Case Report: septic arthritis of the temporomandibular joint in a neonate

Septic arthritis of the temporomandibular joint (TMJ) is rare and can lead to ankylosis and destruction of the joint. It is usually related to an obvious source of infection, and is often caused by the pathogen Staphylococcus aureus. Prompt treatment results in normal growth and development of the TMJ. In this case report we describe the presentation of a 5 week old neonate with septic arthritis of the knee and TMJ, thought to be related to an infected umbilicus.     

化脓性颞下颌关节炎的特征与诊断

目的探讨化脓性颞下颌关节炎的临床特征及其早期诊断方法。方法收集我科近5年的30例化脓性颞下颌关节炎患者,对其临床症状,关节液的性质和量,关节液的组织学和细菌学表现,影像学检查,其它实验室检查及后遗症进行分析。结果患者主要为成年人(>18岁占29/30);血源性感染多见;多数(25/30)局部症状轻,全身反应不明显;关节液组织学检查见大量粒细胞,可伴纤维蛋白或纤维软骨碎片;15/30患者关节液细菌学检查见到细菌,培养出的病原菌主要为金黄色葡萄球菌和腐生葡萄球菌;后遗症轻,主要为继发性骨关节病。结论当今化脓性颞下颌关节炎表现出感染源隐匿性、症状不典型性、后遗症轻等特点;关节腔穿刺和关节液分析是其必要的诊断手段。     

Acute suppurative arthritis of the temporomandibular joint in a patient with rheumatoid arthritis

Septic arthritis of the temporomandibular joint is a rare condition. A case of acute staphylococcal suppurative arthritis of the temporomandibular joint (TMJ) complicating rheumatoid arthritis (RA) in a 53 year old woman is reported. The aetiology of septic arthritis may be traced to several predisposing factors and many specific agents. It would appear that the case presented is the result of predisposition of patients known to have RA to the complication septic arthritis. Some treatment recommendations are given.     

Diagnosis of bone and joint infections

Bone and joint infections are common worldwide and cause considerable morbidity for the patient. Despite recent advances, they are difficult and expensive to treat. Regardless of the infection type (septic arthritis, osteomyelitis, fracture-related infections, or periprosthetic joint infection), patients may suffer from chronic ill health, multiple revision surgeries and prolonged hospital stay. An accurate diagnosis is the first step for successful treatment and infection control. However, due to the lack of a single test providing 100% accuracy, interdisciplinary teamwork is needed to diagnose bone and joint infections more precisely. Nevertheless, the diagnosis remains very challenging, especially in infections caused by low virulence organisms. This review will describe the diagnostic methods for septic arthritis, osteomyelitis, fracture-related infections and periprosthetic joint infections in current use in clinical practice.     

Molecular mechanisms of Staphylococcus aureus nasopharyngeal colonization

Staphylococcus aureus is responsible for a wide range of different infections ranging in severity from mild to fatal. However, it primarily exists as a commensal organism in a number of different anatomical sites including the nasopharynx. Although colonization itself is a harmless state, colonized individuals are at risk of endogenous infection when S. aureus enters otherwise sterile sites via wounds or indwelling medical devices. As such, studies of colonization may identify important targets for vaccines or other prophylactic approaches. Colonization is a dynamic process; S. aureus must attach to host surfaces, overcome immune components and compete with other commensal microbes. This occurs via a number of surface-attached and secreted proteins and other factors such as wall teichoic acid. In addition, colonizing S. aureus must constantly replicate to maintain its niche and exclude other strains. These myriad interactions provide a strong selective pressure for the maintenance or enhancement of mechanisms of adhesion, invasion and immune evasion. The evolutionary implications of this may explain why S. aureus is such a capable pathogen because many of the proteins involved in colonization have also been identified as virulence factors. This review describes the diverse molecular mechanisms used by S. aureus to colonize the host and discusses how the pressures that have selected for these may have led to its virulence.     

巨噬细胞功能和炎症消退机制及与牙周炎关系研究进展

巨噬细胞是人体固有免疫系统中重要的组成部分,具有强大的识别、吞噬、清除细菌及外来异物的功能。牙周炎是一种以牙龈炎症和牙槽骨丧失为特征的慢性感染性疾病,是成年人失牙的主要病因。目前已经明确,牙周炎的组织破坏是由宿主对感染的免疫应答引起的,巨噬细胞作为宿主免疫应答的重要组成部分,在炎症的发生发展中起重要作用。近年研究显示,巨噬细胞在炎症消退过程中亦扮演着重要作用。本文就巨噬细胞在炎症的发生、发展及消退中的作用进行综述,并总结了其在牙周炎发展及治疗中可能的作用。     

Factors affecting susceptibility of Staphylococcus aureus to antibacterial agents

Staphylococcus aureus is a major human pathogen that causes suppurative diseases, toxic shock syndrome, pneumonia, food poisoning, and staphylococcal scalded skin syndrome (SSSS). S. aureus can also cause osteomyelitis and radicular cysts that impact dental health. β-lactam antibiotics are frequently used for the treatment of S. aureus infections, but the emergence of methicillin-resistant S. aureus (MRSA) has caused serious problems for the antibiotic treatment of S. aureus infections. PBP2′ has a low affinity for methicillin antibiotics and is one of the factors responsible for resistance to these antibiotics. However, clinical MRSA isolates show various levels of resistance to methicillin that are not determined by the amount of PBP2′, indicating that other factors are also involved. Furthermore, while vancomycin is very effective against MRSA, vancomycin-resistant and vancomycin-intermediate S. aureus have recently been reported. Many studies have been undertaken to better understand methicillin and vancomycin resistance mechanisms through identification of the factors affecting susceptibility to β-lactams. We recently demonstrated that MRSA showed resistance to antimicrobial peptides produced by humans that are a component of the innate immune system, in addition to various antibiotics.     

The formation of immune complexes is involved in the acute phase of periodontal destruction in rats

Kuramoto A, Yoshinaga Y, Kaneko T, Ukai T, Shiraishi C, Oshino K, Ichimura I, Hara Y. The formation of immune complexes is involved in the acute phase of periodontal destruction in rats. J Periodont Res 2012; 47: 455–462. © 2012 John Wiley & Sons A/S Background and Objective: Loss of clinical attachment and alveolar bone destruction are major symptoms of periodontitis, caused by not only the destructive effect of periodontopathic bacteria but also the overactive response of the host immune system against periodontal pathogens. The details of the participation of the immune system in the onset and progression of periodontitis are unclear. In this study, we attempted to determine whether the host immune system, and in particular the formation of immune complexes, is involved in the periodontal destruction. Material and Methods: We applied ovalbumin or lipopolysaccharide (LPS) as antigens and their specific immunoglobulin G (IgG) antibodies purified from rat serum to rat gingival sulcus alternately. Loss of attachment, alveolar bone destruction and the numbers of inflammatory cells infiltrating the periodontal tissue and osteoclasts on the alveolar bone surface were investigated histometrically. The formation of immune complex was confirmed by immunohistological staining of complement C1qB. Results: Loss of attachment and the presence of C1qB were observed histopathologically in both experimental groups. The group that had been treated with LPS and anti‐LPS IgG showed greater loss of attachment. The number of inflammatory cells in the periodontal tissue was increased in both experimental groups, while osteoclasts at the alveolar bone crest were observed only in the group that had been treated with LPS and anti‐LPS IgG. Conclusion: In the present study, we showed that the formation of immune complex appears to be involved in the acute phase of periodontal destruction and that the biological activity of antigens is also important.     

化脓性颞下颌关节炎病原菌的分离培养和鉴定

目的 分离、培养和保存化脓性颞下颌关节炎的病原菌，了解其种类，探索合适的培养条件。方法 对近5a就诊的30例化脓性颞下颌关节炎患者，抽取关节液，进行涂片、革兰染色，分别采用血琼脂培养基、室温保存菌种培养基、乳酪消化大豆胨琼脂(TSA)和乳酪消化大豆胨肉汤(TSB)等4种培养基在需氧和厌氧条件下进行细菌培养，并对培养出的细菌进行生化鉴定。结果 关节液涂片细菌检出率为50％(15／30)，细菌培养阳性率为17％(5／30)，培养出的病原菌主要为腐生葡萄球菌和金黄色葡萄球菌，所用的培养基以TSB为佳。结论 作者成功地分离出2种病原菌，其中腐生葡萄球菌为首次发现，但检出率较低，尚需进一步完善培养技术。     

Neutrophil-mediated host response to Porphyromonas gingivalis

Periodontal diseases are infections initiated by specific species of microorganisms and are among the most common human infections. The pathogenesis of periodontitis is mediated by interactions between host and microbial factors, complicated by genetic and environmental risk factors. Periodontal disease also represents a unique model in which to study the roles of bacterial and host-related factors, a model in which patients do not suffer from life-threatening disease. The aim of this paper is to focus on recent findings relating to neutrophil-mediated host response mechanisms in Porphyromonas gingivalis-induced periodontal disease. Virulence factors of Porphyromonas gingivalis such as the gingipains, fimbrillin peptides, capsule polysaccharides, lipopolysaccharides, haemagglutinating and haemolysing activities, toxic products of metabolism, outer membrane vesicles, and other enzymes have important roles in eliciting host responses in various ways. These factors significantly affect epithelial/endothelial cells, but their major effect is observed on the modulation of neutrophil response. Periodontitis represents an important model for neutrophil-mediated host tissue injury. In this model, neutrophils, primed or stimulated by the presence or persistence of infection, express an elevated and excessive response. This, in turn, leads to tissue destruction mediated by neutrophil activity. It is essential to understand the mechanisms underlying the interactions between the neutrophils and the microbial virulence factors to be able to develop rational, novel treatment strategies.     

Clindamycin in dentistry: more than just effective prophylaxis for endocarditis?

Clindamycin is a broad-spectrum antibiotic with activity against aerobic, anaerobic, and beta-lactamase-producing pathogens. This antibiotic has been used for many years as prophylactic treatment during dental procedures to prevent endocarditis. However, the spectrum and susceptibility of the bacteria species involved in dental infections indicate that clindamycin would also be an effective treatment option for these conditions. In addition to its antiinfective properties, clindamycin has high oral absorption, significant tissue penetration, including penetration into bone, and stimulatory effects on the host immune system. This review discusses the microbiologic and clinical evidence supporting the efficacy and safety of clindamycin for the successful management of dental infections.     

Septic arthritis of the temporomandibular joint successfully treated with arthroscopic lysis and lavage: case report and review of the literature

Septic arthritis of the temporomandibular joint (TMJ) is infrequently reported. We present a case of septic arthritis of the TMJ following the extraction of the left upper second molar that occurred 1 week before beginning of symptoms. No evident predisposing factors were detected. Arthroscopic diagnosis of septic arthritis, lysis and lavage, and capsular stretch were performed. Cultures taken from the TMJ space grew Streptococcus sp. After 1 month of antimicrobial therapy the patient was asymptomatic and mandibular function was normal. Literature related to septic arthritis of TMJ and its treatment was reviewed. Different surgical procedures are available to treat this condition. Arthroscopy should be preferred as initial treatment on account of the possibility of drainage and accurate lavage under direct visualization of joint space, at the same time allowing confirmation of diagnostic hypotheses. Improving joint mobility with lysis of adhesions and capsular stretch in an early stage of disease may be helpful in stopping the fibrosis process.     

Microbiological, pathological, inflammatory, immunological and molecular biological aspects of periradicular disease

Multimicrobial infection of the dental pulp triggers inflammatory responses and ultimately causes bone destruction in the periradicular tissues. Besides bacteria, noxious substances such as degraded protein components and cholesterol could also act as antigens and elicit a host response, which can be harmful to periradicular tissues. Histologically, a dense infiltration of immunocompetent cells is seen in periradicular lesions and their host reactions may induce bone resorption. Polymorphonuclear leucocytes (PMN) and macrophages migrate to the periapical lesions and phagocytose pathogens as a first line of defence. Dead PMN are quickly phagocytosed by macrophages and this disposal system plays a role in maintaining chronicity of the lesions. The pathological roles of periradicular T cells have been assessed through analysing phenotypic markers of cell types, especially CD antigens, but the results are still controversial. Recently, technical developments in immunology and molecular biology have made it possible to investigate the pathogenesis of many diseases at molecular level. The investigation of functional analysis of the immune cells and their regulatory molecules such as apoptosis-associated molecules and adhesion molecules, will lead to a better understanding of the pathogenesis of periradicular lesions. The role of inflammatory mediators including antibodies, cytokines, matrix metalloproteinases, growth factors and arachidonic metabolism is becoming known for these lesions. Knowledge from these investigations improve the understanding of the pathological mechanisms of periradicular infections.     

(i) Irritable hip and septic arthritis of the hip

Transient synovitis needs to be differentiated from septic arthritis of the hip when a child presents with features of an irritable hip. Although there is considerable overlap in the clinical presentation of the two conditions, the natural history, treatment strategy and potential range of outcomes are quite distinct. While transient synovitis is a self limiting condition, emergent surgical intervention in the form of arthrotomy and wash out of joint is the mainstay of treatment of septic arthritis. Clinical decision algorithms have been developed using a combination of clinical and laboratory parameters to help differentiate the two conditions.     

Staphopains in Staphylococcus aureus bacteremia: Virulence activities related to the onset of septic shock,coagulation disorders,and infectious endocarditis

BackgroundStaphylococcus aureus is an important oral bacterium that enters the bloodstream following dental procedures, causing bacteremia. Infectious endocarditis occurs due to the invasion of blood-borne pathogens into the endocardium. S. aureus is the most frequently isolated bacterium in Gram-positive sepsis, and shock and coagulation disorders are common and potentially fatal consequences of sepsis. Staphopains are the most abundant proteases among extracellular proteolytic enzymes produced by staphylococci, and their virulence activities related to the pathophysiology of S. aureus bacteremia have been elucidated.HighlightStaphopain A (ScpA)—not staphopain B (SspB)—releases bradykinin, and the two staphopains synergistically release a novel kinin, Leu-Met-Lys-bradykinin, directly from human plasma kininogens. These kinins cause vascular leakage. ScpA, similar to the two kinins, lowers blood pressure in guinea pigs in a bradykinin B₂-receptor-dependent manner when administered intra-arterially, and produces septic shock symptoms in them. Kinin generation from human plasma by ScpA is enhanced in the presence of SspB, strongly suggesting a shock induction by the bacterial proteases. Staphopains, SspB being threefold more potent than ScpA, truncate fibrinogen by preferentially cleaving this coagulation factor at the C-terminal region of the Aα chain, which results in loss of fibrinogen clottability, thereby causing bleeding tendency. Staphopains showed a degradation activity for type I collagen similar to that observed in ScpA-mediated skin destruction, indicating that they participate in S. aureus-induced endocardium destruction.ConclusionStaphopains are potent virulence factors and are potentially involved in the onset of septic shock, coagulation disorders, and infectious endocarditis that occurs in S. aureus bacteremia.     

骨免疫在口腔疾病中的作用研究进展

长期以来的研究表明先天免疫和后天免疫在宿主抵御外来微生物入侵的过程中起着至关重要的作用，而在这过程中也会同时造成宿主自身的组织或器官的损害。骨骼系统就是其中之一，在一些诸如类风湿性关节炎、牙周炎等疾病中，免疫系统的反应不仅起到去除外来致病菌的作用，还会同时造成骨骼系统的破坏。长期以来大部分的研究都致力于了解免疫系统对骨组织破坏的机制，而近些年来有研究开始探究骨反作用于免疫系统，由此衍生出了一个全新的研究领域——骨免疫。文章从骨免疫的机制、免疫与骨吸收作用通路以及在口腔相关疾病的作用机制等方面总结了近些年来相关的研究进展。     

树突状细胞在牙髓或牙周组织中的作用机制

牙髓或牙周的急、慢性炎症是由宿主对病原体发生的免疫反应造成的，明确机体抵御病原微生物的免疫机制对弄清牙髓或牙周病的发病机制十分重要。已经知道在牙髓或牙周系统中存在各种炎性和免疫细胞。在这些细胞中，树突状细胞作为专职的抗原呈递细胞，在诱导免疫反应中扮演着不可缺少的角色。树突状细胞捕捉和搬运来自外界的信息给获得性免疫系统的细胞，所以树突状细胞架起了先天性免疫和获得性免疫之间的桥梁。最近，很多研究集中在树突状细胞怎样调控牙髓或牙周病的免疫应答，从而为疾病的治愈和发展可行的免疫治疗提供依据。     

Tissue destruction in periodontitis: bacteria or cytokines fault?

The pathogenesis of periodontal disease involves the sequential activation of a great variety of components of the host immune response, primarily acting to defend periodontal tissues against bacterial aggression, but also functioning as mediators of tissue destruction. The expression of the disease results from the interaction of host, microbiological agents, and environmental factors. Leukocytes play a critical role in the pathogenesis of the disease, producing different cytokines, chemokines, and other mediators, thus generating a host defense response, as well as inducing tissue inflammation and bone destruction. The aim of this review is to address the role of some inflammatory mediators in response to bacterial aggression in periodontitis.     

Role of chronic stress and depression in periodontal diseases

An extensive body of experimental and clinical evidence documents the negative impact of chronic psychological stress and depression on the immune system and health. Chronic stress and depression can result in general dysregulation of the immune system, of both cellular and humoral pathways, which may contribute to pathogenic infection and concomitant periodontal tissue destruction. In general, the evidence is consistent with the hypothesis that stress can modify the host defense and progression of periodontal infections in patients susceptible to periodontitis. However, substantial evidence also indicates that these conditions can mediate risk for disease, including periodontitis, through changes in health‐related behaviors, such as oral hygiene, smoking and diet. The unequivocal interpretation of studies has also been hampered, in part, by issues related to conceptualization of stress and depression, as well as commonly associated comorbidities, such as diabetes, that can modify the onset and progression of periodontal disease. In addition, stress and depression appear to fall into a spectrum, ranging from mild to severe, involving a complex interaction of genetic background, coping strategies and environment. Differences in the conceptualization of stress and depression are probably important in assessing associations with other biologic and clinical measures. Future studies are necessary to clarify the complex interactions of chronic stress and depression in periodontal diseases.