored periodontal membranes were at least twice as thick as those considered normal. Again, it is also possible that the incidence of thickening of the periodontal ligament spaces, observed in our 35 patients radiographically, is a result of the rather severe nature of their dis ease. Previous researchers have found that the pos terior teeth are more frequently involved than the anterior teeth.3 The present work confirms this observation and also indicates that the max illa and the mandible are about equally involved. Unlike previous reports describing a reduced lamina dura around involved teeth, in this study the lamina dura was found to be of normal thick ness around most of the teeth with thickened periodontal ligament spaces. Only twice was it found to be thinned or missing. It was rather striking that roughly half of all patients with changes in the periodontal ligament also had osseous changes in the mandible. In all, radiographs of seven of the patients with PSS demonstrated resorption of some portion of the mandibular angle and/or the coronoid process. Resorption of the mandibular angle occurred twice as frequently as resorption of the coronoid process and both were found to be associated, except in one instance, with people who also demonstrated changes of the periodontal mem brane space. Since radiographs of half the pa tients with periodontal ligament space changes did not demonstrate such osseous lesions, the bone changes would appear to represent a more advanced state of disease. Further, the progressive nature of the defect in the mandibular angle and coronoid process is indicated by the three patients for whom fol low-up radiographs demonstrated clear progres sion of the disease. Of those three patients, the radiographs for only one demonstrated an in creased incidence of thickening of the perio dontal membrane spaces. This patient (P. M.) showed an increase of from zero to one involved tooth. Radiographs for the other patients (I. P. and Z. U.) demonstrated no such progressive changes in the periodontal ligament during the same time. Although the thickening of the periodontal ligament spaces did not seem to present clinical difficulties to the individuals with PSS, the pro gressive loss of bone in the region of the mandib ular angle is more serious. None o f our patients have yet had pathologic fractures in the mandi ble, but such an occurrence is possible. We be 1182 ■ JADA, Vol. 94, June 1977
lieve that it is important to follow all patients known to have PSS with periodic radiography of the jaws in order to monitor this potential prob lem. Resorptive osseous changes have been repor ted in multiple bones including the clavicle, ra dius, ulna, and digits of the hand and foot in pa tients with PSS.14 Although the etiologic factors of the mandibular resorption are unknown, most authors believe that, in some way, pressure atro phy or ischemia is responsible for this defect in other bones. The progressive nature o f the le sions observed in three of our patients over a rel atively short period of time (two years) is com patible with the concept that mandibular lesions are acquired defects secondary to pressure atro phy or ischemia, as proposed for other skeletal lesions. This investigation was supported in part by U SPHS Grants No. 5 S01 R R-05304-14, G M 15759, and No. RR-00865. Dr. W h ite is associate professor and chairm an of oral radiology, University of California, School of Dentistry, T h e C enter for the H ealth Sciences, Los Angeles, 90024. Dr. Frey is in private prac tice in C onneaut, Ohio. Dr. Blaschke is assistant professor, UCLA S chool of Dentistry. Drs. Ross and Furst are fellows in th e Divi sion o f R heum atology, D epartm ent of M edicine, at UCLA. Dr. C lem ents is assistant professor and Dr. Paulus is associate pro fessor in th e Division of R heum atology, Departm ent of M edi cine, UCLA. Address requests for reprints to Dr. W hite. 1. H ollander, J.L., and M cCarty, D.J. A rthritis and allied con ditions. Philadelphia, Lea & Febiger, 1972, p 962. 2. C am pbell, P.M ., and LeRoy, E.C. Pathogenesis of systemic sclerosis: a vascular hypothesis. Sem in Arthritis Rheum 4:351 M ay 1975. 3. Stafne, E.C ., and Austin, L.T. A characteristic dental finding in acrosclerosis and diffuse scleroderm a. Amer J O rthod 30:25 Jan 1944. 4. Sm ith, D.B. Scleroderm a: its oral manifestations. Oral Surg 11:865 Aug 1958. 5. Traiger, J. S cleroderm a; its oral m anifestations. O ral Surg 14:117 Jan 1961. 6. G reen, D. S cleroderm a and its oral m anifestations. Oral Surg 15:1312 Nov 1962. 7. Krogh, H.W. Dental m anifestations of scleroderm a: report o f case. J O ral Surg 8:242 July 1950. 8. Gores, R.J. D ental characteristics associated w ith acro sclerosis and diffuse scleroderm a. JADA 54:755 June 1957. 9. Fullm er, H.M ., and W ite, W .E. Periodontal m em brane affec ted by scleroderm a (a histochem ical study). Arch Pathol 73:184 M arch 1962. 10. Taveras, J.M . The interpretation of radiographs. In Schwartz, L., ed. Disorders o f the tem p orom andibular joint. Philadelphia, W . B. S aunders Co., 1959, p 160. 11. Seifert, M.H.; Steigerw ald, J.C.; and Cliff, M .M . B one re sorption of the m andible in progressive system ic sclerosis. A rth ritis Rheum 18:507 S ept-O ct 1975. 12. W eber, D.D.; Blunt, M.H.; and C aldwell, J.B. Fracture of m an dib ular rami com plicated by scleroderm a: report of case. J Oral Surg 28:860 Nov 1970. 13. M edsger, T.A., and Masi, A.T. Epidem iology of systemic sclerosis (scleroderm a). Ann Intern Med 74:714 May 1971. 14. G ondos, B. R oentgen m anifestation in progressive sys tem ic sclerosis (diffuse scleroderm a). A m er J R oentgenol R adi um T h er Nucl Med 8 4:235 Aug 1960.
Oral radiographic changes in patients with progressive systemic sclerosis (scleroderma) S tu a rt C. W h ite , N e a l W . F re y ,
DDS, PhD, Los Angeles
DDS, MS, Conneaut, Ohio
D o n a ld D. B la s c h k e , M ic h a e l D. R oss,
P h ilip J. C le m e n ts , D a n ie l E. Furst,
DDS
MD MD
MD
H a ro ld E. P a u lu s ,
MD, Los Angeles ■ ■ ■ ■ ■ ■ ■ ■ ■ ■ ■
Progressive systemic sclerosis (PSS) is a gener alized disease that causes sclerosis of the skin and connective tissues. In addition to the skin involvement, the disease may be manifested by abnormalities in the gastrointestinal tract, heart, lungs, and kidneys. It is this involvement of or gans other than the skin that usually results in more serious complications. For example, gas trointestinal involvement can lead to malabsorp tion and cachexia, cardiac involvement can re sult in heart failure, pulmonary involvement can give rise to severe respiratory insufficiency, and renal involvement can develop into uremia, with or without malignant hypertension. Since involvement of the skin is often very obvious, with prominent resultant cutaneous manifestations, several terms have been used to identify this condition. CRST syndrome indi cates the combined occurrence of calcinosis, Raynaud’s phenomenon, sclerodactyly, and telangiectasia; scleroderma denotes the thick1178 ■ JADA, V ol. 94, J u n e 1977
ened hidebound quality of the involved skin (the lack of mobility of the skin over the underlying tissues); acroscleroderma emphasizes cutaneous changes, particularly in the distal portions of the extremities; and Thibierge-Weissenbach syn drome is an eponymic term used to describe ex tensive subcutaneous tissue calcinosis. In these conditions, systemic involvement of organ sys tems other than the skin is extremely common and is often uncovered either concomitantly with the diagnosis of the cutaneous disorder, or on future evaluation. PSS is, therefore, the pre ferred term and should be distinguished from morphea and linear scleroderma, in which the changes are local and limited to the skin. It is a disease that affects about three times more wo men than men. The greatest incidence occurs during ages 30 through 50; the disease rarely be gins during infancy or after age 60. Each year 4.5 persons out of every million find out they have PSS.1 Although the etiologic factors are uncer-
Table 1 ■ Incidence of thickened periodontal ligament spaces in all patients. No. of patients with thickened P P M * spaces Full-m outh Panoram ic No.________________radiographs____________ radiographs Patients with P S S t Control patients
35 40
13 0
No. of teeth with thickened PP M spaces Full-m outh Panoram ic radiographs_________ radiographs
Ï1
0
52 0
37 0
*PPM : periodontal m em brane fP S S : progressive systemic sclerosis
tain at present, various infectious, biochemical, immunologic, and vascular hypotheses have been proposed.2 Oral manifestations of PSS were initially re ported in 1944 by Stafne and Austin,3 who de scribed an increase in the thickness of the per iodontal ligament space on dental radiographs. This finding was noted in about 7% of their pa tients; the increase in the periodontal ligament space was fairly uniform in width and surround ed the entire root of the involved tooth. The pos terior teeth were more commonly affected than the anterior teeth. Despite this widening of the periodontal ligament space, it was noted that the teeth were not mobile and that the gingival at tachment was intact. Clinical or radiographic evaluation of the involved teeth did not reveal evidence of supraocclusion or periodontal dis ease. Since that original report, many other in vestigators have reported the thickening of the periodontal ligament space in such patients.*6 In 1950, Krogh7 described a patient in whom thickening of the periodontal ligament space dis appeared after its earlier occurrence, thereby documenting reversibility of this lesion. Microscopic examination of thickened perio dontal ligament spaces by Gores8 revealed “loss of normal arrangement of collagenous fibers . . . , and thickening of the walls, with accompanying narrowing of the lumina of the blood vessels of the periodontal membrane.” Despite such defin itive radiographic and microscopic descriptions, as well as histochemical studies,9 the cause of these findings is unknown. Resorption of the posteroinferior angle of the mandible was first described in patients with PSS by Taveras10 in 1959. Seifert and co-work ers11 subsequently described 16 patients with PSS; 5 had resorption of the mandibular rami, and 1 had suffered bilateral fractures on trauma. These authors11 reported that their patients with mandibular resorptive changes had restricted oral apertures. Because fractures have been known to complicate this bone resorptive phe nomenon, this change can be of significant clin ical importance.12 In the present study of the oral radiographic changes in patients with PSS, such
mandibular changes are given particular atten tion, in addition to the better known changes of the periodontal ligament space.
Study design Thirty-five patients with PSS were referred to the Oral Radiology Clinic from the Division of Rheumatology. Criteria for diagnosis were the same as those used by Medsger and Masi.13 These patients ranged in age from 24 to 79 with a mean of 44; there were 30 women and 5 men, 1 black and the others white. Panoramic and fullmouth intraoral radiographs were taken on each patient. All patients had at least some teeth re maining. Forty adults of similar age and with a similar distribution by sex, who were seeking general dental care and who did not have PSS, were used as controls. Radiographs of all patients were examined blindly in random sequence simultaneously by two dental radiologists (S. W. and D. B.). Thick ening of the periodontal ligament space was scored when a uniformly thickened space around the entire tooth was observed, when a uniformly thickened space was seen to extend along one side of the root surface from the interdental al veolar crest to the root apex, or when a uniform ly thickened space around the apical third of a tooth was observed and there was no evidence of periodontal or pulpal pathologic conditions, and no reasonable evidence of traumatic occlusion. In all instances, the scored periodontal mem brane spaces were at least twice the width of normal spaces in the same patient. Teeth with uneven thickness of the periodontal ligament, especially near the alveolar crest, were not scored. Other osseous changes were noted as observed.
Results Table 1 shows that radiographs of 13 of 35 of the patients with PSS (37%) demonstrated thickenW h ite -o th e rs : PROGRESSIVE SYSTEMIC SCLEROSIS ■ 1179
Fig
1 ■ Abnormally thickened
periodontal
ligament spaces
are seen around all aspects of both bicuspids and first and sec
Fig 2 ■ Panoramic radiograph of W. K. demonstrating bilateral resorptive changes of posteroinferior angles of mandible.
ond molars.
ing of the periodontal ligament space, whereas radiographs for none of the 40 control patients demonstrated such a finding (Fig 1). The num ber of teeth involved ranged from 1 to 14, with an aver age of 4.5, a median of 3, and a mode of 1. Five patients with PSS had only 1 tooth in volved, six had 2 to 5 teeth involved, and the re maining two patients had 13 and 14 teeth in volved. It was easier to see the thickened perio dontal ligament spaces on the intraoral films than on the panoramic projections. For 16 of the 35 patients with PSS, two or more sets of intraoral radiographs were available, separated by up to two years. In radiographs of two patients, progressive thickening of the per iodontal ligament space was observed. Over time, in one patient, the number of involved teeth increased from 1 to 3; in another, the in crease was 0 to 1. Decrease in the number of affected periodontal ligament spaces was not ob served. Table 2 indicates the distribution of teeth with thickened periodontal ligament spaces as ob served on the intraoral radiographs. The fre quency of affected teeth was similar in the maxil la and the mandible. The lamina dura assoc iated with the thickened spaces around 52 teeth were intact and of normal thickness except around two teeth. There was a strong tendency for lesions to appear in posterior rather than an terior teeth. Forty-seven of the 52 lesions were found around the roots of posterior teeth. In addi tion, all patients with anterior lesions had con2 ■ Distribution of teeth with thickened periodontal ligament spaces in patients with progressive systemic sclerosis.
T a b le
Maxilla Mandible Total
Anterior
Premolar
Molar
Total
3 2 5
7 9 16
16 15 31
26 26 52
1 180 ■ JADA, V ol. 94, J u n e 1977
Fig 3 ■ Schematic drawing of panoramic appearance of man dible illustrating varying degrees of resorptive changes seen in our patients. (Each patient is identified by initials.) Crosshatched lines in region of coronoid process indicate areas of local bone resorption. In B. P. entire left coronoid process is absent.
comitant lesions in the posterior teeth; no in stances of isolated anterior lesions were ob served. Radiographs of 6 of the 35 patients with PSS demonstrated osseous resorption in the region of the mandibular angles. Figure 2 illustrates one of the five instances of bilateral angular resorption. These changes were not observed in radiographs of any of the control patients. The extent of the resorption in the six patients varied from mild to prominent. Figure 3 illustrates schematically the extent of the mandibular osseous defects. All angular lesions were bilaterally symmetrical except one; this lesion was minimal and unilater al. The angular lesions varied in appearance from erosion primarily along the inferior border of the mandibular body near the angle, to loss primarily on the posterior border of the ramus. For three of the six patients with resorption of
Fig 4 ■ Panoramic radiographs of P. M. 15 months apart illus trating interval resorptive changes. Remnants of cortical bone
Fig 5 ■ Portion of panoramic radiograph of B. P. illustrating com
are identified with arrows in bottom photo.
plete absence of left coronoid process.
the mandibular angle, follow-up films for up to two years were available for comparison. In ra diographs of all three, progression of the resorp tion was observed (Fig 4). No instances of path ologic fracture were observed in the current study. Partial or complete resorption of the coronoid process also was observed radiographically in two of the six patients with PSS who had resorp tion of the mandibular angle, and in another pa tient with PSS. The extent of this finding varied from mild resorption, to amputation with a free fragment, to complete resorption of the coronoid process (Fig 5). Bony changes correlated well with thickening of the periodontal ligament spaces, in that radio graphs of six of the seven patients with resorp tion of the mandibular angles and/or coronoid processes also demonstrated thickening of the spaces around one or more teeth (Table 3). Ra diographs of almost half (6 of 13) of the patients with thickened periodontal ligament spaces also demonstrated the osseous mandibular changes.
Discussion
We found thickened periodontal ligament spac es in radiographs of 37% of our patients with PSS. This figure is noticeably higher than the 7% reported by Stafne and Austin. Possible rea sons for this difference are: different criteria may have been used in evaluating the abnormal thick ening of the periodontal membrane, and the ex tent of the disease in our group of 35 patients with PSS may have been more severe than that stud ied by other authors. Radiographs published in articles by other investigators have generally shown noticeable thickening of the periodontal ligament around all surfaces of involved roots. While such lesions were frequendy scored in our sample, radiographs of many patients also demonstrated thickening of the periodontal membrane around only the apical third of a tooth or along one root surface. Inclusion of such less prominent occurrences in our data may account, in part, for the higher incidence of lesions ob
■ Mandibular osseous and periodontal membrane changes in patients with progressive systemic sclerosis.
T a b le 3
Patient W. K. P. M. I. P. B. P. D. R. D. S. Z. U.
Angular resorption Bilateral Unilateral X X X
Coronoid resorption X X
X X X
X
Thickened periodontal spaces 1 1 14 4 3 0 5
W h ite — o th e rs : PR O G R ESSIVE S Y S TE M IC S C LE R O S IS ■
1181
served in this study. In all our patients, how ever, scored periodontal membranes were at least twice as thick as those considered normal. Again, it is also possible that the incidence of thickening of the periodontal ligament spaces, observed in our 35 patients radiographically, is a result of the rather severe nature of their dis ease. Previous researchers have found that the pos terior teeth are more frequently involved than the anterior teeth.3 The present work confirms this observation and also indicates that the max illa and the mandible are about equally involved. Unlike previous reports describing a reduced lamina dura around involved teeth, in this study the lamina dura was found to be of normal thick ness around most of the teeth with thickened periodontal ligament spaces. Only twice was it found to be thinned or missing. It was rather striking that roughly half of all patients with changes in the periodontal ligament also had osseous changes in the mandible. In all, radiographs of seven of the patients with PSS demonstrated resorption of some portion of the mandibular angle and/or the coronoid process. Resorption of the mandibular angle occurred twice as frequently as resorption of the coronoid process and both were found to be associated, except in one instance, with people who also demonstrated changes of the periodontal mem brane space. Since radiographs of half the pa tients with periodontal ligament space changes did not demonstrate such osseous lesions, the bone changes would appear to represent a more advanced state of disease. Further, the progressive nature of the defect in the mandibular angle and coronoid process is indicated by the three patients for whom fol low-up radiographs demonstrated clear progres sion of the disease. Of those three patients, the radiographs for only one demonstrated an in creased incidence of thickening of the perio dontal membrane spaces. This patient (P. M.) showed an increase of from zero to one involved tooth. Radiographs for the other patients (I. P. and Z. U.) demonstrated no such progressive changes in the periodontal ligament during the same time. Although the thickening of the periodontal ligament spaces did not seem to present clinical difficulties to the individuals with PSS, the pro gressive loss of bone in the region of the mandib ular angle is more serious. None o f our patients have yet had pathologic fractures in the mandi ble, but such an occurrence is possible. We be 1182 ■ JADA, Vol. 94, June 1977
lieve that it is important to follow all patients known to have PSS with periodic radiography of the jaws in order to monitor this potential prob lem. Resorptive osseous changes have been repor ted in multiple bones including the clavicle, ra dius, ulna, and digits of the hand and foot in pa tients with PSS.14 Although the etiologic factors of the mandibular resorption are unknown, most authors believe that, in some way, pressure atro phy or ischemia is responsible for this defect in other bones. The progressive nature o f the le sions observed in three of our patients over a rel atively short period of time (two years) is com patible with the concept that mandibular lesions are acquired defects secondary to pressure atro phy or ischemia, as proposed for other skeletal lesions. This investigation was supported in part by U SPHS Grants No. 5 S01 R R-05304-14, G M 15759, and No. RR-00865. Dr. W h ite is associate professor and chairm an of oral radiology, University of California, School of Dentistry, T h e C enter for the H ealth Sciences, Los Angeles, 90024. Dr. Frey is in private prac tice in C onneaut, Ohio. Dr. Blaschke is assistant professor, UCLA S chool of Dentistry. Drs. Ross and Furst are fellows in th e Divi sion o f R heum atology, D epartm ent of M edicine, at UCLA. Dr. C lem ents is assistant professor and Dr. Paulus is associate pro fessor in th e Division of R heum atology, Departm ent of M edi cine, UCLA. Address requests for reprints to Dr. W hite. 1. H ollander, J.L., and M cCarty, D.J. A rthritis and allied con ditions. Philadelphia, Lea & Febiger, 1972, p 962. 2. C am pbell, P.M ., and LeRoy, E.C. Pathogenesis of systemic sclerosis: a vascular hypothesis. Sem in Arthritis Rheum 4:351 M ay 1975. 3. Stafne, E.C ., and Austin, L.T. A characteristic dental finding in acrosclerosis and diffuse scleroderm a. Amer J O rthod 30:25 Jan 1944. 4. Sm ith, D.B. Scleroderm a: its oral manifestations. Oral Surg 11:865 Aug 1958. 5. Traiger, J. S cleroderm a; its oral m anifestations. O ral Surg 14:117 Jan 1961. 6. G reen, D. S cleroderm a and its oral m anifestations. Oral Surg 15:1312 Nov 1962. 7. Krogh, H.W. Dental m anifestations of scleroderm a: report o f case. J O ral Surg 8:242 July 1950. 8. Gores, R.J. D ental characteristics associated w ith acro sclerosis and diffuse scleroderm a. JADA 54:755 June 1957. 9. Fullm er, H.M ., and W ite, W .E. Periodontal m em brane affec ted by scleroderm a (a histochem ical study). Arch Pathol 73:184 M arch 1962. 10. Taveras, J.M . The interpretation of radiographs. In Schwartz, L., ed. Disorders o f the tem p orom andibular joint. Philadelphia, W . B. S aunders Co., 1959, p 160. 11. Seifert, M.H.; Steigerw ald, J.C.; and Cliff, M .M . B one re sorption of the m andible in progressive system ic sclerosis. A rth ritis Rheum 18:507 S ept-O ct 1975. 12. W eber, D.D.; Blunt, M.H.; and C aldwell, J.B. Fracture of m an dib ular rami com plicated by scleroderm a: report of case. J Oral Surg 28:860 Nov 1970. 13. M edsger, T.A., and Masi, A.T. Epidem iology of systemic sclerosis (scleroderm a). Ann Intern Med 74:714 May 1971. 14. G ondos, B. R oentgen m anifestation in progressive sys tem ic sclerosis (diffuse scleroderm a). A m er J R oentgenol R adi um T h er Nucl Med 8 4:235 Aug 1960.