Bacteraemia following periodontal procedures

Kinane, D. F.; Riggio, Marcello P.; Walker, Keith F.; MacKenzie, Duncan; Shearer, Barbara

doi:10.1308/135576105774342974

Cited by 73 publications

(157 citation statements)

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“…7,[40][41][42][43][44][45][46][47] When the tip of the ultrasonic scaler is inserted between the tooth and gingiva, the junctional epithelium and periodontal ligaments are ruptured; bacteria in the sulcus may enter the bloodstream, causing transient bacteremia. Prophylactic management is now indicated for patients who are at risk before such dental procedures.…”

Section: Discussionmentioning

confidence: 99%

“…However, it has been known that bacteremia frequently occurs after professional periodontal treatment procedures such as scaling and root planing. [5][6][7] Previous study has revealed that diode laser treatment might be able to reduce the occurrence of bacteremia associated with ultrasonic scaling. 8 In addition, dental lasers of various wavelengths have been used for the treatment of chronic periodontitis, either as the sole instrument of choice or in an adjunctive capacity to traditional therapy.…”

Section: Introductionmentioning

confidence: 99%

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Morphological Alterations of Periodontal Pocket Epithelium Following Nd:YAG Laser Irradiation

Ting

Fukuda

Watanabe

et al. 2014

Photomedicine and Laser Surgery

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Morphological Alterations of Periodontal Pocket Epithelium Following Nd:YAG Laser Irradiation

Ting

Fukuda

Watanabe

et al. 2014

Photomedicine and Laser Surgery

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show abstract

“…However, 13-23% of humans with periodontal disease develop bacteraemia following periodontal treatment. Even more significantly, nearly 7% of humans with periodontal disease are reportedly affected by a continuous low-level bacteraemia on a daily basis (Kinane et al 2005). However, the prevalence of systemic disease related to this bacteraemia is extremely low.…”

Section: Discussionmentioning

confidence: 99%

“…Systemic complications following equine cheek tooth extraction have been infrequently described, including a small number of cases of exodontia-related bacterial meningioencephalitis (Smith et al 2004;Bach et al 2014). This is surprising, as dental manipulation can lead to bacteraemia in many species, including horses (Nieves et al 1997;Kinane et al 2005;Bienert-Zeit et al 2015). Infections at distant sites related to the spread of dental pathogens have been well described in humans and in small animals (Tou et al 2005;Westermeyer et al 2013).…”

Section: Introductionmentioning

confidence: 99%

Head and neck abscessation and thrombophlebitis following cheek tooth extraction in a pony

Horbal

Reardon

Froydenlund

et al. 2018

Equine Veterinary Education

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Summary Due to their long hypsodont reserve crowns, extraction of equid cheek teeth can be difficult and result in more complications than the extraction of their shorter brachydont counterparts although the more recent resumption of oral extraction has greatly reduced such complications. The more common post‐extraction sequelae in equids include non‐healing alveoli due to retained dental or alveolar sequestrae which may lead to oromaxillary or oronasal fistula formation, chronic external sinus tract formation or osteomyelitis of the supporting bones. Collateral damage to adjacent teeth has also occasionally been reported during dental repulsion. Systemic complications following equine cheek tooth extraction have been infrequently described, including a small number of cases of exodontia‐related bacterial meningioencephalitis. This is surprising, as dental manipulation can lead to bacteraemia in many species, including horses. Infections at distant sites related to the spread of dental pathogens have been well described in humans and in small animals. This report describes deep abscessation of the masseter muscles followed by extensive thrombophlebitis of the jugular, facial and rostral cervical veins following oral cheek tooth extraction in a pony affected by pituitary pars intermedia dysfunction (PPID) that was successfully treated by abscess drainage and thrombectomy of the affected veins.

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“…Transient bacteremia, which may occur daily, is a common feature that may contribute to the cumulative exposure of the vascular system to oral microorganisms. 92,93 Therefore, it is not surprising that oral bacteria have been found in atherothrombotic plaques and AAA. [94][95][96] Massberg et al 97 reported the reciprocal coupling of coagulation and innate immunity in order to trap and kill bacteria.…”

Section: Relation To Weak Pathogen Contaminationmentioning

confidence: 99%

From intraplaque haemorrhages to plaque vulnerability

Michel

Delbosc

Ho‐Tin‐Noé

et al. 2012

Journal of Cardiovascular Medicine

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Intraplaque hemorrhages are mainly related to inward neoangiogenesis, initiated from the adventitia by lipid-dependent outwardly convected signals, and by the immaturity of these neovessels, allowing leaks and hemorrhages. Repeated intraplaque hemorrhages play a major role in the evolution of thrombotic occlusive disease, similar to the role of intraluminal thrombus in the progression of abdominal aortic aneurysm toward rupture. Red blood cells (RBCs) are an important source of unesterified cholesterol, because their membranes are particularly cholesterol rich. This unesterified cholesterol is rapidly organized in cholesterol crystals, highly toxic for cell and membranes. Oxidized cholesterol and LDL provoke the irreversible covalent aggregation of proteins, including hemoglobin, forming ceroids, which are also highly toxic. Hemoglobin play a major role of prooxydant molecules in this context, by its ability to release heme and iron, the main catalyser of oxidative reaction. In the context of type 2 diabetes, the oxidative potential of intraplaque-free hemoglobin play a predominant role in the progression of atherothrombotic disease toward clinical expression. Associated to RBC, intraplaque hemorrhages convey leukocyte, mainly neutrophils in human, and plasma zymogen that are the main source of proteases, including coagulation proteases, activation of the fibrinolytique system, release of leukocyte serine proteases and cathepsins and activation of MMPs. These proteases concentrate in the hemorrhagic/necrotic core rendered plaque highly vulnerable. An adaptive immune response takes place in the adventitia, in regard of hemorrhagic plaques, in relation to outwardly convected oxidized or proteolyzed neoantigens, and chemokinic signals. Finally, intraplaque hemorrhages and thrombi are the site of weak pathogen entrapment, which promote all these oxydative and proteolytic phenomenons.

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Bacteraemia following periodontal procedures

Cited by 73 publications

References 0 publications

Morphological Alterations of Periodontal Pocket Epithelium Following Nd:YAG Laser Irradiation

Morphological Alterations of Periodontal Pocket Epithelium Following Nd:YAG Laser Irradiation

Head and neck abscessation and thrombophlebitis following cheek tooth extraction in a pony

From intraplaque haemorrhages to plaque vulnerability

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