An unexpected death associated with an acute dentoalveolar abscess—report of a case[a/t]

Currie, W.J.R.; Ho, Valerie Wai-Yee

doi:10.1016/0266-4356(93)90063-3

Cited by 30 publications

(23 citation statements)

References 4 publications

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“…However, our finding that gingipain Rs can also readily induce blood coagulation suggest the possibility of bacterial proteinase-induced DIC coagulation in sepsis. It has been reported that a patient with an acute dentoalveolar abscess developed septicemia of Bacteroides melaninogenicus, a bacterium similar to P. gingivalis, and died with DIC (53). The fact that no plasma proteinase inhibitor effectively inactivates gingipain Rs (data not shown) supports this possibility.…”

Section: Discussionsupporting

confidence: 67%

Activation of Blood Coagulation Factor X by Arginine-specific Cysteine Proteinases (Gingipain-Rs) from Porphyromonas gingivalis

Imamura¹,

Potempa²,

Tanase³

et al. 1997

Journal of Biological Chemistry

107

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The effect of two arginine-specific cysteine proteinases (gingipain Rs) from Porphyromonas gingivalis, a causative bacterium of adult periodontitis, on human blood coagulation was investigated. Activated partial thromboplastin time and prothrombin time were shortened by these proteinases, with a 95-kDa gingipain R containing adhesin domains being 5-fold more efficient in comparison to a 50-kDa gingipain R containing the catalytic domain alone. The 50-kDa enzyme reduced each coagulation time in several plasmas deficient in various coagulation factors, while it was ineffective in factor X-deficient plasma unless reconstituted with this protein. Each proteinase activated factor X in a doseand time-dependent manner, with Michaelis constants (K m ) being found to be lower than the normal plasma factor X concentration, strongly suggesting that factor X activation by gingipain Rs, especially the 95-kDa form which is strongly activated by phospholipids, could occur in plasma. This is the first report of factor X activation by bacterial proteinases and indicates that the gingipain Rs could be responsible for the production of thrombin and, indirectly, with the generation of prostaglandins, interleukin-1, etc., which have been found to be associated with the development of periodontitis induced by P. gingivalis infections. Furthermore, the data support the hypothesis that induction of blood coagulation by bacterial proteinases may be a causative agent in the pathogenesis of disseminated intravascular coagulation in sepsis.Periodontitis is an infectious disease associated with a loss of connective tissue, resorption of alveolar bone, and formation of periodontal pockets. It is the most common cause of tooth loss in adults, primarily because of the declining incidence of dental caries in the general population (1, 2). Although the pathogenesis of periodontitis is not completely understood, prostaglandins (3, 4) and interleukin-1 (5, 6), which increase in gingival crevicular fluid in periodontal pockets, are considered to be predominant factors in the tissue destruction process associated with this disease. However, the mechanism of the production of these inflammatory mediators is still unclear.Thrombin, which is primarily associated with the cleavage of fibrinogen to generate fibrin clots (7-11), is a key proteinase in the blood coagulation system. However, besides its central role in hemostasis, this proteinase is also a potent stimulator of prostaglandin synthesis in osteoblasts (12), with in vitro bone resorption appearing to be dependent, at least in part, on thrombin-stimulated prostaglandin synthesis (13,14). In addition, thrombin also potentiates lipopolysaccharide-stimulated interleukin-1 production by macrophages (15). These facts suggest that thrombin may play a major role in the development of periodontitis by indirectly causing tissue breakdown including alveolar bone resorption. However, whether thrombin is produced at periodontitis sites is still unknown.A close relationship between Porphyromonas gingivalis (...

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Section: Discussionsupporting

confidence: 67%

Activation of Blood Coagulation Factor X by Arginine-specific Cysteine Proteinases (Gingipain-Rs) from Porphyromonas gingivalis

Imamura¹,

Potempa²,

Tanase³

et al. 1997

Journal of Biological Chemistry

107

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“…They may also spread into the cavernous cavity causing thrombosis of the area. Systemic spread of infections from oro-facial regions resulting in disseminated intravascular coagulation (DIVC) and septic shock had also been reported (2).…”

Section: Introductionmentioning

confidence: 99%

Clinical Patterns Of Oro-facial Infections

Rahman

Hamimah

Bunyarit

2005

ADUM

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were included in this retrospective study. The list of patients were taken from record of patients attendance. The patients' case notes were retrieved and reviewed using specially designed proforma. The data on patients' demography, clinical presentation, source and site of infection and treatment were collected. Patients with inadequate information and unavailable case notes were excluded from this study. RESULTSA total of 409 patients were included in this study. There were 258 (63.1%) males and 151 (36.9%) females. The male to female ratio was 1.7:1.The incidence of oro-facial infections was highest in the 20-29 year age-group. This age group accounted for about 33% of the total cases. This was followed by the 30-39 year age group, which accounted for 20.1% of total cases ( ABSTRACTThe aim of this retrospective study was to study the clinical patterns of oro-facial infections presented and their management (or trends of management) at the Department of Oral and Maxillofacial Surgery, Dental Faculty, University of Malaya. These included the predisposing factors, presentations and management. This study reviewed the oro-facial infection cases over 15 years. The data was obtained from case note reviews of patients using specially designed proforma. A total number of 409 samples were included in this study. Majority of the patients were generally healthy with about 6.6% having diabetes mellitus. The common presentations were pain (47.4%), pus discharges (16.9%) and limitation of mouth opening (12.5%). The major site was in the submandibular region (18.9%) followed by cheek (13.2%). Most of the infections were from odontogenic source (63.2%). Other sources includes cysts (15.4%) and tumours (6.7%). Incision and drainage were the treatment of choice performed on 57.55% of patients. Monoantimicrobial therapy was the treatment instituted in 20.8% of cases.

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“…3 Progression to Ludwig's angina increases the risk of mortality. With routine use of intravenous antimicrobial therapy as an adjunct to surgical incision and drainage the mortality associated with Ludwig's angina is now less than 10%.…”

Section: Discussionmentioning

confidence: 99%