[Analysis of related factors affecting treatment results in 126 patients with oral and maxillofacial space infection].

PURPOSE: This study was aimed to retrospectively investigate the related factors of oral and maxillofacial space infection in 126 patients. METHODS: The clinical data of 126 patients with oral and maxillofacial space infection were collected from the Department of Oral and Maxillofacial Surgery, The First Affiliated Hospital of Xinjiang Medical University during the period of 2015 to 2017. The clinical features (e.g. body mass index, the number of days from onset to hospital admission, and the number of inflammatory spaces, and etc.) as well as laboratory examination variables (e.g. leucocytic count, the number of neutrophilic granulocyte, interleukin-6, C reactive protein, calcitonin, blood glucose, blood lipids, albumin, and etc.). Pearson correlation method were used to analyze the correlated factors and multiple linear regression analysis was used to analyze the related factors with SPSS20.0 software package. RESULTS: Correlation analysis showed that there was a significant correlation in the hospitalization days with the ages, white blood cells, neutrophilic granulocyte, neutrophil ratio, C reactive protein, body mass index, triglyceride, high density lipoprotein, the number of inflammatory spaces. The results of multiple linear regression analysis showed that there were 4 independent variables (P<0.05), which were the number of inflammatory spaces, the number of days from onset to hospital admission, triglyceride and neutrophilic granulocyte. CONCLUSIONS: There was a positive correlation between the hospitalization days with the number of inflammatory spaces, triglyceride, inflammatory cells and cytokines in patients with oral and maxillofacial space infection. In addition, the related factors affecting the treatment results of oral and maxillofacial space infection include the number of inflammatory spaces, the number of days from onset to hospital admission, triglycerides and neutrophils.

A review of pathogenesis, diagnosis, treatment options, and differential diagnosis of odontogenic infections: a rather mundane pathology?

Odontogenic infections are common in the dental practice and their treatment should be a standard procedure for every dentist. For optimal management of septic intraoral problems, the practitioner must understand the underlying causes and etiologies of odontogenic infections. Therefore, the purpose of this article is to outline basic inflammatory processes involved in the development of odontogenic and intraoral infections including relevant pathogens, biochemical processes mediated by pro-inflammatory molecules, the basics of abscess formation, the host response, and the clinical appearance of intraoral septic processes. Furthermore, treatment modalities of odontogenic infections and associated lesions are discussed and a brief explanation of possible complications and their management is provided.

Impact of tooth loss on oral and systemic health.

Periodontitis is a primarily bacterial infection that is common in dentate individuals, while denture stomatitis is a predominantly fungal infection that is common among denture wearers. Both infections may increase a patient's risk for chronic systemic infection dissemination, and may in turn increase the risk of chronic, inflammatory-based systemic diseases. Systemic diseases for which chronic oral infections are believed to confer attributable risk include atherosclerotic and coronary disease, stroke, chronic obstructive pulmonary disease, diabetes, and hypertension. It appears that invasive oral pathogens trigger a systemic inflammatory response via mediators released by the cardiovascular system and liver, putting the patient at increased risk for these diseases. Data comparing gene expression between denture wearers with and without denture stomatitis (and associated Candida albicans infections) has demonstrated unique up- and down-regulation patterns for a number of genes. It appears that down-regulated genes (whose functions are thereby diminished) are associated with reduced epithelial barrier integrity. By contrast, there appears to be an association between up-regulated genes (which have enhanced function) and inflammatory responses that facilitate the ability of C. albicans to bind with and penetrate the oral mucosa. Molecular biological approaches suggest that future therapeutic development could target reducing either the local inflammatory processor, the binding and attachment of C. albicans to the oral mucosa, or both. Ongoing investigations are attempting to incorporate interventions into matrices, to provide a local and sustained presence to therapeutic interventions.

Non-surgical periodontal therapy improves serum levels of C-reactive protein and edematous states in female patients with idiopathic edema.

BACKGROUND: The relationship between periodontal disease and systemic disease is revealing new and exciting associations. Idiopathic edema presents a clinical syndrome with obscure pathophysiology. The present study investigates whether non-surgical periodontal therapy is beneficial in patients who are not responding to conventional treatment of idiopathic edema. METHODS: Thirty patients with idiopathic edema were allocated to intervention and control groups. All the subjects were assessed for systemic (body weight, body mass index, visual scale of edema, serum C-reactive protein, and serum albumin) and periodontal (plaque index, calculus index, and gingival index) parameters. Non-surgical periodontal therapy, including oral hygiene instructions, scaling and root planing, and systemic antibiotic therapy, was provided in the intervention group. Both groups were reevaluated after 4 weeks. RESULTS: Both groups were comparable at baseline. All parameters, except serum albumin, showed significant improvement after periodontal therapy. The control group showed further worsening of these parameters. CONCLUSIONS: This study shows that sources for systemic inflammation, such as periodontal disease, could affect the pathogenesis of idiopathic edema. Successful elimination of such covert sources of inflammation leads to a clinical benefit in patients who are distressed by this condition.

Review: Pathogen-induced inflammation at sites distant from oral infection: bacterial persistence and induction of cell-specific innate immune inflammatory pathways.

A hallmark of infection with the gram-negative pathogen Porphyromonas gingivalis is the induction of a chronic inflammatory response. P. gingivalis induces a local chronic inflammatory response that results in oral inflammatory bone destruction, which manifests as periodontal disease. In addition to chronic inflammation at the initial site of infection, mounting evidence has accumulated supporting a role for P. gingivalis-mediated periodontal disease as a risk factor for several systemic diseases including, diabetes, preterm birth, stroke, and atherosclerotic cardiovascular disease. A growing number of in vitro studies have demonstrated that P. gingivalis infection stimulates cell activation commensurate with expected responses paralleling inflammatory atherosclerotic-type responses. Furthermore, various mouse models have been used to examine the ability of P. gingivalis to stimulate chronic inflammatory plaque accumulation and recent studies have pointed to a pivotal role for innate immune signaling via the Toll-like receptors in the chronic inflammation associated with P. gingivalis infection. In this review we discuss the pathogen and host cell specificity of these responses and discuss possible mechanisms by which this oral pathogen can induce and maintain a chronic state of inflammation at sites distant from oral infection.

The flavonoids luteolin and quercetagetin inhibit lipoteichoic acid actions on H9c2 cardiomyocytes.

Dental focal infections are infections in the mouth that cause subsequent infection and symptoms in other parts of the body. Dental conditions such as periodontitis have been associated with coronary heart disease. In this study, we investigated the effect of flavonoids on activation of mitogen-activated protein kinase (MAPK) family members, protein kinase B (AKT), and IL-1 beta expression by rat heart embryonic (H9c2) cells upon stimulation with LTA. Pretreatment with four flavonoids, including quercetin, genistein, quercetagetin, and luteolin diminished LTA-induced ERK1/2, JNK, p38, and AKT phosphorylation and IL-1 beta gene expression. Our findings indicate that flavonoids interfere with LTA signal transduction.

Too old to fight? Aging and its toll on innate immunity.

Elderly individuals display increased susceptibility to chronic inflammatory diseases and microbial infections, such as periodontitis and oral aspiration pneumonia. The resurgent interest in innate immunity in the 2000s has been accompanied by parallel studies to understand the impact of aging on the function of the innate immune system, which not only provides first-line defense but is essential for the development of adaptive immunity. This review summarizes and discusses our current understanding of age-associated molecular alterations in neutrophils and macrophages, key inflammatory phagocytes implicated in both protective and destructive host responses. The analysis of recent literature suggests that, in advanced age, phagocytes undergo significant changes in signal transduction pathways that may affect their ability to perform antimicrobial functions or regulate the inflammatory response. These abnormalities are expected to contribute to the pathology of oral infection-driven inflammatory diseases in the elderly. Moreover, the elucidation of age-associated defects in the innate immune system will facilitate the development of intervention therapeutic strategies to promote or restore innate immune function and improve the quality of health in old age.

[Diagnostic and prognostic value of determination of the endogenic intoxication and functional activity of neutrophils indices in odontogenic phlegmon].

There were studied up the peripheral blood indices in 109 patients, suffering odontogenic phlegmon (OPH), coexistant with severe and of medium severity systemic inflammatory response syndrome (SIRS). In the patients with OPH and severe SIRS (with the complicated course), the blood neutrophils indices, concerning endogenic intoxication and functional activity, differ essentially from those parameters, present in patients, suffering noncomplicated course of the disease.

[Local ocular immunity parameters in chronic rhino- or odontogenic infection].

Thirty-four patients with foci of chronic rhino- or odontogenic infection were examined. All the patients underwent physical examination, biochemical blood analysis, immunological test for immunoglobulins A, G, and M, circulating immune complexes, leukocyte migration inhibition test with phytohemagglutinin, Con A, with antigens of the retina, vitreous body, iris, and lens, scrapes from the dentogingival pocket, conjunctival and nasal cavities for Chlamydia, followed by direct immunofluorescence, polymerase chain reaction, and culture. Chronic rhino- or odontogenic infection foci impair local ocular immunity in ophthalmologically healthy patients. The foci of chronic rhinogenic infection cause more pronounced changes in systemic and local ocular immunity than those of chronic odontogenic infection. In half the patients with chronic rhino- or odontogenic infection foci, Chlamydia are detectable in the oral, nasal, and ocular mucosae, which suggests that there is generalized infection and there is a need for complex sanitation of the body. Isolated local treatment for Chlamydia infection is not promising.

[Preparation glycosaminosulphate efficacy in comprehensive treatment of patients with odontogenic phlegmon of maxillofacial region].

The results of 20 patients (with odontogenic phlegmon of maxillofacial region) treatment by glycosaminosulphate were compared with the results of patients received traditional treatment. Significant speeding-up of the blood indices normalization terms, humoral immunity factors and postoperative wound regeneration after odontogenic phlegmon of maxillofacial region lancing was determined.

Cardiovascular and oral disease interactions: what is the evidence?

This paper reviews the evidence for the interaction of oral disease (more specifically, periodontal infections) with cardiovascular disease. Cardiovascular disease is a major cause of death worldwide, with atherosclerosis as the underlying aetiology in the vast majority of cases. The importance of the role of infection and inflammation in atherosclerosis is now widely accepted, and there has been increasing awareness that immune responses are central to atherogenesis. Chronic inflammatory periodontal diseases are among the most common chronic infections, and a number of studies have shown an association between periodontal disease and an increased risk of stroke and coronary heart disease. Although it is recognised that large-scale intervention studies are required, pathogenic mechanism studies are nevertheless required so as to establish the biological rationale. In this context, a number of hypotheses have been put forward; these include common susceptibility, inflammation via increased circulating cytokines and inflammatory mediators, direct infection of the blood vessels, and the possibility of cross-reactivity or molecular mimicry between bacterial and self-antigens. In this latter hypothesis, the progression of atherosclerosis can be explained in terms of the immune response to bacterial heat shock proteins (HSPs). Because the immune system may not be able to differentiate between self-HSP and bacterial HSP, an immune response generated by the host directed at pathogenic HSP may result in an autoimmune response to similar sequences in the host. Furthermore, endothelial cells express HSPs in atherosclerosis, and cross-reactive T cells exist in the arteries and peripheral blood of patients with atherosclerosis. Each of these hypotheses is reviewed in light of current research. It is concluded that although atherosclerotic cardiovascular disease is almost certainly a multifactorial disease, there is now strong evidence that infection and inflammation are important risk factors. As the oral cavity is one potential source of infection, it is wise to try to ensure that any oral disease is minimised. This may be of significant benefit to cardiovascular health and enables members of the oral health team to contribute to their patients' general health.

[Periodontitis and systemic disease relationships]. / Zwiazek miedzy chorobami przyzebia, a rozwojem niektórych schorzen systemowych.

Recently, it has been recognized, that oral infection especially periodontitis may affect the pathomechanism and course of a number of systemic diseases, such as: cardiovascular, cerebrovascular diseases, atheromatous peripheral vascular disease bacterial pneumonia, diabetes mellitus, osteoporosis, or cause adverse pregnancy outcome. This review will focus on the current knowledge linking periodontal infections to a set of above mentioned systemic diseases. While a number of their mutual interactions have been already identified, additional research will be required to determine with certainty, whether these associations are casual or coincidental and to evaluate disease pathogenesis and potential therapeutic interventions.

[The impact of periodontal infection on systemic inflammatory process and atherosclerosis]. / Wplyw chorób przyzebia na powstanie ogólnoustrojowej reakcji zapalnej i rozwój miazdzycy.

It is becoming increasingly clear that infections and chronic inflammatory conditions, such as periodontitis can be linked with atherosclerotic process. Periodontitis and atherosclerosis have many pathogenetic mechanisms in common. The objective of this based on current knowledge review is to present the putative mechanisms whereby periodontitis which is chronic and inflammatory in nature and initiated by microbial plaque can influence the atherosclerosis. Two main processes in particular are worthy of consideration and may provide the link between these two diseases. Induction of the chronic systemic inflammation has been proposed to be of pathogenetic relevance in the association of infection and atherosclerosis, and may rely in part on the endothelial toxicity of bacterial endotoxin and the action of proinflammatory cytokines (PGE-2, IL-1beta, TNF-alpha). Another well-founded proatherogenetic property of infectious illness may be the induction of autoimmunity and autoagression. It has been suggested that humoral immune cross-reaction of the same antibodies to heat shock proteins (HSP), both bacterial mHSP65 and human endothelial HSP60 may play an important role in the process of vascular endothelial injury. Both of these mechanisms are believed to be a key event in the pathogenesis of artheriosclerosis.

[The role of chronic dental bacterial infections in the aetiopathogenesis of ischaemic heart disease]. / Rola przewleklych bakteryjnych zakazen zkbopochodnych w etiopatogenezie choroby niedokrwiennej serca.

Chronic dental infections, even of low intensity, may cause the development of atherosclerotic changes in arteries, that lead to coronary heart disease. There are many risk factors for atherosclerosis, but the most important are endothelium function disturbances, platelets activation and oxidative changes of plasmatic lipoproteins. Among factors that can induce the epithelium lesions bacterial factor may play an important role. In consequence of the bacterial cell breakdown place the release of endotoxins takes, that lead directly to the damage of endothelial cells. Apart from this direct effect endotoxins activate the fagocytes releasing superoxide reactive radicals, that cause lesions of endothelium. Probably the most widespread chronic bacterial infections in human are the diseases of periodontium and teeth and their inflammatory complications. Oral cavity is colonized by 300-400 bacterial species. In the case of dental bacterial infections bacteriemia occurs after such procedures as tooth extraction, endodontic treatment, therapeutic and hygienic interventions on periodontal tissues. The results of many investigations show the relationship between the oral status (dental and periodontal diseases as chronic oral infections) and disorders of cardiovascular system.

[The monitoring of immunological indices in odontogenic abscesses and phlegmons and their differential diagnostic meaning]. / Monitoring immunologicheskikh pokazatelei pri odontogennykh abstsessakh i flegmonakh i ikh differentsial'no-diagnosticheskaia znachimost.

The immune homeostasis parameters have been monitored in 31 patients with odontogenic abscesses and phlegmons. Immunological values possessing differential diagnostic significance have been detected. Activation of phagocytosis, spontaneous and stimulated activity of phagocytes in parallel with a moderate decrease in the cellular functional reserve, increased immunoregulatory index, and moderate shifts in the concentrations of IgG and IgM are characteristic of odontogenic abscesses, while odontogenic phlegmons are characterized by deep depression of the phagocyte function and failure of cellular and humoral immunity. The disorders in the immune functions of patients with odontogenic phlegmons normalized 2 weeks later than in those with odontogenic abscesses. Both diseases run a wave-like course and are characterized by phasic changes in immunological parameters, which is significant for determining pathogenesis and choosing appropriate immunocorrective therapy.

[A comparative analysis of the course of odontogenic phlegmons of the face and neck area in patients from Yakutsk and Moscow]. / Sravnitel'nyi analiz techeniia odontogennykh flegmon oblasti litsa i shei u bol'nykh Iakutska i Moskvy.

A total of 126 patients with odontogenic inflammatory diseases were examined, 54 of these in Moscow and 72 in Yakutsk. The clinical and immunological parameters were assessed on days 2 and 6 after similar operations. In residents of Yakutsk the inflammatory process was associated with a more expressed intoxication and coursed 1.5 to 2 days longer than in Muscovites; moreover, the residents of Yakutsk developed higher leukocytosis and a drop of T-lymphocyte level with the predominance of T-helpers. Hence, odontogenic inflammations take mainly a hyperergic course in Yakutsk and a normergic one in Moscow.