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Osteosarcoma of the jaw bones
Oral Oncology 37 (2001) 545±547
www.elsevier.com/locate/oraloncology
Review
Osteosarcoma of the jaw bones Mark L. Chindia Faculty of Dental Sciences, PO Box 19676, Nairobi, Kenya Received 27 September 2000; accepted 8 November 2000
Abstract Currently, it has been established that osteosarcoma (OS) of bone is not a stereotyped disease, and several varieties have been identi®ed by clinical ®ndings, radiographic and histopathologic appearances. Generally, it is the most common primary malignant bone neoplasm that accounts for at least 30% of all primary tumours of bone. In the jaw bones, OS accounts for about 4% of all the primary malignant neoplasms. In the general skeleton, the highest incidence is observed in the second decade of life; the neoplasm is said to be unusual before the age of 5 years and very rare after age 50 years. The aetiology and precise pathogenesis of this disease remain unknown. A diagnosis of clinically and radiologically suspicious OS requires meticulous histologic examination. However, histologic diagnosis may also be dicult since the dierent varieties of OS may have dierent morphological patterns in dierent sample sites. Currently, the two therapeutic modalities used in the primary treatment of OS include radical surgery and cytotoxic chemotherapy. In the general skeleton, the use of surgery alone results in a 90% rate of recurrence of OS. Notably, the advent of adjuvant and neoadjuvant cytotoxic chemotherapy as an adjunct to radical surgery has greatly improved the prognosis of many cases of OS of the jaw bones. # 2001 Elsevier Science Ltd. All rights reserved. Keywords: Osteosarcoma; Jaw bones
1. Introduction
2. Clinical features and diagnosis
Osteosarcoma (OS) is a tumour in which the malignant spindle cell produces osteoid [1,2]. It is, generally, the most common malignant bone tumour constituting at least 30% of all primary tumours of the skeleton [3]. In the general skeleton, the annual incidence has been reported as 1.6±2.8 per million children under 15 years; and that it occurs in males more commonly than females at a ratio of 1.6:1 [4]. Between 6.5 and 10% of all OSs are found in the bones of the skull, with the majority in the jaw bones [5]. More recently, it has been shown that in the jaws, OS is an unusual lesion representing less than 4% of all the cases documented [6]. In the jaws, the biologic behaviour of OS diers from tumours involving the other skeletal bones: the average age of onset is 10±20 years later than for skeletal lesions, the histopathologic variables are more favourable, distant metastases occur less frequently; and survival rates are higher [7,8]. In this article, a review is presented of OSs of the jaw bones with respect to the clinical features, diagnosis, pathogenesis, management and the factors that may in¯uence prognosis.
The most common symptoms of OS include persistent pain, swelling and paraesthesia/anaesthesia [9,10]. General manifestations of disease, such as fever or considerable weight loss are rare [3]. Notably, a signi®cant proportion of patients with OS may present without any pain except jaw swelling. The age range of cases of OS appears variable in diverse studies worldwide. Among the thirty cases presented recently by August et al. [6], the age range was 4±84 years. Notably, Chindia et al. [11] presented a 1-week-old female patient in their series of 14 cases of OS. Thus, this disease may manifest at any age. The diagnostic evaluation of OS should delineate the extent of the primary tumour and the presence or absence of metastatic disease [2]. Thus, in addition to a de®nitive incisional biopsy, basic diagnostic evaluation should include: a clear history, physical examination, plain radiographs of the aected jaw including those of the chest; and computerized tomography or magnetic resonance imaging of the aected area. Radiologically, the ®ndings may be the same as those of OS in other sites: osteolytic, osteoblastic or a mixture of the two with poorly de®ned irregular margins that are characteristic
1368-8375/01/$ - see front matter # 2001 Elsevier Science Ltd. All rights reserved. PII: S1368-8375(00)00129-9
546
M.L. Chindia / Oral Oncology 37 (2001) 545±547
of malignant lesions [12]. It is important to note that some cases may present with no evident radiological changes, while others may exhibit variable appearances including sclerotic, laminated and the classic sunburst patterns [13]. Histopathologically, classi®cation of OS is based on the predominant type of stroma: osteoblastic, chondroblastic, ®broblastic, telangiectatic, ®brohistiocystic and juxta cortical tumours Ð parosteal and periosteal [8]. 3. Aetiology and pathology The exact aetiology of OS remains unknown [3]. However, there is no doubt that ionizing radiation may induce development of OS since a high incidence of this tumour has been observed in workers who painted watch faces during the period in which ¯uorescent paints containing traces of radium and mesothorium were used. On the other hand, current knowledge [2] indicates that certain other factors which appear to correlate with the occurrence of OS include linear bone growth (the most common sites being metaphyseal in the most rapidly growing bones such as the distal femur), genetic and environmental factors. There is evidence that age, sex and anatomical site of OS correlate well with periods of rapid growth in man and animals [3]. Other predisposing factors associated with the occurrence of OS include trauma and ®brous dysplasia [14], and Paget's disease of bone [15]. OS can be broadly divided into intramedullary (central) and juxtacortical (peripheral) types on the basis of clinical, histopathologic and radiographic characteristics [16]. Current classi®cation is presented in Table 1 [2]. Although the small cell type, giant cell type; and spindle cell type may be confused with Ewing's sarcoma, giant cell tumour and ®brosarcoma respectively, in all cases the anaplastic stromal cells produce osteoid, which distinguishes them as OSs. Dahlin and Coventry [15] de®ned OS as a sarcoma whose malignant cells produced osteoid even if in only small foci, recognizing that such
Table 1 Classi®cation of osteosarcoma [2] I.
II. III. IV. V. VI. VII.
Classic A. Osteoblastic. B. Chondroblastic. C. Fibroblastic. Telangiectatic Small cell Giant cell Spindle cell Periosteal Parosteal
tumours had dominant chondroblastic or ®broblastic components and that a few with the same basic cytological features produced no ground substance. OS is not a stereotyped disease since several varieties have so far been identi®ed [13] among which some may run a particularly indolent course [17]. Raubenheimer and Noke [18] have described the low-grade intraosseous OS of the jaws which they noted had often been inappropriately diagnosed as a benign neoplasm. Indeed, low-grade central OSs are well-dierentiated lesions that can be mistaken for benign processes such as ®brous dysplasia or ossifying ®broma [17]. On the other hand, parosteal OS of the jaws must also be dierentiated from benign lesions that may occupy a juxtacortical position such as osteochondroma and myositis ossi®cans [19,20]. Microscopic evidence of malignancy is subtle in early disease; and initially, these lesions consist of mature bone trabeculae with a sparse ®brous stroma of spindle-shaped cells that vary in appearance from well-dierentiated to moderately atypical. Ultrastructurally, parosteal OS presents quite characteristic features composed chie¯y of ®broblast-like or elongated osteoblast-like tumour cells and abundant myo®broblasts [1]. The other entity of the juxtacortical varieties of OS is the periosteal OS which is histologically welldierentiated and occurs extremely rarely in the jaws; and radiographically appears as a very dense, lobulated mass attached by a broad base to the underlying bone [21,22]. 4. Management and prognosis The cornerstone of curative treatment of primary OS is adequate surgical extirpation [4,7,13,20]. This view should apply for all entities of OS including the juxtacortical types. The periosteal OS is capable of local recurrence and distant metastasis while the parosteal OS is generally regarded as a low-grade neoplasm that is locally aggressive and may recur if incompletely excised [16]. It must be emphasized that inadequate surgical procedures yield very poor results [13]. Available evidence indicates that there has been a remarkable improvement in the survival for patients treated with multiple drug chemotherapy as a routine in conjunction with surgery [23]. Indeed, eective chemotherapy improves the outcome of patients with high grade surface OS [23]. August et al. [6] have noted that when a group of patients receiving chemotherapy was evaluated by the number of antineoplastic drugs used, a suggestive trend towards improved survival was found in those receiving treatment with four or more agents. In the general skeleton, some of the surface OS are associated with a better prognosis, compared with the usual high-grade intramedullary tumours [24,25].
M.L. Chindia / Oral Oncology 37 (2001) 545±547
Prognostic factors in overall survival include tumour size, location and histologic grade [26]. In comparison with OS of the extremeties, jaw OS is characterized by an increased 5-year survival rate and a lower incidence of metastasis although, there is no dierence in histological degree of malignancy of the disease in the two sites, at least with respect to mitotic activity [27]. As a group, parosteal OSs can be associated with a good prognosis if the diagnosis is restricted to surface tumours that lack medullary involvement and that are histologically low-grade [25]. Similarly, periosteal OSs form a less common but equally distinct group with speci®c prognostic implications if the diagnosis is restricted to surface tumours that lack medullary involvement and that are lobulated and predominantly chondroblastic. Because of the small number of cases reported, and the lack of uniformity in histologic description, the value of the histologic grade of the jaw tumours with respect to prognosis remains unclear [20]. While it is well known that jaw OS is particularly resistant to radiation therapy (RT), it has been shown that there is a role for RT combined with chemotherapy in the treatment of advanced OS since it can be used to palliate the bulky primary tumour when the patient presents with metastatic disease [28]. However, it cannot be relied upon to completely eradicate a large primary tumour. When surgical treatment fails, radiation and/or chemotherapy may extend survival for some patients [8]. It is worthy of note that the overall prognosis for patients with OS has improved over the years, but the extent to which this has been achieved varies [4]. References [1] Martinez-Tello FJ, Navas-Palacios JJ. The ultrastructure of conventional, parosteal and periosteal osteosarcomas. Cancer 1982; 50:949±61. [2] Lanzkowsky P. Malignant bone tumours In: Redner A, editor. Manual of paediatric hematology and oncology, 3rd ed. London: Academic Press, 2000. p. 555±70. [3] Bonadona G, della Cuna GR. Osteosarcoma. In: Bonadona G, Robustelli della Cuna G, editors. Handbook of Medical Oncology. Milano: Masson S.P.A, Milano, 1988. p. 708±18. [4] Craft AW. Osteosarcoma and Chondrosarcoma. In: Voute PA, Barrett A, Lemerle J, editors. Cancer in children. Clinical management. London: Springer-Verlag, 1992. p. 282±94. [5] Batsakis JG. Osteogenic and chondrogenic sarcomas of the jaws. Ann Otol Rhinol Laryngol 1987;96:474±5. [6] August M, Magennis P, Dewitt D. Osteogenic sarcoma of the jaws: factors in¯uencing prognosis. Int J Oral Maxillofac Surg 1997;26:198±204. [7] Russ JE, Jesse RH. Management of osteosarcoma of the maxilla and mandible. American J Surg 1980;140:572±6.
547
[8] Regezi JA, Zarbo RJ, McClatchey KD, Courtney RM, Crissman JD. Osteosarcomas and Chondrosarcomas of the jaws: immunohistochemical correlations. Oral Surg Oral Med Oral Pathol 1987;64:207±302. [9] Pindborg JJ, Eversole LR. Malignant neoplasms of the jaw bones including those metastatic to the region. In: Prabhu, Wilson, Daftary, Johnson, editors. Oral diseases in the tropics. Oxford: Oxford University Press, 1992. p. 470±7. [10] Archer D, Langdon JO. Primary tumours of the jaws. In: Langdon, Henk, editors. Malignant tumours of the mouth, jaws and salivary glands. London: Edward Arnold, 1995. p. 222±39. [11] Chindia ML, Guthua SW, Awange DO, Wakoli KA. Osteosarcomas of the maxillofacial bones in Kenyans. Journal of Cranio-Maxillofac Surg 1998;26:98±101. [12] Doval DC, Baosy PP, Kumar RV, Kannan V, Sabitha KS, Kumarswamy SV. Osteosarcomas of the jaw bones. Br J Oral Maxillofac Surg 1997;35:337±62. [13] Bertoni F, Dallera P, Bacchini P, Marchetti C, Campobassi A. The Istuto Rizzoli Ð Beretta experience with osteosarcoma of the jaw. Cancer 1991;68:1555±63. [14] Ajagbe HA, Junaid TA, Daramola JO. Osteogenic sarcoma of the jaws in an African community: report of twenty-one cases. J Oral Maxillofac Surg 1986;44:104±6. [15] Dahlin DC, Coventry MB. Osteogenic sarcoma: a study of six hundred cases. The J of Bone and Joint Surg 1967;49A:101±10. [16] Zarbo RJ, Regezi JA, Baker SR. Periosteal osteogenic sarcoma of the mandible. Oral Surg 1984;57:643±7. [17] Koury ME, Regezi JA, Perrot DH, Kaban LB. ``Atypical'' ®broosseous lesions: diagnostic challenges and treatment. Int J Oral Maxillofac Surg 1995;24:162±9. [18] Raubenheimer EJ, Noke CE. Low-grade intraosseous osteosarcoma of the jaws. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 1998;86:82±5. [19] Newland JR, Ayala AG. Parosteal osteosarcoma of the maxilla. Oral Surg 1977;43:727±33. [20] Bras JM, Donner R, Van der Kwast WAM, Snow GB, Van der Waal I. Juxtacortical osteogenic sarcoma of the jaws: review of the literature and report of a case. Oral Surg 1980;50:535±44. [21] Bertoni F, Boriani S, Laus M, Campanacci M. Periosteal chondrosarcoma and periosteal osteosarcoma: two distinct entities. Journal of Bone and Joint Surgery 1982;64-B:370±6. [22] Minic AJ. Periosteal osteosarcoma of the mandible. Int J Oral Maxillofac Surg 1995;24:226±8. [23] Huvos AG, Rosen G, Bretsky SS, Butler A. Telangiectatic osteogenic sarcoma: a clinicopathologic study of 124 patients. Cancer 1982;49:1679±89. [24] Okada K, Unni KK, Swee RG, Sim FH. High grade surface osteosarcoma: a clinicopathologic study of 46 cases. Cancer 1999;85:1044±54. [25] Wold LE, Beabout JW, Unni KK, Pritchard DJ. High-grade surface osteosarcomas. Am J Surg Pathol 1984;8:181±6. [26] Ruiz-Godoy RLM, Meneses-Garcia A, Mosqueda-Taylor A, Dela la Garza-Salar J. Well-dierentiated intraosseous osteosarcoma of the jaws: experience of two cases from the Intituto Nacional de Cancerologia, Mexico. Oral Oncology 1999;35:530±3. [27] Slootweg PJ, Muller H. Osteosarcoma of the jaw bones: analysis of 18 cases. J Max-fac Surg 1985;13:158±66. [28] Rosen G, Tet M, Martinez A, Cham W, Murphy ML. Combination chemotherapy and radiation therapy in the treatment of metastatic osteogenic sarcoma. Cancer 1975;35:622±30.
www.elsevier.com/locate/oraloncology
Review
Osteosarcoma of the jaw bones Mark L. Chindia Faculty of Dental Sciences, PO Box 19676, Nairobi, Kenya Received 27 September 2000; accepted 8 November 2000
Abstract Currently, it has been established that osteosarcoma (OS) of bone is not a stereotyped disease, and several varieties have been identi®ed by clinical ®ndings, radiographic and histopathologic appearances. Generally, it is the most common primary malignant bone neoplasm that accounts for at least 30% of all primary tumours of bone. In the jaw bones, OS accounts for about 4% of all the primary malignant neoplasms. In the general skeleton, the highest incidence is observed in the second decade of life; the neoplasm is said to be unusual before the age of 5 years and very rare after age 50 years. The aetiology and precise pathogenesis of this disease remain unknown. A diagnosis of clinically and radiologically suspicious OS requires meticulous histologic examination. However, histologic diagnosis may also be dicult since the dierent varieties of OS may have dierent morphological patterns in dierent sample sites. Currently, the two therapeutic modalities used in the primary treatment of OS include radical surgery and cytotoxic chemotherapy. In the general skeleton, the use of surgery alone results in a 90% rate of recurrence of OS. Notably, the advent of adjuvant and neoadjuvant cytotoxic chemotherapy as an adjunct to radical surgery has greatly improved the prognosis of many cases of OS of the jaw bones. # 2001 Elsevier Science Ltd. All rights reserved. Keywords: Osteosarcoma; Jaw bones
1. Introduction
2. Clinical features and diagnosis
Osteosarcoma (OS) is a tumour in which the malignant spindle cell produces osteoid [1,2]. It is, generally, the most common malignant bone tumour constituting at least 30% of all primary tumours of the skeleton [3]. In the general skeleton, the annual incidence has been reported as 1.6±2.8 per million children under 15 years; and that it occurs in males more commonly than females at a ratio of 1.6:1 [4]. Between 6.5 and 10% of all OSs are found in the bones of the skull, with the majority in the jaw bones [5]. More recently, it has been shown that in the jaws, OS is an unusual lesion representing less than 4% of all the cases documented [6]. In the jaws, the biologic behaviour of OS diers from tumours involving the other skeletal bones: the average age of onset is 10±20 years later than for skeletal lesions, the histopathologic variables are more favourable, distant metastases occur less frequently; and survival rates are higher [7,8]. In this article, a review is presented of OSs of the jaw bones with respect to the clinical features, diagnosis, pathogenesis, management and the factors that may in¯uence prognosis.
The most common symptoms of OS include persistent pain, swelling and paraesthesia/anaesthesia [9,10]. General manifestations of disease, such as fever or considerable weight loss are rare [3]. Notably, a signi®cant proportion of patients with OS may present without any pain except jaw swelling. The age range of cases of OS appears variable in diverse studies worldwide. Among the thirty cases presented recently by August et al. [6], the age range was 4±84 years. Notably, Chindia et al. [11] presented a 1-week-old female patient in their series of 14 cases of OS. Thus, this disease may manifest at any age. The diagnostic evaluation of OS should delineate the extent of the primary tumour and the presence or absence of metastatic disease [2]. Thus, in addition to a de®nitive incisional biopsy, basic diagnostic evaluation should include: a clear history, physical examination, plain radiographs of the aected jaw including those of the chest; and computerized tomography or magnetic resonance imaging of the aected area. Radiologically, the ®ndings may be the same as those of OS in other sites: osteolytic, osteoblastic or a mixture of the two with poorly de®ned irregular margins that are characteristic
1368-8375/01/$ - see front matter # 2001 Elsevier Science Ltd. All rights reserved. PII: S1368-8375(00)00129-9
546
M.L. Chindia / Oral Oncology 37 (2001) 545±547
of malignant lesions [12]. It is important to note that some cases may present with no evident radiological changes, while others may exhibit variable appearances including sclerotic, laminated and the classic sunburst patterns [13]. Histopathologically, classi®cation of OS is based on the predominant type of stroma: osteoblastic, chondroblastic, ®broblastic, telangiectatic, ®brohistiocystic and juxta cortical tumours Ð parosteal and periosteal [8]. 3. Aetiology and pathology The exact aetiology of OS remains unknown [3]. However, there is no doubt that ionizing radiation may induce development of OS since a high incidence of this tumour has been observed in workers who painted watch faces during the period in which ¯uorescent paints containing traces of radium and mesothorium were used. On the other hand, current knowledge [2] indicates that certain other factors which appear to correlate with the occurrence of OS include linear bone growth (the most common sites being metaphyseal in the most rapidly growing bones such as the distal femur), genetic and environmental factors. There is evidence that age, sex and anatomical site of OS correlate well with periods of rapid growth in man and animals [3]. Other predisposing factors associated with the occurrence of OS include trauma and ®brous dysplasia [14], and Paget's disease of bone [15]. OS can be broadly divided into intramedullary (central) and juxtacortical (peripheral) types on the basis of clinical, histopathologic and radiographic characteristics [16]. Current classi®cation is presented in Table 1 [2]. Although the small cell type, giant cell type; and spindle cell type may be confused with Ewing's sarcoma, giant cell tumour and ®brosarcoma respectively, in all cases the anaplastic stromal cells produce osteoid, which distinguishes them as OSs. Dahlin and Coventry [15] de®ned OS as a sarcoma whose malignant cells produced osteoid even if in only small foci, recognizing that such
Table 1 Classi®cation of osteosarcoma [2] I.
II. III. IV. V. VI. VII.
Classic A. Osteoblastic. B. Chondroblastic. C. Fibroblastic. Telangiectatic Small cell Giant cell Spindle cell Periosteal Parosteal
tumours had dominant chondroblastic or ®broblastic components and that a few with the same basic cytological features produced no ground substance. OS is not a stereotyped disease since several varieties have so far been identi®ed [13] among which some may run a particularly indolent course [17]. Raubenheimer and Noke [18] have described the low-grade intraosseous OS of the jaws which they noted had often been inappropriately diagnosed as a benign neoplasm. Indeed, low-grade central OSs are well-dierentiated lesions that can be mistaken for benign processes such as ®brous dysplasia or ossifying ®broma [17]. On the other hand, parosteal OS of the jaws must also be dierentiated from benign lesions that may occupy a juxtacortical position such as osteochondroma and myositis ossi®cans [19,20]. Microscopic evidence of malignancy is subtle in early disease; and initially, these lesions consist of mature bone trabeculae with a sparse ®brous stroma of spindle-shaped cells that vary in appearance from well-dierentiated to moderately atypical. Ultrastructurally, parosteal OS presents quite characteristic features composed chie¯y of ®broblast-like or elongated osteoblast-like tumour cells and abundant myo®broblasts [1]. The other entity of the juxtacortical varieties of OS is the periosteal OS which is histologically welldierentiated and occurs extremely rarely in the jaws; and radiographically appears as a very dense, lobulated mass attached by a broad base to the underlying bone [21,22]. 4. Management and prognosis The cornerstone of curative treatment of primary OS is adequate surgical extirpation [4,7,13,20]. This view should apply for all entities of OS including the juxtacortical types. The periosteal OS is capable of local recurrence and distant metastasis while the parosteal OS is generally regarded as a low-grade neoplasm that is locally aggressive and may recur if incompletely excised [16]. It must be emphasized that inadequate surgical procedures yield very poor results [13]. Available evidence indicates that there has been a remarkable improvement in the survival for patients treated with multiple drug chemotherapy as a routine in conjunction with surgery [23]. Indeed, eective chemotherapy improves the outcome of patients with high grade surface OS [23]. August et al. [6] have noted that when a group of patients receiving chemotherapy was evaluated by the number of antineoplastic drugs used, a suggestive trend towards improved survival was found in those receiving treatment with four or more agents. In the general skeleton, some of the surface OS are associated with a better prognosis, compared with the usual high-grade intramedullary tumours [24,25].
M.L. Chindia / Oral Oncology 37 (2001) 545±547
Prognostic factors in overall survival include tumour size, location and histologic grade [26]. In comparison with OS of the extremeties, jaw OS is characterized by an increased 5-year survival rate and a lower incidence of metastasis although, there is no dierence in histological degree of malignancy of the disease in the two sites, at least with respect to mitotic activity [27]. As a group, parosteal OSs can be associated with a good prognosis if the diagnosis is restricted to surface tumours that lack medullary involvement and that are histologically low-grade [25]. Similarly, periosteal OSs form a less common but equally distinct group with speci®c prognostic implications if the diagnosis is restricted to surface tumours that lack medullary involvement and that are lobulated and predominantly chondroblastic. Because of the small number of cases reported, and the lack of uniformity in histologic description, the value of the histologic grade of the jaw tumours with respect to prognosis remains unclear [20]. While it is well known that jaw OS is particularly resistant to radiation therapy (RT), it has been shown that there is a role for RT combined with chemotherapy in the treatment of advanced OS since it can be used to palliate the bulky primary tumour when the patient presents with metastatic disease [28]. However, it cannot be relied upon to completely eradicate a large primary tumour. When surgical treatment fails, radiation and/or chemotherapy may extend survival for some patients [8]. It is worthy of note that the overall prognosis for patients with OS has improved over the years, but the extent to which this has been achieved varies [4]. References [1] Martinez-Tello FJ, Navas-Palacios JJ. The ultrastructure of conventional, parosteal and periosteal osteosarcomas. Cancer 1982; 50:949±61. [2] Lanzkowsky P. Malignant bone tumours In: Redner A, editor. Manual of paediatric hematology and oncology, 3rd ed. London: Academic Press, 2000. p. 555±70. [3] Bonadona G, della Cuna GR. Osteosarcoma. In: Bonadona G, Robustelli della Cuna G, editors. Handbook of Medical Oncology. Milano: Masson S.P.A, Milano, 1988. p. 708±18. [4] Craft AW. Osteosarcoma and Chondrosarcoma. In: Voute PA, Barrett A, Lemerle J, editors. Cancer in children. Clinical management. London: Springer-Verlag, 1992. p. 282±94. [5] Batsakis JG. Osteogenic and chondrogenic sarcomas of the jaws. Ann Otol Rhinol Laryngol 1987;96:474±5. [6] August M, Magennis P, Dewitt D. Osteogenic sarcoma of the jaws: factors in¯uencing prognosis. Int J Oral Maxillofac Surg 1997;26:198±204. [7] Russ JE, Jesse RH. Management of osteosarcoma of the maxilla and mandible. American J Surg 1980;140:572±6.
547
[8] Regezi JA, Zarbo RJ, McClatchey KD, Courtney RM, Crissman JD. Osteosarcomas and Chondrosarcomas of the jaws: immunohistochemical correlations. Oral Surg Oral Med Oral Pathol 1987;64:207±302. [9] Pindborg JJ, Eversole LR. Malignant neoplasms of the jaw bones including those metastatic to the region. In: Prabhu, Wilson, Daftary, Johnson, editors. Oral diseases in the tropics. Oxford: Oxford University Press, 1992. p. 470±7. [10] Archer D, Langdon JO. Primary tumours of the jaws. In: Langdon, Henk, editors. Malignant tumours of the mouth, jaws and salivary glands. London: Edward Arnold, 1995. p. 222±39. [11] Chindia ML, Guthua SW, Awange DO, Wakoli KA. Osteosarcomas of the maxillofacial bones in Kenyans. Journal of Cranio-Maxillofac Surg 1998;26:98±101. [12] Doval DC, Baosy PP, Kumar RV, Kannan V, Sabitha KS, Kumarswamy SV. Osteosarcomas of the jaw bones. Br J Oral Maxillofac Surg 1997;35:337±62. [13] Bertoni F, Dallera P, Bacchini P, Marchetti C, Campobassi A. The Istuto Rizzoli Ð Beretta experience with osteosarcoma of the jaw. Cancer 1991;68:1555±63. [14] Ajagbe HA, Junaid TA, Daramola JO. Osteogenic sarcoma of the jaws in an African community: report of twenty-one cases. J Oral Maxillofac Surg 1986;44:104±6. [15] Dahlin DC, Coventry MB. Osteogenic sarcoma: a study of six hundred cases. The J of Bone and Joint Surg 1967;49A:101±10. [16] Zarbo RJ, Regezi JA, Baker SR. Periosteal osteogenic sarcoma of the mandible. Oral Surg 1984;57:643±7. [17] Koury ME, Regezi JA, Perrot DH, Kaban LB. ``Atypical'' ®broosseous lesions: diagnostic challenges and treatment. Int J Oral Maxillofac Surg 1995;24:162±9. [18] Raubenheimer EJ, Noke CE. Low-grade intraosseous osteosarcoma of the jaws. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 1998;86:82±5. [19] Newland JR, Ayala AG. Parosteal osteosarcoma of the maxilla. Oral Surg 1977;43:727±33. [20] Bras JM, Donner R, Van der Kwast WAM, Snow GB, Van der Waal I. Juxtacortical osteogenic sarcoma of the jaws: review of the literature and report of a case. Oral Surg 1980;50:535±44. [21] Bertoni F, Boriani S, Laus M, Campanacci M. Periosteal chondrosarcoma and periosteal osteosarcoma: two distinct entities. Journal of Bone and Joint Surgery 1982;64-B:370±6. [22] Minic AJ. Periosteal osteosarcoma of the mandible. Int J Oral Maxillofac Surg 1995;24:226±8. [23] Huvos AG, Rosen G, Bretsky SS, Butler A. Telangiectatic osteogenic sarcoma: a clinicopathologic study of 124 patients. Cancer 1982;49:1679±89. [24] Okada K, Unni KK, Swee RG, Sim FH. High grade surface osteosarcoma: a clinicopathologic study of 46 cases. Cancer 1999;85:1044±54. [25] Wold LE, Beabout JW, Unni KK, Pritchard DJ. High-grade surface osteosarcomas. Am J Surg Pathol 1984;8:181±6. [26] Ruiz-Godoy RLM, Meneses-Garcia A, Mosqueda-Taylor A, Dela la Garza-Salar J. Well-dierentiated intraosseous osteosarcoma of the jaws: experience of two cases from the Intituto Nacional de Cancerologia, Mexico. Oral Oncology 1999;35:530±3. [27] Slootweg PJ, Muller H. Osteosarcoma of the jaw bones: analysis of 18 cases. J Max-fac Surg 1985;13:158±66. [28] Rosen G, Tet M, Martinez A, Cham W, Murphy ML. Combination chemotherapy and radiation therapy in the treatment of metastatic osteogenic sarcoma. Cancer 1975;35:622±30.