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Apical periodontitis (AP) is an inflammatory lesion around the apex of a tooth caused by bacterial infection of the pulp canal system. AP appears radiographically as a radiolucent periapical lesion (RPL). The elective treatment for teeth with AP is root canal treatment (RCT). No study is available about the frequency of RPL and RCT in patients with inherited coagulation disorders (ICD). The aim of this study was to investigate the prevalence of RPL and RCT in patients with ICD and control subjects. In a cross-sectional study, the radiographic records of 58 patients with haemophilia A, haemophilia B or von Willebrand’s disease (study group) and 58 control subjects were examined. The frequency of RPL and RCT was assessed using digital panoramic radiographs and the Periapical Index. RPL in one or more teeth was found in 67.2% of patients with ICD and in 48.3% of control subjects (odds ratio = 2.20; P = 0.038). At least one RCT was found in 34.5% and 65.5% of subjects in the study and control groups respectively (odds ratio = 0.28; P = 0.001). Multivariate logistic regression analysis indicated that subjects with ICD had RPL with higher likelihood than control subjects (odds ratio = 7.4; P = 0.0005). Patients with ICD disorders showed a significantly higher prevalence of RPL and lower frequency of RCT than control patients.

Laser use in dentistry was suggested approximately 35 years ago as a means of using energy generated by light to remove or modify soft and hard tissues in the oral cavity. A Laser is an acronym for Light Amplification by Stimulated Emission of Radiation. The radiation involved in generating laser light is nonionizing and does not produce the same effects attributed to X-radiation. The Food and Drug Administration has approved the use of various lasers as devices to remove diseased gingival tissues and for other soft tissue applications, in the removal of dental caries, as an aid in placing tooth-colored restorations and as an adjunct in root canal procedures, such as pulpotomies. This position paper concentrates on laser use in root canal treatment.

The true age of dental composites was launched with this initial science into coupling agents. In the late 1950s and early 1960s, the word “composite” was still new to dentistry. Its predecessor, the adjective “reinforced,” dominated the dental materials nomenclature instead. In this landmark article by Bowen, the term “composite” does not even appear. Dental materials science was just beginning to deal with the extreme challenges of chemically connecting internal interfaces of things to make ceramic-polymer composites.

We thank the authors of the letters for their interest in our publication. Their comments focused on Chlamydia pneumoniae–negative finding, role of infection burden and coexistence of multiple pathogens, clinical usefulness of findings, and how the chronic oral infectionis involved in acute coronary events.

INTRODUCTION:

Clinical studies suggest a direct influence of periodontal disease (PD) on serum inflammatory markers and disease assessment of patients with established rheumatoid arthritis (RA). However, the influence of PD on arthritis development remains unclear. This investigation was undertaken to determine the contribution of chronic PD to immune activation and development of joint inflammation using the collagen-induced arthritis (CIA) model.

METHODS:

DBA1/J mice orally infected with Porphyromonas gingivalis were administered with collagen II (CII) emulsified in complete Freund’s adjuvant (CFA) or incomplete Freund’s adjuvant (IFA) to induce arthritis. Arthritis development was assessed by visual scoring of paw swelling, caliper measurement of the paws, mRNA expression, paw micro-computed tomography (micro-CT) analysis, histology, and tartrate resistant acid phosphatase for osteoclast detection (TRAP)-positive immunohistochemistry. Serum and reactivated splenocytes were evaluated for cytokine expression.

RESULTS:

Mice induced for PD and/or arthritis developed periodontal disease, shown by decreased alveolar bone and alteration of mRNA expression in gingival tissues and submandibular lymph nodes compared to vehicle. P. gingivalis oral infection increased paw swelling and osteoclast numbers in mice immunized with CFA/CII. Arthritis incidence and severity were increased by P. gingivalis in mice that received IFA/CII immunizations. Increased synovitis, bone erosions, and osteoclast numbers in the paws were observed following IFA/CII immunizations in mice infected with P gingivalis. Furthermore, cytokine analysis showed a trend toward increased serum Th17/Th1 ratios when P. gingivalis infection was present in mice receiving either CFA/CII or IFA/CII immunizations. Significant cytokine increases induced by P. gingivalis oral infection were mostly associated to Th17-related cytokines of reactivated splenic cells, including IL-1β, IL-6, and IL-22 in the CFA/CII group and IL-1β, tumor necrosis factor-α, transforming growth factor-β, IL-6 and IL-23 in the IFA/CII group.

CONCLUSIONS:

Chronic P. gingivalis oral infection prior to arthritis induction increases the immune system activation favoring Th17 cell responses, and ultimately accelerating arthritis development. These results suggest that chronic oral infection may influence RA development mainly through activation of Th17-related pathways.

Autoimmune/autoinflammatory syndrome induced by adjuvants (ASIA) has been recently proposed by Shoenfeld and Agmon-Levin as a new entity that comprises several conditions: the macrophagic-myofasciitis syndrome, the Gulf War syndrome, silicosis and post-vaccination phenomena, autoimmunity related to infectious fragments, hormones, aluminum, silicone, squalene oil, and pristane. We report the case of a 23-year-old woman who developed serial episodes of high fever, extreme fatigue, transient thrombocytopenia, multiple cervical adenopathies, hepatosplenomegaly, anemia, neutropenia, severe proteinuria and urine sediment abnormalities, elevated serum ferritin levels, and transient low positive antinuclear antibodies 1 year after she had a nickel-titanium chin implant for cosmetic reasons. The clinical picture simulated a variety of probable diseases: systemic lupus erythematosus, Kikuchi-Fujimoto syndrome, adult onset Still’s disease, antiphospholipid syndrome, and hemophagocytic syndrome, among others, so she underwent an extensive medical investigation including two lymph node biopsies. She received treatment accordingly with steroids, methotrexate, and mofetil mycophenolate, with initial improvement of her symptoms, which recurred every time the dose was reduced. Two and a half years later the patient decided to retire the chin implant and afterwards all her systemic symptoms have disappeared. She remains in good health, without recurrence of any symptom and off medications until today. Albeit this patient fulfills proposed major ASIA criteria, to our knowledge it would be the first description of systemic features of autoinflammation in connection with a metal implant.