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Growth changes and orthodontic treatment in a patient with condylolysis
American Journal of ORTHODONTICS and DENTOFACIAL ORTHOPEDICS Founded in 1915
Volunze 102 Number 4
October 1992
Copyright 9 1992 by the American Association of Orthodontists
CASE REPORT
Growth changes and orthodontic treatment in a patient with condylolysis Takafumi Susami, DDS, PhD, ~ Takayuki Kuroda, DDS, PhD, b Yoshito Yano, DDS, c and Touru Nakamura, DDS, PhD ~ ToL3'o, Japan A patient with acquired bilateral degeneration of the mandibular condyles was treated orthodontically. The flattening of condyles and the shortening of the ramus began at adolescence. The facial profile changed to a convex type, with a marked mandibular retrognathia and severe Class II malocclusion. The cause seems to be due to a condylolysis of the mandible. (AM J ORTHOO DENTOFACORTHOP 1992;102:295-301 .)
This is an important article because of recent attempts to link orthodontics with changes in condylar structure during therapy. There are several cases now in litigation in which there has been reduction in condylar mass and a change in shape, resulting in the shortening of the ramus height and an open bite. Despite attempts to close the bite, the condylolysis may continue. Rasmussen has shown that this can often stabilize after 4 to 5 years, but the cause is unknown. The importance here lies in the fact that there was no orthodontic therapy and no apparent trauma, and yet the process occurred. This case provides an important link in the defense of orthodontists against contingency-fee lawyer litigation. --T. M. Graber
Fig. 1. Facial appearance at first examination. A n o m a l i e s o f the mandibular condyle, such as absence, incomplete formation or degeneration, cause severe facial dysmorphosis. There are several eiiologic factors in the abnormal development o f mandibular condyle. Congenital anomalies, trauma, and infection of the mandibular condyle in growing children often lead to skeletal disharmony with severe malocclusion. ~.2 From Tokyo Medical and Dental University and Takahashi Orthodontic Office. ~Instructor, The Second Department of Orthodontics. bProfessor and Chairman, The Second Department of Orthodontics. 'Director, Takahashi Orthodontic Office. dtnstructor, Takahashi Orthodontic Office. 814139O99
The purpose o f this article is to present a case report on a patient with acquired bilateral degeneration o f the mandibular condyle that started at adolescence. Morphologic and growth change analyses have been completed. The results o f the orthodontic treatment are illustrated.
CASE REPORT The first examination A girl who was 11 years and I0 months old had a complaint of anterior crowding. Her facial profile was slightly concave and no asymmetry was observed (Figs. 1 and 2). Anteroposterior molar relations were Class I at the left side and Class Ill at the right side. Overjet was 4 mm, and over
295
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Susami et al.
Am. J. Orthod. Dentofac. Orthop. October 1992
Fig. 2. Occlusion at time of first examination.
bite was 2.5 mm. Arch shape was tapered in both maxillary and mandibular arches. Full-mouth intraoral radiographs showed no dental abnormalities. All four third molars were developing. Cephalometric analysis indicated a skeletal Class III tendency with relatively retruded maxilla and protruded mandible (Fig. 3). The mandibular plane, Y-axis, and gonial angle were within normal range; the maxillary and mandibular incisors showed labial and lingual tipping, respectively. There were no specific abnormal forms in the mandibular ramus and the condyle. These findings indicated the major problem was an arch length discrepancy. The extraction of four premolars and the alignment of individual teeth, with careful attention to the remaining facial growth, was recommended. Nevertheless, the treatment was postponed for economic reasons.
The second examination After a protracted interval, the patient came in for an examination again at the age of 17 years and 1 month. She showed peculiar morphologic changes. The facial profile was changed to a convex type, with a marked mandibular retrognathia (Fig. 4). Lip incompetence was seen at the rest position, and the hypertonicity of perioral musculature was noted at lip closure. The overjet was increased abnormally to 11 mm, and the overbite was decreased to - 1 mm, presenting anterior open bite (Fig. 5). The molar relations were changed
to bilateral Class II. The arch shape was still tapered and showed crowding in both maxilla and mandible. The cephalometric analysis represented the shortening of the mandible in size, especially in the ramus (Fig. 6). The mandible was retruded posteriorly and was rotated downward and backward, presenting a typical retrognathia, with a large mandibular plane angle and Y-axis. The maxillary incisors were tipped more labially, and the FMIA angle was decreased. The mandibular condyles were obscure, and typical antegonial notching was observed in the cephalogram. The degenerated condylar form was clearly shown by the orthopantomograph and the transcranial projection (Fig. 7). The condylar processes became thin, and the condylar heads were flattened on the articular surface. The amount of maximum mouth opening, as measured between upper and lower incisor edge, was 42 mm, and the mouth opening movement was not restricted. There was no apparent history concerning facial trauma or infection between the first and the second examination, except the chin was bruised while playing volleyball. Hematologic examinations were performed on the routine biochemical examinations (mineral, sugar, lipid, protein, and enzymes), hemogram, and a specific examination for antistreptolysin O (ASO), C-reactive protein (CRP), and rheumatoid factors (RA-test). There were no particular findings
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Fig. 4. Facial appearance at second examination.
Fig. 3. Lateral cephalograms taken at first examination.
suggesting systemic bone disease, infection, or rheumatoid arthritis. Negative findings concerning the systemic diseases were also observed in hand-wrist and foot-wrist radiographs. The masticatory muscle activiiies--masseter, anterior and posterior parts of temporalis, and anterior belly of digastricus--were checked with an electromyograph (Fig. 8). Although the activities of these muscles in an 0.8 second tapping movement were relatively low, they were working harmoniously. In the functional movements, such as chewing and biting, the activities were quite normal. There were also no findings indicating abnormal muscle activity that pointed to the cause of the degeneration. Orthodontic treatment After l-year growth observation in which no progressive skeletal changes were noticed, active orthodontic treatment was started. The treatment planning was as follows: 1. Maximum anchorage for the maxillary molars. 2. Retraction and lingual tipping of the maxillary incisors with bilateral extraction of the maxillary first premolars. 3. Anterior expansion of the mandibular arch to eliminate the crowding and to correct the ovcrjet.
4. Keeping the occlusal plane unchanged during orthodontic treatment. The treatment was performed with multibracket appliances with standard 0.018 • 0.022-inch slot. A leveling of the maxillary arch preceded that of the mandible arch. A Nance holding arch was placed in the maxillary arch and a cervical pull J-hook extraoral appliance was used for canine retraction (Fig. 9). The active treatment period was 2 years and l month. The following changes were observed by superimpositional comparison of the cephalograms taken before and after active treatment (Fig. 10). The medial movement of the maxillary molars was about 1.5 mm, and there was no extrusion. Lingual tipping of the maxillary incisors and some labial tipping of the mandibular incisors was found. Mandibular downward and backward rotation occurred during the treatment period. Retention was performed with a Hawley-type retainer in the maxilla and with a bonded canine-to-canine lingual retainer in the mandible. Occlusal stability was well maintained, as shown in Figs. 11 and 12. DISCUSSION The cause o f the degeneration of the condyles in this patient is unknown. It is rather questionable to attribute this to congenital etiologic effects, because o f a normal mandibular growth without any symptoms until her first visit. There are no similar familial anomalies. Reports 1,2"3 suggested several causes, such as osteoarthritis, trauma, local infection, and rheumatoid arthritis, as a basis o f this developmental anomaly. However, there is no proof o f any o f these factors for this patient. Hematologic examinations, especially a specific examination for antistreptolysin O (ASO), C-reactive protein, and rheumatoid factors, eliminated the possibility o f the local infection or o f rheumatoid arthritis. The effects o f the masticatory muscle deficiency were also not seen in the electromyographic examination. The American A c a d e m y o f Craniomandibuiar Disorders 4 has recommended classifying the congenital
998
Susami el al.
Am. J. Orthod. Dentofac. Orthop. October 1992
J
0111 Fig. 5. Occlusion at second examination.
l O
llY10M 17YIM
,,"Y'7 ", ,/ ~
! ,,ps
Fig. 6. Facial and dental changes between first and second examinations. Cephalometric tracings were superimposed on the structures in the anterior cranial base.
and developmental disorders in five categories: agenesis, hypoplasia, condylolysis, hyperplasia, and neoplasia. In condylolysis, the condyle becomes progressively smaller and may disappear in a severe case. It is differentiated from aplasia and is not associated with ankylosis or erosive changes. Normal development proceeds until a lytic event occurs, and serologic tests are negative. These definitions were coincident with this patient. The cephalometric characteristics of this patient, a small and backward-rotated mandible, a large gonial angle, a decreased facial angle because of retrognathia and antegonial notching, were similar to the findings in other congenital and acquired mandibular disorders, such as mandibulofacial dysostosis, 57 Pierre Robin syndrome, 8 hemifacial microsomia, 9.~~and rheumatoid arthritis. 7"~'~2 These features seem to be common with the growth disturbances in the mandible. B j r r k 13 s u m m a r i z e d the characteristic features of the facial and the occlusal patterns in a case of bilateral condylar hypoplasia; a retrognathia of the lower face with a retruded chin, a strongly overdeveloped angular process, forming a typical notching at its inferior border, an abnormally high anterior part of the alveolar process, pronounced alveolar prognathism, accompanied by proclination of the incisors, mandibular posterior rotation, which often results in anterior open bite, abnormally
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Number 4
A
B
Fig. 7. Degeneration of condyle. A, Transcranial projection. B, Magnification from orthopantomograph.
A
B
large overjet, severely crowded teeth, and mandibular third molar impaction. These characteristics were also RTA seen in this patient. Antegonial notching is a specific characteristic in LTA - - ~ - ' ~ - ~ , ~ ' ~ - - these patients. This feature is divided into two types, congenital and acquired. 5''4 In the congenital disorders, the concave curve is a long arc, extending from the RTP gonion to menton. In acquired antegonial notching, the concave curve is closer to the angular process (gonion). This patient showed the typical antegonial notching of LTP the acquired type. On the oral function of the patients with degenerated mandibular condyles, several studies have described the changes. In rheumatoid arthritis, Stabrun et al. :5 reported the reduction of condylar translatory capacity i ~ ;'-" and maximum mouth opening. Kreiborg et a l . t6 concluded that dysplastic growth of the mandible led to increasingly unstable occlusion, with poor working DIG conditions for the masticatory muscles. The muscles Fig. 8. Muscle activities checked by electromyograph. A, 0.8 became weaker and even revealed marked structural .... second tapping movement; B, maximum biting. RTA,Right temhistologic and histochemical changes. In this case, the poralis anterior; LTA, left temporalis anterior; RTP, right temmandibular movement seems not to be restricted, at poralis posterior; LTP, left temporalis posterior; RM, right masseter; LM, left masseter; DIG, digastricus (right side). least with clinical observation. The maximum incisal
300
Susami et al.
Ant. J. Ortbod. Dentofac. Orthop. October 1992
Fig. 9. Orthodontic treatment. The treatment of the maxillary arch was preceded that of the mandibular arch. A Nance holding arch was placed in the maxillary arch and a cervical pull J-hook headgear was used for canine retraction.
Fig. 11. Facial appearance after orthodontic treatment.
opening, 42 mm, indicated little or no restriction. The muscle activities in the masticatory muscles were relatively low in a tapping movement, but maximum bite force showed a normal level. These findings seemed to be due to an unstable occlusion rather than the muscle disorders. This case clearly demonstrates the facial and the occlusal changes caused by condylolysis. Despite satisfactory orthodontic treatment results, however, further long-term observation is needed. Fig. 10. Facial and occlusal change before (17 years and 1 month old) and after (21 years) active orthodontic treatment. Cephalometric tracings were superimposed on the structures in the anterior cranial base.
REFERENCES
1. Pruzansky S. The temporomandibularjoint. Otolaryngol Clin North Am 1973;6:523-48.
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Fig. 12. Occlusion after orthodontic treatment including retention.
2. Ogus HD, Toiler PA. Common disorders of the temporomandibular joint. 2nd ed. Briston: Wright, 1986. 3. Bell WE. Temporomandibular disorders. Classification, diagnosis, management. 3rd ed. Chicago: Year Book, 1990. 4. American Academy of Craniomandibular Disorders. Craniomandibular disorders. Guidelines for evaluation, diagnosis, and management. Chicago: Quintessence, 1990. 5. Roberts RF, Pruzansky S, Aduss H. An x-radiocephalometric study of mandibulofacial dysostosis in man. Archs Oral Biol 1975;20:265-81. 6. Grayson BH, Bookstein FL, Mccarthy JG. The mandible in mandibulofacial dysostosis: a cephalomctric study. AMJ Oa'rHOD 1986;86:393-8. 7. Bj6rk A, Skieller V. Contrasting mandibular growth and facial development in long face syndrome, juvenile rheumatoid polyarthritis, and mandibulofacial dysostosis. J Craniofac Genet Dev Biol 1985;5(Suppl): 127-38. 8. Markovic M. Growth changes in cases of mandibular micrognathia. Trans Eur Orthod Soc 1972;133-45. 9. Grayson BH. Unilateral craniofacial mlcrosomia. Part I. Mandibular analysis. AM J ORTttOD 1983;84:225-30. 10. Susami T, Motohashi N, Baba Y, et al. Investigation of the facial dysmorphology and malocclusion in hemifacial microsomia. Jpn J Orthod Soc 1991;50:87-99.
! i. Engle MB, Richmond JR, Brodie AG. Mandibular growth disturbance in rheumatoid arthritis of childhood. Am J Dis Child 1949;78:728-43. 12. Koski K. The mandibular complex. Trans Eur Orthod Soc 1974:53-67. 13. Bj6rk A. Facial growth in bilateral hypoplasia of the mandibular condyles. In: Kravs BS, Riedel RA, eds. Vistas in orthodontics. Philadelphia: Lea & Febiger, 1962:347-58. 14. Becker MH, Coccaro PJ, Converse JM. Antegonial notching of the mandible. An often overlooked mandibular deformity in congenital and acquired disorders. Radiology 1976;121:149-51. 15. Stabrun AE, Larheim TA, Rosier M, Haanaes HR. Impaired mandibular function and its possible effect on mandibular growth in juvenile rheumatoid arthritis. Eur J Orthod 1987;9:43-50. 16. Kreibolg S, Bakke M, Kirkeby S, et al. Facial growth and oral function in a case of juvenile rheumatoid arthritis during an 8year period. Eur J Orthod 1990;12:119-34. Reprint requests to: Dr. Takafumi Susami The Second Department of Orthodontics, Faculty of Dentistry Tokyo Medical and Dental University 1-5-45, Yushima, Bunkyo-ku, Tokyo 113, Japan
Volunze 102 Number 4
October 1992
Copyright 9 1992 by the American Association of Orthodontists
CASE REPORT
Growth changes and orthodontic treatment in a patient with condylolysis Takafumi Susami, DDS, PhD, ~ Takayuki Kuroda, DDS, PhD, b Yoshito Yano, DDS, c and Touru Nakamura, DDS, PhD ~ ToL3'o, Japan A patient with acquired bilateral degeneration of the mandibular condyles was treated orthodontically. The flattening of condyles and the shortening of the ramus began at adolescence. The facial profile changed to a convex type, with a marked mandibular retrognathia and severe Class II malocclusion. The cause seems to be due to a condylolysis of the mandible. (AM J ORTHOO DENTOFACORTHOP 1992;102:295-301 .)
This is an important article because of recent attempts to link orthodontics with changes in condylar structure during therapy. There are several cases now in litigation in which there has been reduction in condylar mass and a change in shape, resulting in the shortening of the ramus height and an open bite. Despite attempts to close the bite, the condylolysis may continue. Rasmussen has shown that this can often stabilize after 4 to 5 years, but the cause is unknown. The importance here lies in the fact that there was no orthodontic therapy and no apparent trauma, and yet the process occurred. This case provides an important link in the defense of orthodontists against contingency-fee lawyer litigation. --T. M. Graber
Fig. 1. Facial appearance at first examination. A n o m a l i e s o f the mandibular condyle, such as absence, incomplete formation or degeneration, cause severe facial dysmorphosis. There are several eiiologic factors in the abnormal development o f mandibular condyle. Congenital anomalies, trauma, and infection of the mandibular condyle in growing children often lead to skeletal disharmony with severe malocclusion. ~.2 From Tokyo Medical and Dental University and Takahashi Orthodontic Office. ~Instructor, The Second Department of Orthodontics. bProfessor and Chairman, The Second Department of Orthodontics. 'Director, Takahashi Orthodontic Office. dtnstructor, Takahashi Orthodontic Office. 814139O99
The purpose o f this article is to present a case report on a patient with acquired bilateral degeneration o f the mandibular condyle that started at adolescence. Morphologic and growth change analyses have been completed. The results o f the orthodontic treatment are illustrated.
CASE REPORT The first examination A girl who was 11 years and I0 months old had a complaint of anterior crowding. Her facial profile was slightly concave and no asymmetry was observed (Figs. 1 and 2). Anteroposterior molar relations were Class I at the left side and Class Ill at the right side. Overjet was 4 mm, and over
295
296
Susami et al.
Am. J. Orthod. Dentofac. Orthop. October 1992
Fig. 2. Occlusion at time of first examination.
bite was 2.5 mm. Arch shape was tapered in both maxillary and mandibular arches. Full-mouth intraoral radiographs showed no dental abnormalities. All four third molars were developing. Cephalometric analysis indicated a skeletal Class III tendency with relatively retruded maxilla and protruded mandible (Fig. 3). The mandibular plane, Y-axis, and gonial angle were within normal range; the maxillary and mandibular incisors showed labial and lingual tipping, respectively. There were no specific abnormal forms in the mandibular ramus and the condyle. These findings indicated the major problem was an arch length discrepancy. The extraction of four premolars and the alignment of individual teeth, with careful attention to the remaining facial growth, was recommended. Nevertheless, the treatment was postponed for economic reasons.
The second examination After a protracted interval, the patient came in for an examination again at the age of 17 years and 1 month. She showed peculiar morphologic changes. The facial profile was changed to a convex type, with a marked mandibular retrognathia (Fig. 4). Lip incompetence was seen at the rest position, and the hypertonicity of perioral musculature was noted at lip closure. The overjet was increased abnormally to 11 mm, and the overbite was decreased to - 1 mm, presenting anterior open bite (Fig. 5). The molar relations were changed
to bilateral Class II. The arch shape was still tapered and showed crowding in both maxilla and mandible. The cephalometric analysis represented the shortening of the mandible in size, especially in the ramus (Fig. 6). The mandible was retruded posteriorly and was rotated downward and backward, presenting a typical retrognathia, with a large mandibular plane angle and Y-axis. The maxillary incisors were tipped more labially, and the FMIA angle was decreased. The mandibular condyles were obscure, and typical antegonial notching was observed in the cephalogram. The degenerated condylar form was clearly shown by the orthopantomograph and the transcranial projection (Fig. 7). The condylar processes became thin, and the condylar heads were flattened on the articular surface. The amount of maximum mouth opening, as measured between upper and lower incisor edge, was 42 mm, and the mouth opening movement was not restricted. There was no apparent history concerning facial trauma or infection between the first and the second examination, except the chin was bruised while playing volleyball. Hematologic examinations were performed on the routine biochemical examinations (mineral, sugar, lipid, protein, and enzymes), hemogram, and a specific examination for antistreptolysin O (ASO), C-reactive protein (CRP), and rheumatoid factors (RA-test). There were no particular findings
Volume 102 Number 4
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297
Fig. 4. Facial appearance at second examination.
Fig. 3. Lateral cephalograms taken at first examination.
suggesting systemic bone disease, infection, or rheumatoid arthritis. Negative findings concerning the systemic diseases were also observed in hand-wrist and foot-wrist radiographs. The masticatory muscle activiiies--masseter, anterior and posterior parts of temporalis, and anterior belly of digastricus--were checked with an electromyograph (Fig. 8). Although the activities of these muscles in an 0.8 second tapping movement were relatively low, they were working harmoniously. In the functional movements, such as chewing and biting, the activities were quite normal. There were also no findings indicating abnormal muscle activity that pointed to the cause of the degeneration. Orthodontic treatment After l-year growth observation in which no progressive skeletal changes were noticed, active orthodontic treatment was started. The treatment planning was as follows: 1. Maximum anchorage for the maxillary molars. 2. Retraction and lingual tipping of the maxillary incisors with bilateral extraction of the maxillary first premolars. 3. Anterior expansion of the mandibular arch to eliminate the crowding and to correct the ovcrjet.
4. Keeping the occlusal plane unchanged during orthodontic treatment. The treatment was performed with multibracket appliances with standard 0.018 • 0.022-inch slot. A leveling of the maxillary arch preceded that of the mandible arch. A Nance holding arch was placed in the maxillary arch and a cervical pull J-hook extraoral appliance was used for canine retraction (Fig. 9). The active treatment period was 2 years and l month. The following changes were observed by superimpositional comparison of the cephalograms taken before and after active treatment (Fig. 10). The medial movement of the maxillary molars was about 1.5 mm, and there was no extrusion. Lingual tipping of the maxillary incisors and some labial tipping of the mandibular incisors was found. Mandibular downward and backward rotation occurred during the treatment period. Retention was performed with a Hawley-type retainer in the maxilla and with a bonded canine-to-canine lingual retainer in the mandible. Occlusal stability was well maintained, as shown in Figs. 11 and 12. DISCUSSION The cause o f the degeneration of the condyles in this patient is unknown. It is rather questionable to attribute this to congenital etiologic effects, because o f a normal mandibular growth without any symptoms until her first visit. There are no similar familial anomalies. Reports 1,2"3 suggested several causes, such as osteoarthritis, trauma, local infection, and rheumatoid arthritis, as a basis o f this developmental anomaly. However, there is no proof o f any o f these factors for this patient. Hematologic examinations, especially a specific examination for antistreptolysin O (ASO), C-reactive protein, and rheumatoid factors, eliminated the possibility o f the local infection or o f rheumatoid arthritis. The effects o f the masticatory muscle deficiency were also not seen in the electromyographic examination. The American A c a d e m y o f Craniomandibuiar Disorders 4 has recommended classifying the congenital
998
Susami el al.
Am. J. Orthod. Dentofac. Orthop. October 1992
J
0111 Fig. 5. Occlusion at second examination.
l O
llY10M 17YIM
,,"Y'7 ", ,/ ~
! ,,ps
Fig. 6. Facial and dental changes between first and second examinations. Cephalometric tracings were superimposed on the structures in the anterior cranial base.
and developmental disorders in five categories: agenesis, hypoplasia, condylolysis, hyperplasia, and neoplasia. In condylolysis, the condyle becomes progressively smaller and may disappear in a severe case. It is differentiated from aplasia and is not associated with ankylosis or erosive changes. Normal development proceeds until a lytic event occurs, and serologic tests are negative. These definitions were coincident with this patient. The cephalometric characteristics of this patient, a small and backward-rotated mandible, a large gonial angle, a decreased facial angle because of retrognathia and antegonial notching, were similar to the findings in other congenital and acquired mandibular disorders, such as mandibulofacial dysostosis, 57 Pierre Robin syndrome, 8 hemifacial microsomia, 9.~~and rheumatoid arthritis. 7"~'~2 These features seem to be common with the growth disturbances in the mandible. B j r r k 13 s u m m a r i z e d the characteristic features of the facial and the occlusal patterns in a case of bilateral condylar hypoplasia; a retrognathia of the lower face with a retruded chin, a strongly overdeveloped angular process, forming a typical notching at its inferior border, an abnormally high anterior part of the alveolar process, pronounced alveolar prognathism, accompanied by proclination of the incisors, mandibular posterior rotation, which often results in anterior open bite, abnormally
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Number 4
A
B
Fig. 7. Degeneration of condyle. A, Transcranial projection. B, Magnification from orthopantomograph.
A
B
large overjet, severely crowded teeth, and mandibular third molar impaction. These characteristics were also RTA seen in this patient. Antegonial notching is a specific characteristic in LTA - - ~ - ' ~ - ~ , ~ ' ~ - - these patients. This feature is divided into two types, congenital and acquired. 5''4 In the congenital disorders, the concave curve is a long arc, extending from the RTP gonion to menton. In acquired antegonial notching, the concave curve is closer to the angular process (gonion). This patient showed the typical antegonial notching of LTP the acquired type. On the oral function of the patients with degenerated mandibular condyles, several studies have described the changes. In rheumatoid arthritis, Stabrun et al. :5 reported the reduction of condylar translatory capacity i ~ ;'-" and maximum mouth opening. Kreiborg et a l . t6 concluded that dysplastic growth of the mandible led to increasingly unstable occlusion, with poor working DIG conditions for the masticatory muscles. The muscles Fig. 8. Muscle activities checked by electromyograph. A, 0.8 became weaker and even revealed marked structural .... second tapping movement; B, maximum biting. RTA,Right temhistologic and histochemical changes. In this case, the poralis anterior; LTA, left temporalis anterior; RTP, right temmandibular movement seems not to be restricted, at poralis posterior; LTP, left temporalis posterior; RM, right masseter; LM, left masseter; DIG, digastricus (right side). least with clinical observation. The maximum incisal
300
Susami et al.
Ant. J. Ortbod. Dentofac. Orthop. October 1992
Fig. 9. Orthodontic treatment. The treatment of the maxillary arch was preceded that of the mandibular arch. A Nance holding arch was placed in the maxillary arch and a cervical pull J-hook headgear was used for canine retraction.
Fig. 11. Facial appearance after orthodontic treatment.
opening, 42 mm, indicated little or no restriction. The muscle activities in the masticatory muscles were relatively low in a tapping movement, but maximum bite force showed a normal level. These findings seemed to be due to an unstable occlusion rather than the muscle disorders. This case clearly demonstrates the facial and the occlusal changes caused by condylolysis. Despite satisfactory orthodontic treatment results, however, further long-term observation is needed. Fig. 10. Facial and occlusal change before (17 years and 1 month old) and after (21 years) active orthodontic treatment. Cephalometric tracings were superimposed on the structures in the anterior cranial base.
REFERENCES
1. Pruzansky S. The temporomandibularjoint. Otolaryngol Clin North Am 1973;6:523-48.
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C a s e report
301
Fig. 12. Occlusion after orthodontic treatment including retention.
2. Ogus HD, Toiler PA. Common disorders of the temporomandibular joint. 2nd ed. Briston: Wright, 1986. 3. Bell WE. Temporomandibular disorders. Classification, diagnosis, management. 3rd ed. Chicago: Year Book, 1990. 4. American Academy of Craniomandibular Disorders. Craniomandibular disorders. Guidelines for evaluation, diagnosis, and management. Chicago: Quintessence, 1990. 5. Roberts RF, Pruzansky S, Aduss H. An x-radiocephalometric study of mandibulofacial dysostosis in man. Archs Oral Biol 1975;20:265-81. 6. Grayson BH, Bookstein FL, Mccarthy JG. The mandible in mandibulofacial dysostosis: a cephalomctric study. AMJ Oa'rHOD 1986;86:393-8. 7. Bj6rk A, Skieller V. Contrasting mandibular growth and facial development in long face syndrome, juvenile rheumatoid polyarthritis, and mandibulofacial dysostosis. J Craniofac Genet Dev Biol 1985;5(Suppl): 127-38. 8. Markovic M. Growth changes in cases of mandibular micrognathia. Trans Eur Orthod Soc 1972;133-45. 9. Grayson BH. Unilateral craniofacial mlcrosomia. Part I. Mandibular analysis. AM J ORTttOD 1983;84:225-30. 10. Susami T, Motohashi N, Baba Y, et al. Investigation of the facial dysmorphology and malocclusion in hemifacial microsomia. Jpn J Orthod Soc 1991;50:87-99.
! i. Engle MB, Richmond JR, Brodie AG. Mandibular growth disturbance in rheumatoid arthritis of childhood. Am J Dis Child 1949;78:728-43. 12. Koski K. The mandibular complex. Trans Eur Orthod Soc 1974:53-67. 13. Bj6rk A. Facial growth in bilateral hypoplasia of the mandibular condyles. In: Kravs BS, Riedel RA, eds. Vistas in orthodontics. Philadelphia: Lea & Febiger, 1962:347-58. 14. Becker MH, Coccaro PJ, Converse JM. Antegonial notching of the mandible. An often overlooked mandibular deformity in congenital and acquired disorders. Radiology 1976;121:149-51. 15. Stabrun AE, Larheim TA, Rosier M, Haanaes HR. Impaired mandibular function and its possible effect on mandibular growth in juvenile rheumatoid arthritis. Eur J Orthod 1987;9:43-50. 16. Kreibolg S, Bakke M, Kirkeby S, et al. Facial growth and oral function in a case of juvenile rheumatoid arthritis during an 8year period. Eur J Orthod 1990;12:119-34. Reprint requests to: Dr. Takafumi Susami The Second Department of Orthodontics, Faculty of Dentistry Tokyo Medical and Dental University 1-5-45, Yushima, Bunkyo-ku, Tokyo 113, Japan