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Massive sequestration of the upper jaw: a case report
British Journal
of Oral and Maxiliofaciai
Surgery
(1990)
28, 55-56
@ 1990The British Association of Oral and Maxillofacial Surgeons
Massive sequestration of the upper jaw: a case report H. Nandakumar,
K. B. Shankaramba
Department of Oral and Maxillofacial Surgery, Bapuji Dental College and Hospital, Davavgere-577 Karnataka State, India
004,
SUMMARY. Massive sequestration of the upper jaw has been reported only rarely in the literature. A case is presented of a 65year-old diabetic male with massive sequestration of the maxilla. The relevant literature is reviewed.
They suggest that ischaemia with superadded infection caused massive sequestration of the maxilla. A further case of massive sequestration of the upper jaw is reported.
INTRODUCTION
Bone is a specialised tissue of the body forming the skeletal architecture. It reacts in a dynamic fashion to stimuli from thermal, electrical, bacterial and radiation sources, either by hyperplasia or necrosis, depending upon the degree and strength of stimulation. Inflammation and infection may produce pus which can spread into the medullary spaces and also outwards and along the surface of the bone causing ischaemia and later necrosis by separating the periosteum from the bone (Killey & Kay, 1975). The inflammatory process may also result in intravascular thrombosis with profound local circulatory disturbance. When the nutrition and oxygenation to the specialised bone cells is impeded both from the cortical surface as well as centrally from the medullary cavity, the normal metabolism of the bone cells ceases, the bone cells die and along with t&em a volume of bone which eventually will form a sequestrum (Archer, 1975; Boyde, 1977). Sequestration iS a slow process because not only the osteoclastic but also the osteoblastic activity of the bone is inhibited. Sequestration occurs when a piece of bone becomes necrotic due to a combination of suppuration and ischaemia and then separates from the adjacent viable tissues. The surrounding healthy bone then usually proliferates to form an ensheathing involucrum. Sequestration of the mandible is more common than that of the maxilla, as it is supplied centrally almost entirely by the inferior alveolar artery alone, whereas the maxilla has a vascular supply from several anastomosing arteries (Thoma, 1969; Kruger, 1984; Laskin, 1985). Cornah and O’Hare (1981) have reported a case where following a severe facial injury total necrosis of the maxilla occurred due to the wide periosteal stripping resulting in local ischaemia and bone death which became apparent 6 days after injury. Parnes and Becker (1972) report the necrosis of the anterior maxilla following an osteotomy which had involved extensive stripping of mucoperiosteum and frbm which they later cultured Pseudomonas aboginosa.
Case report A 6.5year-old male patient presented to the Department of Oral and Maxillofacial Surgery of Bapuji Dental College and Hospital, Davangere in January 1986 complaining that for the last 3 months when he opened his mouth a hard tissue mass descended into his oral cavity. The patient had sought treatment 1 year previously for pain and swelling of the upper jaw from his doctor, but unfortunately the particulars of this treatment are unavailable. Over the succeeding month the patient had noticed a nodular swelling which gradually increased in size which ultimately broke down and gaped open to expose the underlying bone. The breakdown of the soft tissues extended to involve the palatal and alveolar processes of the maxilla with separation of the bone. Later the patient noticed increasing difficulty in opening his mouth due to the descent of the hard tissue mass into the oral cavity. From the medical &story it was known that the patient was receiving treatment for diabetes and asthma. His family history was otherwise not contributory. It was
Fig. l-Exposed mucoperiosteal 5.5
necrotic maxillary bone showing remaining attachment on left side (arrowed).
56
British Journal of Oral and Maxillofacial Surgery
claimed that all the patient’s teeth had gradually exfoliated and that he had never sought dental assistance. Extraoral examination did not reveal any abnormality. Intraorally the patient’s mouth was edentulous with a brownish-yellow hard necrotic mass, covered with food debris and slough, which was hanging in the oral cavity suspended by a 3 to 4 cm mucosal attachment anteroposteriorly in the left palatal and tuberosity region (Fig. 1). The hard, mobile mass descended when the mouth was opened. The nasopalatine foramen and canal could be readily identified. The patient’s general clinical examination was normal. The laboratory haematological investigations, including serum VDRL were within normal limits. Under local anaesthesia, the sequestrated maxilla was lifted gently from its soft tissue bed (Fig. 2). The soft tissues were closed with black silk. A 10 day prescription of antibiotics was given. Histopathological examination confirmed that the mass was made up of necrotic bone. After a further 3 weeks the patient was subjected under general anaesthesia, to the closure of the residual oroantral fistula by means of a transposition flap of palatal mucosa. The postoperatire healing was uneventful and no further exposure of bone has occurred.
DISCUSSION Prior to the advent of chemotherapeutic agents and antibiotics, sequestration of bone following specific or non-specific forms of osteomyelitis was not uncommon. Infection and trauma superimposed upon ischaemic radiation damage may lead also to
bone necrosis and sequestration. In addition, chemical agents must be excluded as possible causes of bone necrosis. Specific infections causing osteomyelitis such as tuberculosis, syphilis and actinomycosis must be considered and excluded as a cause of bone necrosis and sequestration (Shafer et al., 1983). Debilitating systemic diseases such as diabetes mellitus, predispose an individual to bone infection by pyogenic organisms and haematogenous spread and invasion by streptococci and pneumococci has also been cited in the literature as a further cause (Thoma, 1969; Laskin, 1985). Though the exact cause for the massive necrosis and separation of the maxilla could not be arrived at in the present patient, the history of diabetes and asthma together with the natural exfoliation of teeth are strongly suggestive of the presence of advanced chronic periodontal disease. It is postulated that the patient’s diabetes mellitus might have predisposed the patient to bone infection by pyogenic organisms introduced by a periodontal pathway leading in turn to gradual separation of periosteum from the bone with the end result of ischaemia and bone necrosis. The review of the literature yielded very few reports of massive sequestration of the maxilla in the adult and this does appear to be a rare entity. References Archer, W. H. (1975). Textbook of Oral and Maxillofacial Surgery. 5th Ed. pp. 502-504; 1632-1643; 1825. Philadelphia, London &Toronto: Saunders. Boyde, W. (1977). Introduction to Study of Diseases. Indian edition; Huntington Sheldon, pp. 45@452. K. M. Verghese Co., Bombay. Philadelphia: Lea & Febiger. Cornah, J. & O’Hare, P. M. (1981). Total maxillary necrosis following severe facial injury. British Journal of Oral and Maxillofacial Surgery, 19,148. Killey, H. C., Seward G. R. & Kay, L. W. (1975). An Outline of Oral Surgery. Part 1. pp. 129. Bristol: John Wright & Sons Ltd. Kruger, G. 0. (1984). Textbook of Oral and Maxillofacial Surgery. 6th Ed., pp. 217-218. St. Louis &Toronto: C. V. Mosby Co. Laskin, D M. (1985). Textbook of Oral and Maxillofacial Surgery. Vol. II. pp. 26&264. St. Louis &Toronto: C. V. Mosby Co. Parnes, E. I. &Becker, M. L. (1972). Necrosis of anterior maxilla following osteotomy. Oral Surgery, Oral Medicine, Oral Pathology, 33,326.
Fig. 2-Soft tissue bed after removal of sequestrum revealing oro-antral communication (arrowed).
Shafer, W. G., Hine, N. K. & Levy, B. N. (1983). Textbook of Oral Pathology, 4th Ed., pp. 500. Philadelphia & London: Saunders. Thoma, K. H. (1969). Textbook of Oral Surgery, Vol. II. 5th Ed., pp. 781-798. St. Louis &Toronto: C. V. Mosby Co.
The Authors Professor H. Nandakumar BSc, ML%, FIAOS, Head of Department Dr (Mrs) K. B. Shankaramba BSc, MDS Reader Department of Oral and Maxillofacial Surgery Bapuji Dental College and Hospital Davavgere-577 044 Karnataka State India Correspondence Nandakumar Fig. 3-Complete sequestrum. Nasopalatine foramen arrowed.
and requests for offprints to Professor H.
Paper received 2 June 1988 Accepted 31 January 1989
of Oral and Maxiliofaciai
Surgery
(1990)
28, 55-56
@ 1990The British Association of Oral and Maxillofacial Surgeons
Massive sequestration of the upper jaw: a case report H. Nandakumar,
K. B. Shankaramba
Department of Oral and Maxillofacial Surgery, Bapuji Dental College and Hospital, Davavgere-577 Karnataka State, India
004,
SUMMARY. Massive sequestration of the upper jaw has been reported only rarely in the literature. A case is presented of a 65year-old diabetic male with massive sequestration of the maxilla. The relevant literature is reviewed.
They suggest that ischaemia with superadded infection caused massive sequestration of the maxilla. A further case of massive sequestration of the upper jaw is reported.
INTRODUCTION
Bone is a specialised tissue of the body forming the skeletal architecture. It reacts in a dynamic fashion to stimuli from thermal, electrical, bacterial and radiation sources, either by hyperplasia or necrosis, depending upon the degree and strength of stimulation. Inflammation and infection may produce pus which can spread into the medullary spaces and also outwards and along the surface of the bone causing ischaemia and later necrosis by separating the periosteum from the bone (Killey & Kay, 1975). The inflammatory process may also result in intravascular thrombosis with profound local circulatory disturbance. When the nutrition and oxygenation to the specialised bone cells is impeded both from the cortical surface as well as centrally from the medullary cavity, the normal metabolism of the bone cells ceases, the bone cells die and along with t&em a volume of bone which eventually will form a sequestrum (Archer, 1975; Boyde, 1977). Sequestration iS a slow process because not only the osteoclastic but also the osteoblastic activity of the bone is inhibited. Sequestration occurs when a piece of bone becomes necrotic due to a combination of suppuration and ischaemia and then separates from the adjacent viable tissues. The surrounding healthy bone then usually proliferates to form an ensheathing involucrum. Sequestration of the mandible is more common than that of the maxilla, as it is supplied centrally almost entirely by the inferior alveolar artery alone, whereas the maxilla has a vascular supply from several anastomosing arteries (Thoma, 1969; Kruger, 1984; Laskin, 1985). Cornah and O’Hare (1981) have reported a case where following a severe facial injury total necrosis of the maxilla occurred due to the wide periosteal stripping resulting in local ischaemia and bone death which became apparent 6 days after injury. Parnes and Becker (1972) report the necrosis of the anterior maxilla following an osteotomy which had involved extensive stripping of mucoperiosteum and frbm which they later cultured Pseudomonas aboginosa.
Case report A 6.5year-old male patient presented to the Department of Oral and Maxillofacial Surgery of Bapuji Dental College and Hospital, Davangere in January 1986 complaining that for the last 3 months when he opened his mouth a hard tissue mass descended into his oral cavity. The patient had sought treatment 1 year previously for pain and swelling of the upper jaw from his doctor, but unfortunately the particulars of this treatment are unavailable. Over the succeeding month the patient had noticed a nodular swelling which gradually increased in size which ultimately broke down and gaped open to expose the underlying bone. The breakdown of the soft tissues extended to involve the palatal and alveolar processes of the maxilla with separation of the bone. Later the patient noticed increasing difficulty in opening his mouth due to the descent of the hard tissue mass into the oral cavity. From the medical &story it was known that the patient was receiving treatment for diabetes and asthma. His family history was otherwise not contributory. It was
Fig. l-Exposed mucoperiosteal 5.5
necrotic maxillary bone showing remaining attachment on left side (arrowed).
56
British Journal of Oral and Maxillofacial Surgery
claimed that all the patient’s teeth had gradually exfoliated and that he had never sought dental assistance. Extraoral examination did not reveal any abnormality. Intraorally the patient’s mouth was edentulous with a brownish-yellow hard necrotic mass, covered with food debris and slough, which was hanging in the oral cavity suspended by a 3 to 4 cm mucosal attachment anteroposteriorly in the left palatal and tuberosity region (Fig. 1). The hard, mobile mass descended when the mouth was opened. The nasopalatine foramen and canal could be readily identified. The patient’s general clinical examination was normal. The laboratory haematological investigations, including serum VDRL were within normal limits. Under local anaesthesia, the sequestrated maxilla was lifted gently from its soft tissue bed (Fig. 2). The soft tissues were closed with black silk. A 10 day prescription of antibiotics was given. Histopathological examination confirmed that the mass was made up of necrotic bone. After a further 3 weeks the patient was subjected under general anaesthesia, to the closure of the residual oroantral fistula by means of a transposition flap of palatal mucosa. The postoperatire healing was uneventful and no further exposure of bone has occurred.
DISCUSSION Prior to the advent of chemotherapeutic agents and antibiotics, sequestration of bone following specific or non-specific forms of osteomyelitis was not uncommon. Infection and trauma superimposed upon ischaemic radiation damage may lead also to
bone necrosis and sequestration. In addition, chemical agents must be excluded as possible causes of bone necrosis. Specific infections causing osteomyelitis such as tuberculosis, syphilis and actinomycosis must be considered and excluded as a cause of bone necrosis and sequestration (Shafer et al., 1983). Debilitating systemic diseases such as diabetes mellitus, predispose an individual to bone infection by pyogenic organisms and haematogenous spread and invasion by streptococci and pneumococci has also been cited in the literature as a further cause (Thoma, 1969; Laskin, 1985). Though the exact cause for the massive necrosis and separation of the maxilla could not be arrived at in the present patient, the history of diabetes and asthma together with the natural exfoliation of teeth are strongly suggestive of the presence of advanced chronic periodontal disease. It is postulated that the patient’s diabetes mellitus might have predisposed the patient to bone infection by pyogenic organisms introduced by a periodontal pathway leading in turn to gradual separation of periosteum from the bone with the end result of ischaemia and bone necrosis. The review of the literature yielded very few reports of massive sequestration of the maxilla in the adult and this does appear to be a rare entity. References Archer, W. H. (1975). Textbook of Oral and Maxillofacial Surgery. 5th Ed. pp. 502-504; 1632-1643; 1825. Philadelphia, London &Toronto: Saunders. Boyde, W. (1977). Introduction to Study of Diseases. Indian edition; Huntington Sheldon, pp. 45@452. K. M. Verghese Co., Bombay. Philadelphia: Lea & Febiger. Cornah, J. & O’Hare, P. M. (1981). Total maxillary necrosis following severe facial injury. British Journal of Oral and Maxillofacial Surgery, 19,148. Killey, H. C., Seward G. R. & Kay, L. W. (1975). An Outline of Oral Surgery. Part 1. pp. 129. Bristol: John Wright & Sons Ltd. Kruger, G. 0. (1984). Textbook of Oral and Maxillofacial Surgery. 6th Ed., pp. 217-218. St. Louis &Toronto: C. V. Mosby Co. Laskin, D M. (1985). Textbook of Oral and Maxillofacial Surgery. Vol. II. pp. 26&264. St. Louis &Toronto: C. V. Mosby Co. Parnes, E. I. &Becker, M. L. (1972). Necrosis of anterior maxilla following osteotomy. Oral Surgery, Oral Medicine, Oral Pathology, 33,326.
Fig. 2-Soft tissue bed after removal of sequestrum revealing oro-antral communication (arrowed).
Shafer, W. G., Hine, N. K. & Levy, B. N. (1983). Textbook of Oral Pathology, 4th Ed., pp. 500. Philadelphia & London: Saunders. Thoma, K. H. (1969). Textbook of Oral Surgery, Vol. II. 5th Ed., pp. 781-798. St. Louis &Toronto: C. V. Mosby Co.
The Authors Professor H. Nandakumar BSc, ML%, FIAOS, Head of Department Dr (Mrs) K. B. Shankaramba BSc, MDS Reader Department of Oral and Maxillofacial Surgery Bapuji Dental College and Hospital Davavgere-577 044 Karnataka State India Correspondence Nandakumar Fig. 3-Complete sequestrum. Nasopalatine foramen arrowed.
and requests for offprints to Professor H.
Paper received 2 June 1988 Accepted 31 January 1989