897
RUBIN ET AL
21.
22.
23. 24. 25. 26.
27.
28.
29.
30.
31.
a two-radiopharmaceutical approach. Pediatrics 73:661, 1984 Gilday DL, Eng B, Paul DJ, et al: Diagnosis of osteomyelitis in children by combined blood pool and bone imaging. Radiology 117:331, 1975 Alexander JM: Radionuclide bone scanning in the diagnosis of lesions of the maxillofacial region. J Oral Surg 34:249, 1976 Lisbona R, Rosenthal] L: An update on radionuclide imaging in benign bone disorders. J Can Assoc Radio1 29: 188, 1978 Nelson HT. Taylor A: Bone scanning in the diagnosis of acute osteomyelitis. Eur J Nucl Med 5:267, 1980 Capitanio MA. Kirkpatrick JA: Early roentgen observations in acute osteomyelitis. AJR 108:488, 1970 Galasko CSB: Infection, in Galasko CSB, Weber DA (eds): Scintigraphy in Orthopaedics. Edinburgh, Churchill Livingstone, 1984, p 138 Alazraki N, Fierer J, Resnick D: Chronic osteomyelitis, monitoring by Tc-99m phosphate and Ga-67 citrate imaging, AJR 145:767, 1985 Graham CD, Lundy MM, Moreno AJ, et al: The role of Tc-99m MDP and Ga-67 citrate in predicting the cure of osteomyelitis. Clin Nucl Med 8:344. 1983 Shafer RB, Marlette JM, Browne GA, et al: The role of Tc-99m phosphate complexes and Gallium-67 in the diagnosis and management of maxillofacial disease. concise communication. J Nucl Med 22:8. 1981 Dhawan VJ, Sziklas JJ, Spencer RP, et al: Computerized double-tracer subtraction scanning with Gallium-67 citrate in inflammatory diseases. J Nucl Med 19:1297, 1978 Hartshorne MF, Graham G. Lancaster J, et al: Gallium67/Technetium99m methylene diphosphonate ratio imag-
J Oral Maxillofac
32.
33.
34.
35.
36.
37.
38.
39. 40.
41.
42.
ing. early rabbit osteomyelitis and fracture. J Nucl Med 26~272. 1985 Francis MD: The inhibition of calcium hydroxyapatite crystal growth by polyphosphonates and polyphosphates. Calcif Tissue Res 3: 151, I%9 Wiegmann T, Kirsh J. Rosenthal1 L, Kaye M: Relationship between bone uptake of Tc-99m pyrophosphate and hydroxyproline in blood and urine. J Nucl Med 17:711, 1976 Zimmer AM, Isitman AT, Holmes RA: Enzymatic inhibition of diphosphonate: A proposed mechanism of tissue uptake. J Nucl Med 16:352, 1975. Gelrud LG. Arseneau JC, Milder MS: The kinetics of gallium-67 incorporation into inflammatory lesions: Experimental and c&al studies. J Lab Clin Med 83:489, i974 Hammerslev PAG. Tavlor DM: The mechanism of the localization of gallium-67 citrate in experimental abscesses. Eur J Nucl Med 4:271, 1979 Menon S. Wagner HN, Tsan MF: Studies on gallium accumulation in inflammatory lesions, II, uptake by staphylococcus aureus. concise communication. J Nucl Med 1944. 1978 Weiner R, Hoffer PB, Thakus ML: Lactoferrin. its role as a Ga-67 binding protein in polymorphonuclear leukocytes. J Nucl Med 22:32, 1981 Hoffer P: Gallium and infection. J Nucl Med 21:484, 1980 Hopkins GB, Mende CW: Gallium-67 and subphrenic abscesses-Is delayed scintigraphy necessary? J Nucl Med 16609, 1975 Mauer AH, Chen DCP, Camargo EC, et al: Utility of threephase skeletal scintigraphy in suspected osteomyelitis. concise communication. J Nucl Med 22:941. 1981 Rosenthal] L, Lisbona R: Skeletal Imaging. Norwalk, CT, Appleton-Century-Crofts, 1984. p 117
Surg
49:997-900.1991
Vertebral Osteomyelitis Secondary Oral Infection MITCHELL
Pyogenic infections the intervening disc mon. For this reason, tions tend to manifest ion, correct diagnosis
M. RUBIN, DMD,* ROSS J. SANFILIPPO, AND RORY S. SADOFF, DDS*
of the vertebral bodies and spaces are relatively uncomand also because these infecthemselves in a bizarre fashis often delayed. Attention is
Received from the Department of Oral and Maxillofacial Surgery, Nassau County Medical Center, East Meadow, NY. * Attending Surgeon: in private practice, Rockville Centre, NY. t Senior Resident. t Director of Advanced Training. Address correspondence and reprint requests to Dr Rubin: South Shore Oral Surgery Associates, P.C., 155 W Merrick Rd. Freeport. NY 11530. 0 1991 American Association of Oral and Maxillofacial geons 0278-2391/9114906/0018$3.00/0
Sur-
to an
DMD,t
frequently directed away from the spine by abdominal pain, neuromuscular disturbances, or genitourinary symptoms. ’ Before the development of antibiotics, acute hematogenous osteomyelitis was associated with a mortality rate of 20% to 30% and a morbidity rate of 50%. The introduction of chemotherapeutic agents, however, together with improved nutrition, has made associated death uncommon and has greatly reduced morbidity.’ Vertebral osteomyelitis may cause the rapid onset of back pain, occasionally with radicular features and the general systemic signs of acute infection. More often, however, the onset is insidous and gradually progressive, with no malaise and little or no fever. Back pain that eventually becomes severe is the most constant feature. It is present even at rest. but is accentuated by movement. Analge-
898
sits, bed rest, and heat have little alleviating effects.3 The most common site of occurrence is the vertebrae of the lower thoracic and upper lumbar spine.4 Elderly men and diabetics are particularly susceptible to the disease.’ Vertebral osteomyelitis, primarily a disease of adults, should be distinguished from the disc space infection of children. It has been shown that until about 20 years of age, there are vascular channels perforating the vertebral end plates and these channels provide a pathway by which blood-borne organisms can reach the intervertebral disc. Adjacent vertebral bodies then become secondarily involved as the disc is destroyed by the lysosomal action of leukocytes accompanying the closed-space infection. In the adult, there are no direct routes of communication to the intervertebral disc, and bacteria lodge in the capillary end-organ system along the vertebral trabeculae. The disc is involved only after considerable destruction of bone.3 In the early stages of hematogenous vertebral osteomyelitis, radiographic examination may disclose rarefaction or loss of trabecular detail, usually in the superior or inferior part of the vertebral body close to the cartilagenous plate, or narrowing of the vertebral disc space. Collapse of the vertebral body may occur later, but vertebral osteomyelitis is often accompanied by rapid bony regeneration so that spurs and dense new bone may form even as the vertebral body is being destroyed. The new bone formation can lead to bony bridging and fusion of the opposing vertebral bodies.6 Technetium bone scans may show discrete abnormalities of the vertebrae before radiologic changes are observedS5 Vertebral osteomyelitis in adults may follow skin infection, extension from an adjacent area, or uri-
VERTEBRAL
OSTEOMYELITIS
DUE TO ORAL INFECTION
nary tract infection after catheterization or genitourinary surgical procedure. Under these circumstances, the infection probably spreads to the vertebrae through the paravertebral veins as discussed by Batson.’ One case of osteomyelitis of the cervical spine was reported following an open, infected mandibular fracture.* The following is the first case report of vertebral osteomyelitis following a generalized peridontal infection. Report of a Case A 5%year-old white man presented to the orthopedic service at the Nassau County Medical Center for evaluation of lower back pain of approximately 4 months’ duration. His past medical history was positive for type II diabetes mellitus, a hiatus hernia, and hypertension. His current medications included glipizide 10 mg twice per day, and gemfibrozil 300 mg twice per day. Physical examination was unremarkable except for lower back pain, which did not radiate to the legs. Preliminary computed tomography (CT) (Fig 1) and magnetic resonance imaging (MRI) (Fig 2) studies showed a lytic lesion of T-12 to L-l. Results of a fluoroscopically guided needle biopsy was consistent with vertebral osteomyelitis, with disc space infection. Tissue specimens were also sent for culture and antibiotic sensitivity testing, and were positive for growth of Streptococcus sanguis II, Fusobacterium species, and Staphylococcus aurem. At this time the infectious disease department was consulted. They suggested an oral and maxillofacial surgery consultation because of the unusual bacteriologic findings. It was felt that a bacteremia from an intraoral focus was the source of this infection. Clinical and radiographic oral examination (Fig 3) showed an extremely poor peridontial condition, with large amounts of plaque and calculus accumulation, and friable gingival tissues that bled easily on gentle manipulation. Also, a large lateral periodontal defect was noted involving the maxillary left first premolar due to a perfo-
899
RUBIN ET AL
rated post preparation. The patient reported bleeding while brushing, as well as continual pain in the area. A diagnosis of hematogenous vertebral osteomyelitis secondary to oral bacteremia was made. The infectious disease service suggested that the patient’s current antibiotic regimen of clindamycin 900 mg every 8 hours would be an adequate prophylaxis for subsequent dental treatment. The premolar was extracted and the patient was referred to the dental service for peridontal scaling and curettage. He was also instructed to insist on antibiotic prophylaxis prior to future dental treatment. He was discharged from the hospital with a body jacket, and instructed to continue his present course of antibiotic ther-
apy for 8 weeks, with strict bed rest. His back pain has since resolved without residual neurologic
deficit.
Discussion The infectious agent most frequently found in vertebral osteomyelitis is Staphylococcus aureus. This organism is responsible for infection in 90% of the adult cases when septic material is recovered and positive cultures are obtained. E. coli is the next most frequently isolated organism.3 The presence of more than one organism in vertebral osteomyelitis has rarely been described.5 In our case, Streptococcus sanguis II was cultured from the vertebral tissue specimen, along with a Fusobacterium
FIGURE 2. Magnetic resonance image showing narrowing of the T12/L-l disc space, loss of normal disc signal, and abnormal signal from the vertebral bodies T-12 to L-l.
species and Staphylococcus uureus. This is an unusual mixed bacterial infection to be cultured from the vertebrae. These microorganisms are all normal inhabitants of the oral cavity, and are commonly isolated from oral infections. As such, this patient’s severe gingival infection was the most likely source of his vertebral osteomyelitis. The primary habitat of S. sunguis is the dental plaque. In adults it constitutes 20% to 50% of the faculative streptococci present in the dental plaque. It is found only in low numbers in the saliva and throat, occurring in the order of 5,000 to 10,000 times less than in the plaque.’ Because S. sun&s preferentially colonizes the surface of the teeth and is constantly present in plaque in high numbers, it has been suggested that the tissues surrounding the teeth are the main sites of entrance of S. sung&s into the blood stream. It is thought that the oral cavity is more likely than the intestinal tract to be the source of the organism in subacute bacterial endocarditis in view of its much smaller concentration in the intestine and the relative ease with which it enters the blood on dental manipulation.” Under certain conditions, particularly injury to normal mucous membranes, nutritional deficiency, or concomitant infection of the epithelium. the nor-
900
VERTEBRAL
OSTEOMYELITIS
DUE TO ORAL INFECTION
FIGURE 3. Panoramic radiograph showing multiple peridontal defects, including one associated with a perforated canal on the maxillary left first premolar.
ma1 spirochetes of the mouth, together with anaerobic fusiform baccili (fusobacteria), find suitable conditions for a vast increase in number. This occurs commonly in ulcerative gingivostomatitis. Necrotic tissue provides the anaerobic environment required by the fusobacteria. Fusobacterial disease is generally not transmitted through direct contact because everybody carries the organism in the mouth.” Fusobacteria have been isolated more frequently from bone infections resulting from periodontal disease than abscesses of the soft tissues. Fusobacterium plauf~-vincenrj and Fusobacferium nucleatum are the species most commonly isolated from the oral cavity.” Staphylococcus aureus is also a commun inhabitant of the oral cavity, with about one half of the subjects tested yielding some from the saliva, although the total numbers were low. The organism is found more commonly and in greater numbers in the nose and throat. I2 Once the diagnosis of vertebral osteomyelitis has been made, the treatment consists of the appropriate antibiotic therapy and strict bed rest.3 When blood cultures are negative, trocar biopsy is not only a valuable aid to diagnosis but mandatory for accurate therapy. I3 The erythrocyte sedimentation rate has been used as a diagnositic feature and indication of continuing activity during treatment.5 Antibiotics should be continued until the temperature and sedimentation rate become normal, and the radiographic findings remain unchanged for one month.r3 The clinical response to bed rest and antibiotics was found to be equivalent to that obtained with rigid immobilization. This regimen avoids the inconvenience and hazards of casts and the duration of hospitalization may be shortened. ’ When the
disease is diagnosed early, the prognosis of hematogenous vertebral osteomyelitis has been good. The incidence of residual neurologic deficit following infection is less than 7% and that of paraplegia less than 4%.5 References 1. Jordan MC, Kirby WM: Pyogenic vertebral osteomyelitis, treatment with antimicrobial agents and bed rest. Arch Intern Med 128:405, 1970 2. Emslie KR, Nade S: Pathogenesis and treatment of acute hematogenous osteomyelitis: Evaluation of current views with reference to an animal model. Rev Infect Dis 8: 841, 1986 3. Stauffer RN: Pyogenic vertebral osteomyelitis. Orthop Clin North Am 6:1015, 1975 4. Salter RB: Textbook of Disorders and Injuries of Musculoskeletal System. Baltimore, MD, Williams & Wilkins, 1970, p 165 5. Sapico Fl, Montgomerie JZ: Pyogenic vertebral osteomyelitis, report of nine cases and review of the literature. Rev Infect Dis 1:754, 1979 6. Stone DB, Bonliglio M: Pyogenic vertebral osteomyelitis, a diagnostic pitfall for the internist. Arch Intern Med 112:491, 1963 7. Bonliglio M, Lange TA, Kim YM: Pyogenic vertebral osteomvelitis: Disk suace infections, Clin Orthon 96:234. 1973 8. Fein-DJ, Torg JS,.Mohnac AM, et al: Infection of the cervical spine associated with a fracture of the mandible. J Oral Surg 27: 145, 1969 9. Nolte WA: Oral Microbiology: With Basic Microbiology and Immunology (ed 4). St Louis, MO, Mosby, 1982, p 307 10. Van Houte J, Jordan HV, Bellack S: Proportions of Streptococcus sanguis, an organism associated with subacute bacterial endocarditis, in human feces and dental plaque. Infect Immun 4:658, 1971 11. Jawitz E, Melnick JL, Adelberg EA: Review of Medical Microbiology (ed 12). Los Altos, CA, Lange Medical Publications, 1976, p 231 12. Topazian RG, Goldberg MH: Management of Infections of the Oral and Maxillofacial Regions. Philadelphia, PA, Saunders, 1981, pp 39-87 13. Ambrose GB, Alpert M, Neer CS: Vertebral osteomyelitis, a diagnostic problem. JAMA 197: 101, 1966
RUBIN ET AL
21.
22.
23. 24. 25. 26.
27.
28.
29.
30.
31.
a two-radiopharmaceutical approach. Pediatrics 73:661, 1984 Gilday DL, Eng B, Paul DJ, et al: Diagnosis of osteomyelitis in children by combined blood pool and bone imaging. Radiology 117:331, 1975 Alexander JM: Radionuclide bone scanning in the diagnosis of lesions of the maxillofacial region. J Oral Surg 34:249, 1976 Lisbona R, Rosenthal] L: An update on radionuclide imaging in benign bone disorders. J Can Assoc Radio1 29: 188, 1978 Nelson HT. Taylor A: Bone scanning in the diagnosis of acute osteomyelitis. Eur J Nucl Med 5:267, 1980 Capitanio MA. Kirkpatrick JA: Early roentgen observations in acute osteomyelitis. AJR 108:488, 1970 Galasko CSB: Infection, in Galasko CSB, Weber DA (eds): Scintigraphy in Orthopaedics. Edinburgh, Churchill Livingstone, 1984, p 138 Alazraki N, Fierer J, Resnick D: Chronic osteomyelitis, monitoring by Tc-99m phosphate and Ga-67 citrate imaging, AJR 145:767, 1985 Graham CD, Lundy MM, Moreno AJ, et al: The role of Tc-99m MDP and Ga-67 citrate in predicting the cure of osteomyelitis. Clin Nucl Med 8:344. 1983 Shafer RB, Marlette JM, Browne GA, et al: The role of Tc-99m phosphate complexes and Gallium-67 in the diagnosis and management of maxillofacial disease. concise communication. J Nucl Med 22:8. 1981 Dhawan VJ, Sziklas JJ, Spencer RP, et al: Computerized double-tracer subtraction scanning with Gallium-67 citrate in inflammatory diseases. J Nucl Med 19:1297, 1978 Hartshorne MF, Graham G. Lancaster J, et al: Gallium67/Technetium99m methylene diphosphonate ratio imag-
J Oral Maxillofac
32.
33.
34.
35.
36.
37.
38.
39. 40.
41.
42.
ing. early rabbit osteomyelitis and fracture. J Nucl Med 26~272. 1985 Francis MD: The inhibition of calcium hydroxyapatite crystal growth by polyphosphonates and polyphosphates. Calcif Tissue Res 3: 151, I%9 Wiegmann T, Kirsh J. Rosenthal1 L, Kaye M: Relationship between bone uptake of Tc-99m pyrophosphate and hydroxyproline in blood and urine. J Nucl Med 17:711, 1976 Zimmer AM, Isitman AT, Holmes RA: Enzymatic inhibition of diphosphonate: A proposed mechanism of tissue uptake. J Nucl Med 16:352, 1975. Gelrud LG. Arseneau JC, Milder MS: The kinetics of gallium-67 incorporation into inflammatory lesions: Experimental and c&al studies. J Lab Clin Med 83:489, i974 Hammerslev PAG. Tavlor DM: The mechanism of the localization of gallium-67 citrate in experimental abscesses. Eur J Nucl Med 4:271, 1979 Menon S. Wagner HN, Tsan MF: Studies on gallium accumulation in inflammatory lesions, II, uptake by staphylococcus aureus. concise communication. J Nucl Med 1944. 1978 Weiner R, Hoffer PB, Thakus ML: Lactoferrin. its role as a Ga-67 binding protein in polymorphonuclear leukocytes. J Nucl Med 22:32, 1981 Hoffer P: Gallium and infection. J Nucl Med 21:484, 1980 Hopkins GB, Mende CW: Gallium-67 and subphrenic abscesses-Is delayed scintigraphy necessary? J Nucl Med 16609, 1975 Mauer AH, Chen DCP, Camargo EC, et al: Utility of threephase skeletal scintigraphy in suspected osteomyelitis. concise communication. J Nucl Med 22:941. 1981 Rosenthal] L, Lisbona R: Skeletal Imaging. Norwalk, CT, Appleton-Century-Crofts, 1984. p 117
Surg
49:997-900.1991
Vertebral Osteomyelitis Secondary Oral Infection MITCHELL
Pyogenic infections the intervening disc mon. For this reason, tions tend to manifest ion, correct diagnosis
M. RUBIN, DMD,* ROSS J. SANFILIPPO, AND RORY S. SADOFF, DDS*
of the vertebral bodies and spaces are relatively uncomand also because these infecthemselves in a bizarre fashis often delayed. Attention is
Received from the Department of Oral and Maxillofacial Surgery, Nassau County Medical Center, East Meadow, NY. * Attending Surgeon: in private practice, Rockville Centre, NY. t Senior Resident. t Director of Advanced Training. Address correspondence and reprint requests to Dr Rubin: South Shore Oral Surgery Associates, P.C., 155 W Merrick Rd. Freeport. NY 11530. 0 1991 American Association of Oral and Maxillofacial geons 0278-2391/9114906/0018$3.00/0
Sur-
to an
DMD,t
frequently directed away from the spine by abdominal pain, neuromuscular disturbances, or genitourinary symptoms. ’ Before the development of antibiotics, acute hematogenous osteomyelitis was associated with a mortality rate of 20% to 30% and a morbidity rate of 50%. The introduction of chemotherapeutic agents, however, together with improved nutrition, has made associated death uncommon and has greatly reduced morbidity.’ Vertebral osteomyelitis may cause the rapid onset of back pain, occasionally with radicular features and the general systemic signs of acute infection. More often, however, the onset is insidous and gradually progressive, with no malaise and little or no fever. Back pain that eventually becomes severe is the most constant feature. It is present even at rest. but is accentuated by movement. Analge-
898
sits, bed rest, and heat have little alleviating effects.3 The most common site of occurrence is the vertebrae of the lower thoracic and upper lumbar spine.4 Elderly men and diabetics are particularly susceptible to the disease.’ Vertebral osteomyelitis, primarily a disease of adults, should be distinguished from the disc space infection of children. It has been shown that until about 20 years of age, there are vascular channels perforating the vertebral end plates and these channels provide a pathway by which blood-borne organisms can reach the intervertebral disc. Adjacent vertebral bodies then become secondarily involved as the disc is destroyed by the lysosomal action of leukocytes accompanying the closed-space infection. In the adult, there are no direct routes of communication to the intervertebral disc, and bacteria lodge in the capillary end-organ system along the vertebral trabeculae. The disc is involved only after considerable destruction of bone.3 In the early stages of hematogenous vertebral osteomyelitis, radiographic examination may disclose rarefaction or loss of trabecular detail, usually in the superior or inferior part of the vertebral body close to the cartilagenous plate, or narrowing of the vertebral disc space. Collapse of the vertebral body may occur later, but vertebral osteomyelitis is often accompanied by rapid bony regeneration so that spurs and dense new bone may form even as the vertebral body is being destroyed. The new bone formation can lead to bony bridging and fusion of the opposing vertebral bodies.6 Technetium bone scans may show discrete abnormalities of the vertebrae before radiologic changes are observedS5 Vertebral osteomyelitis in adults may follow skin infection, extension from an adjacent area, or uri-
VERTEBRAL
OSTEOMYELITIS
DUE TO ORAL INFECTION
nary tract infection after catheterization or genitourinary surgical procedure. Under these circumstances, the infection probably spreads to the vertebrae through the paravertebral veins as discussed by Batson.’ One case of osteomyelitis of the cervical spine was reported following an open, infected mandibular fracture.* The following is the first case report of vertebral osteomyelitis following a generalized peridontal infection. Report of a Case A 5%year-old white man presented to the orthopedic service at the Nassau County Medical Center for evaluation of lower back pain of approximately 4 months’ duration. His past medical history was positive for type II diabetes mellitus, a hiatus hernia, and hypertension. His current medications included glipizide 10 mg twice per day, and gemfibrozil 300 mg twice per day. Physical examination was unremarkable except for lower back pain, which did not radiate to the legs. Preliminary computed tomography (CT) (Fig 1) and magnetic resonance imaging (MRI) (Fig 2) studies showed a lytic lesion of T-12 to L-l. Results of a fluoroscopically guided needle biopsy was consistent with vertebral osteomyelitis, with disc space infection. Tissue specimens were also sent for culture and antibiotic sensitivity testing, and were positive for growth of Streptococcus sanguis II, Fusobacterium species, and Staphylococcus aurem. At this time the infectious disease department was consulted. They suggested an oral and maxillofacial surgery consultation because of the unusual bacteriologic findings. It was felt that a bacteremia from an intraoral focus was the source of this infection. Clinical and radiographic oral examination (Fig 3) showed an extremely poor peridontial condition, with large amounts of plaque and calculus accumulation, and friable gingival tissues that bled easily on gentle manipulation. Also, a large lateral periodontal defect was noted involving the maxillary left first premolar due to a perfo-
899
RUBIN ET AL
rated post preparation. The patient reported bleeding while brushing, as well as continual pain in the area. A diagnosis of hematogenous vertebral osteomyelitis secondary to oral bacteremia was made. The infectious disease service suggested that the patient’s current antibiotic regimen of clindamycin 900 mg every 8 hours would be an adequate prophylaxis for subsequent dental treatment. The premolar was extracted and the patient was referred to the dental service for peridontal scaling and curettage. He was also instructed to insist on antibiotic prophylaxis prior to future dental treatment. He was discharged from the hospital with a body jacket, and instructed to continue his present course of antibiotic ther-
apy for 8 weeks, with strict bed rest. His back pain has since resolved without residual neurologic
deficit.
Discussion The infectious agent most frequently found in vertebral osteomyelitis is Staphylococcus aureus. This organism is responsible for infection in 90% of the adult cases when septic material is recovered and positive cultures are obtained. E. coli is the next most frequently isolated organism.3 The presence of more than one organism in vertebral osteomyelitis has rarely been described.5 In our case, Streptococcus sanguis II was cultured from the vertebral tissue specimen, along with a Fusobacterium
FIGURE 2. Magnetic resonance image showing narrowing of the T12/L-l disc space, loss of normal disc signal, and abnormal signal from the vertebral bodies T-12 to L-l.
species and Staphylococcus uureus. This is an unusual mixed bacterial infection to be cultured from the vertebrae. These microorganisms are all normal inhabitants of the oral cavity, and are commonly isolated from oral infections. As such, this patient’s severe gingival infection was the most likely source of his vertebral osteomyelitis. The primary habitat of S. sunguis is the dental plaque. In adults it constitutes 20% to 50% of the faculative streptococci present in the dental plaque. It is found only in low numbers in the saliva and throat, occurring in the order of 5,000 to 10,000 times less than in the plaque.’ Because S. sun&s preferentially colonizes the surface of the teeth and is constantly present in plaque in high numbers, it has been suggested that the tissues surrounding the teeth are the main sites of entrance of S. sung&s into the blood stream. It is thought that the oral cavity is more likely than the intestinal tract to be the source of the organism in subacute bacterial endocarditis in view of its much smaller concentration in the intestine and the relative ease with which it enters the blood on dental manipulation.” Under certain conditions, particularly injury to normal mucous membranes, nutritional deficiency, or concomitant infection of the epithelium. the nor-
900
VERTEBRAL
OSTEOMYELITIS
DUE TO ORAL INFECTION
FIGURE 3. Panoramic radiograph showing multiple peridontal defects, including one associated with a perforated canal on the maxillary left first premolar.
ma1 spirochetes of the mouth, together with anaerobic fusiform baccili (fusobacteria), find suitable conditions for a vast increase in number. This occurs commonly in ulcerative gingivostomatitis. Necrotic tissue provides the anaerobic environment required by the fusobacteria. Fusobacterial disease is generally not transmitted through direct contact because everybody carries the organism in the mouth.” Fusobacteria have been isolated more frequently from bone infections resulting from periodontal disease than abscesses of the soft tissues. Fusobacterium plauf~-vincenrj and Fusobacferium nucleatum are the species most commonly isolated from the oral cavity.” Staphylococcus aureus is also a commun inhabitant of the oral cavity, with about one half of the subjects tested yielding some from the saliva, although the total numbers were low. The organism is found more commonly and in greater numbers in the nose and throat. I2 Once the diagnosis of vertebral osteomyelitis has been made, the treatment consists of the appropriate antibiotic therapy and strict bed rest.3 When blood cultures are negative, trocar biopsy is not only a valuable aid to diagnosis but mandatory for accurate therapy. I3 The erythrocyte sedimentation rate has been used as a diagnositic feature and indication of continuing activity during treatment.5 Antibiotics should be continued until the temperature and sedimentation rate become normal, and the radiographic findings remain unchanged for one month.r3 The clinical response to bed rest and antibiotics was found to be equivalent to that obtained with rigid immobilization. This regimen avoids the inconvenience and hazards of casts and the duration of hospitalization may be shortened. ’ When the
disease is diagnosed early, the prognosis of hematogenous vertebral osteomyelitis has been good. The incidence of residual neurologic deficit following infection is less than 7% and that of paraplegia less than 4%.5 References 1. Jordan MC, Kirby WM: Pyogenic vertebral osteomyelitis, treatment with antimicrobial agents and bed rest. Arch Intern Med 128:405, 1970 2. Emslie KR, Nade S: Pathogenesis and treatment of acute hematogenous osteomyelitis: Evaluation of current views with reference to an animal model. Rev Infect Dis 8: 841, 1986 3. Stauffer RN: Pyogenic vertebral osteomyelitis. Orthop Clin North Am 6:1015, 1975 4. Salter RB: Textbook of Disorders and Injuries of Musculoskeletal System. Baltimore, MD, Williams & Wilkins, 1970, p 165 5. Sapico Fl, Montgomerie JZ: Pyogenic vertebral osteomyelitis, report of nine cases and review of the literature. Rev Infect Dis 1:754, 1979 6. Stone DB, Bonliglio M: Pyogenic vertebral osteomyelitis, a diagnostic pitfall for the internist. Arch Intern Med 112:491, 1963 7. Bonliglio M, Lange TA, Kim YM: Pyogenic vertebral osteomvelitis: Disk suace infections, Clin Orthon 96:234. 1973 8. Fein-DJ, Torg JS,.Mohnac AM, et al: Infection of the cervical spine associated with a fracture of the mandible. J Oral Surg 27: 145, 1969 9. Nolte WA: Oral Microbiology: With Basic Microbiology and Immunology (ed 4). St Louis, MO, Mosby, 1982, p 307 10. Van Houte J, Jordan HV, Bellack S: Proportions of Streptococcus sanguis, an organism associated with subacute bacterial endocarditis, in human feces and dental plaque. Infect Immun 4:658, 1971 11. Jawitz E, Melnick JL, Adelberg EA: Review of Medical Microbiology (ed 12). Los Altos, CA, Lange Medical Publications, 1976, p 231 12. Topazian RG, Goldberg MH: Management of Infections of the Oral and Maxillofacial Regions. Philadelphia, PA, Saunders, 1981, pp 39-87 13. Ambrose GB, Alpert M, Neer CS: Vertebral osteomyelitis, a diagnostic problem. JAMA 197: 101, 1966
