Intracranial abscesses of odontogenic origin

Hollin, Sidney A.; Hayashi, Hiroshi; Gross, Sidney W.

doi:10.1016/0030-4220(67)90138-7

Cited by 65 publications

(22 citation statements)

References 39 publications

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“…These infections are mixed and anaerobic in nature, and are associated with high morbidity and mortality if bacterial dissemination occurs from the root canal into the tissues or the circulation. In this regard, pulpal infections may cause cellulitis, are the most common source of infecting microorganisms in Ludwig's angina (15), and have been implicated in cavernous sinus thrombosis, brain abscesses, mediastinitis, and osteomyelitis (7,14). Oral bacteria are also a primary source of infections in transplant patients (13) and in immunodeficient and immunosuppressed individuals (22).…”

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confidence: 99%

B-Cell Deficiency Predisposes Mice to Disseminating Anaerobic Infections: Protection by Passive Antibody Transfer

Hou¹,

Sasakj²,

Stashenko³

2000

Infect Immun

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We have previously demonstrated that a high proportion of RAG-2 SCID knockout mice, which lack T and B cells, develop orofacial abscesses and disseminated infections following pulpal infection, whereas immunocompetent control mice do not. In the present study, we sought to identify the components of the adaptive immune response which contribute to protection against disseminating anaerobic infections and sepsis. For this purpose, various genetically engineered immunodeficient mice were employed, including RAG-2 SCID, Igh-6 (B-cell deficient), Tcrb Tcrd (T-cell deficient) and Hc 0 (C5 deficient). For abscess induction, the mandibular first molars were subjected to pulp exposure on day 0. Teeth were infected with a mixture of four anaerobic pathogens, including Prevotella intermedia, Streptococcus intermedius, Fusobacterium nucleatum, and Peptostreptococcus micros, and teeth were sealed to prevent communication with the oral cavity. The findings demonstrate that both RAG-2 SCID and B-cell-deficient mice, but not T-cell-or C5-deficient mice, have increased susceptibility to the development of disseminating anaerobic infections. Abscess-susceptible RAG-2 SCID and B-cell-deficient mice also showed a significant loss of body weight, splenomegaly, and absent antibacterial antibody production. Furthermore, dissemination was significantly reduced, from 74 to 25%, in susceptible RAG-2 mice by passively transferred antibody, predominantly immunoglobulin G2b (IgG2b) and IgM, against the infecting bacterial innoculum. Fractionated IgG-enriched preparations were more efficient in transferring protection than IgM preparations. We conclude that an antibody-mediated mechanism(s), most likely bacterial opsonization, is of importance in localizing anaerobic root canal infections and in preventing their systemic spread.Bacterial infection of the dental pulp occurs as a consequence of caries, trauma, and operative dental procedures. These infections are mixed and anaerobic in nature, and are associated with high morbidity and mortality if bacterial dissemination occurs from the root canal into the tissues or the circulation. In this regard, pulpal infections may cause cellulitis, are the most common source of infecting microorganisms in Ludwig's angina (15), and have been implicated in cavernous sinus thrombosis, brain abscesses, mediastinitis, and osteomyelitis (7,14). Oral bacteria are also a primary source of infections in transplant patients (13) and in immunodeficient and immunosuppressed individuals (22).Pulpal infections induce local immune responses in the periapical region surrounding the root of the tooth. This response consists of a typical mixed inflammatory infiltrate and is composed of T cells, B cells, plasma cells, macrophages, and neutrophils (21,23,31,32). However, it is unknown which of these responses protect the host against bacterial egress and dissemination. In previous studies, we developed a model of induced pulpal infection in RAG-2 severe combined immunodeficient (SCID) mice (34). RAG-2 SCID mice were foun...

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confidence: 99%

B-Cell Deficiency Predisposes Mice to Disseminating Anaerobic Infections: Protection by Passive Antibody Transfer

Hou¹,

Sasakj²,

Stashenko³

2000

Infect Immun

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“…The brain is remarkably resistant to bacterial and fungal infection, due in part to the brain's abundant blood supply and the relatively impermeable blood-brain barrier [1]. Although rare, BAs are still challenging conditions because the mortality rate is quite high (36-90 %) [1][2][3][4]. A study of 400 patients with BA found that the most common cause of this lesion was ear infection.…”

Section: Discussionmentioning

confidence: 99%

“…Brain abscesses (BAs) are rare, but can be life-threatening with an incidence of 1 per 100,000 persons and a mortality rate between 36 and 90 % [1][2][3][4]. Half of all BAs arise from a contiguous source of infection, such as the middle ear, paranasal sinuses, mastoids, oropharynx, or teeth [1].…”

Section: Introductionmentioning

confidence: 99%

“…Moreover, BA may arise in patients with a history of major systemic or lung infection, or congenital cyanotic heart disease, although the origin of infection is not apparent in 10-20 % of patients [1,5]. The incidence of BAs caused by oral infection or dental treatment procedures is low, due to the function of blood-brain barrier [1][2][3][4][5]. The origin of BAs is usually determined by the presence of acute infectious lesions or definite abscess formation.…”

Section: Introductionmentioning

confidence: 99%

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Use of FDG-PET to detect a chronic odontogenic infection as a possible source of the brain abscess

et al. 2015

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This study describes the use of (18)F-fluoro-2-deoxyglucose positron emission tomography (FDG-PET) to detect a chronic odontogenic infection as the possible origin of a brain abscess (BA). A 74-year-old man with esophageal carcinoma was referred to our department to determine the origin of a BA in his oral cavity. He had no acute odontogenic infections. The BA was drained, and bacteria of the Staphylococcus milleri group were detected. Whole body FDG-PET revealed that the only sites of definite uptake of FDG were the esophageal carcinoma and the left upper maxillary region (SUVmax: 4.5). These findings suggested that the BA may have originated from a chronic periodontal infection. Six teeth with progressive chronic periodontal disease were extracted to remove the possible source of BA. These findings excluded the possibility of direct spread of bacteria from the odontogenic infectious lesion to the intracranial cavity. After extraction, there was no relapse of BA.

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“…It usually occurs after cranial trauma or surgery, or secondary to a 'septic' focus elsewhere, spread either by direct extension or haematologically (Corson et al, 2001). Initially, it was resistant to antimicrobial chemotherapy, having been one of the rare bacterial infections where morbidity and mortality rates remained almost unaffected by the improvements in antimicrobial therapy until the late 1960s (Hollin et al, 1967). Recently, the advances in neuro-scanning techniques such as CT and MRI, as well as the introduction of more effective antibiotics, have reduced the mortality rate to 0-24% (Matheison and Johnson, 1997).…”

Section: Introductionmentioning

confidence: 99%