Streptococcal Gingivitis: A Report of Case with a Description of a Unique Gingival Prothesis

2004 ◽  
Vol 5 (3) ◽  
pp. 150-157 ◽  
Author(s):  
Yasin Çiçek ◽  
Mehmet Özgöz ◽  
Varol Çanakçi ◽  
Recep Orbak

Abstract Acute streptococcal gingivitis is an acute inflammation of the oral mucosa. Specific bacterial infections of the gingiva may be due to neisseria gonorrhea, treponema pallidum, streptococci, and other organisms. Streptococcal infections are seen rarely. This case report describes a patient who presented with severe gingival inflammation and pain that was diagnosed as an acute streptococcal infection. Bacterial cultures were obtained from the lesion, and biopsies were obtained from the gingiva of lower incisors for histopathologic evaluation. The patient was successfully treated using conventional periodontal therapy (scaling, root planning, curettage) and antibacterial agents. The reconstructive phase for this patient consisted of the fabrication of a heat-cured acrylic gingival facade to mask the gingival recession. The treatment of acute gingivostomatitis is of importance because of the possibility of systemic secondary infections. When esthetics is important, a gingival prostheses can be considered. The differential diagnosis, etiology, and treatment of acute streptococcal gingivitis are discussed and the literature is reviewed in this report. Citation Çiçek Y, Özgöz M, Çanakçi, et. al Streptococcal Gingivitis: A Report of Case with a Description of a Unique Gingival Prosthesis. J Contemp Dent Pract 2004 August;(5)3:150-157.

2007 ◽  
Vol 01 (04) ◽  
pp. 251-255 ◽  
Author(s):  
Cankat Kara ◽  
Turgut Demir ◽  
Adnan Tezel ◽  
Meltem Zihni

ABSTRACTAcute streptococcal gingivitis is an acute inflammation of the oral mucosa and also may be seen with the other oral diseases as aggressive periodontitis that is characterized by a considerable attachment loss over a relatively short period of time. Streptococcal infections of gingiva are seen rarely; also the origin of this gingival inflammation is occasionally different from that of routine plaque-associated gingivitis. The clinical features and treatment methods of these diseases are already reported in previous literatures. This case report describes a patient who presented with severe gingival inflammation and attachment loss that was diagnosed as an acute streptococcal infection associated with aggressive periodontitis. In this study a supportive treatment option was demonstrated based on these data and antacid treatment as adjunctive to the recommended treatment modalities was used for streptococcal gingivitis. (Eur J Dent 2007;1:251-255)


2016 ◽  
Vol 6 (1) ◽  
Author(s):  
Jana Ninkovic ◽  
Vidhu Anand ◽  
Raini Dutta ◽  
Li Zhang ◽  
Anuj Saluja ◽  
...  

Abstract Opioid drug abusers have a greater susceptibility to gram positive (Gram (+)) bacterial infections. However, the mechanism underlying opioid modulation of Gram (+) versus Gram (−) bacterial clearance has not been investigated. In this study, we show that opioid treatment resulted in reduced phagocytosis of Gram (+), when compared to Gram (−) bacteria. We further established that LPS priming of chronic morphine treated macrophages leads to potentiated phagocytosis and killing of both Gram (+) and Gram (−) bacteria in a P-38 MAP kinase dependent signaling pathway. In contrast, LTA priming lead to inhibition of both phagocytosis and bacterial killing. This study demonstrates for the first time the differential effects of TLR4 and TLR2 agonists on morphine induced inhibition of phagocytosis. Our results suggest that the incidence and severity of secondary infections with Gram (+) bacteria would be higher in opioid abusers.


Author(s):  
Bharat Bhushan Awasthi ◽  
Saurabh Singh

Background: Periodontitis is a common chronic inflammatory dental disease, which occurs due to the existence of pathogenic microorganisms within the gingival plaque and lead to the formation of periodontal pocket. This study was aimed to evaluate the effectiveness of satranidazole and ornidazole in the treatment of chronic periodontal diseases along with mechanical debridement.Methods: Forty subjects were randomly selected to access the effectiveness of selected drugs on the basis of clinical and microbiological investigations over a period of 14 days. Six Ramfjord teeth (i.e. 16, 21, 24, 36, 41 and 44) were examined for investigating clinical parameters such as gingival inflammation, pocket depth and bleeding on probing. Microbiological investigations were carried out to examine the presence of gram positive (cocci and bacilli), gram negative (cocci and bacilli) and spirochaetes.Results: A substantial progress was recorded in treating gingival inflammation, pocket depth and bleeding on probing. The results of microbiological investigations suggest that the satranidazole and ornidazole were equally effective when used alone and with scaling and root planning in reducing microbial infections. The results indicated a significant (p <0.0001) effect of model drugs on clinical and microbiological parameters in different study subjects at baseline (pre-treatment), and 7 days and 14 days post treatment.Conclusions: The results concluded that ornidazole is better than satranidazole in treating periodontal diseases.


2020 ◽  
Vol 17 (2) ◽  
pp. 54
Author(s):  
Anindita L. ◽  
Aris Aji K. ◽  
Arcadia Sulistijo J.

Hypertension presents an increase in blood pressure following the oral manifestations, such as gingival enlargement. A 42-year-old woman came to the General Sudirman University Dental and Oral Hospital complaining of enlarged front gums seven years ago. The patient had a history of hypertension and regularly consumed drugs, amlodipine 5 mg. Extraoral examination revealed no lymphadenopathy and no swelling of the head and neck area. Intraoral examination revealed a gingival enlargement involving the papilla to the gingival margin present on the entire upper and lower labial gingival surface. The patient's diagnosis was gingival enlargement caused by gingival enlargement due to the use of amlodipine. Gingival enlargement has been noted with long-term or high-dose amlodipine use. The mechanism of amlodipine in causing gingival enlargement is through the role of fibroblasts with abnormal susceptibility to the drug, resulting in increased levels of protein synthesis, especially collagen. The role of pro-inflammatory cytokines occurs through an increase in interleukin-1β (IL-1β) and IL-6 in the inflamed gingival tissue due to the gingival fibrogenic response to drugs. Therapies were DHE and scaling and root planning as phase I in periodontal treatment. Plaque elimination is vital to reduce gingival inflammation that may occur. Substitution of the drug amlodipine may be needed if there is no improvement. Based on case reports, hypertension patients who took amlodipine could have gingival enlargement. The therapy given was plaque elimination in the form of DHE and Scaling and regular check-ups with the dentist.


Author(s):  
Vicky Sender ◽  
Karina Hentrich ◽  
Birgitta Henriques-Normark

Secondary bacterial infections enhance the disease burden of influenza infections substantially. Streptococcus pneumoniae (the pneumococcus) plays a major role in the synergism between bacterial and viral pathogens, which is based on complex interactions between the pathogen and the host immune response. Here, we discuss mechanisms that drive the pathogenesis of a secondary pneumococcal infection after an influenza infection with a focus on how pneumococci senses and adapts to the influenza-modified environment. We briefly summarize what is known regarding secondary bacterial infection in relation to COVID-19 and highlight the need to improve our current strategies to prevent and treat viral bacterial coinfections.


Circulation ◽  
2015 ◽  
Vol 131 (suppl_2) ◽  
Author(s):  
Kentaro Ueno

Objective: Circulating platelet-neutrophil aggregates play a crucial role in amplifying acute inflammation and could promote adverse effects involving vascular injury. The aim of this study was to clarify the role of platelet-neutrophil aggregates in patients with Kawasaki disease (KD). Methods: We analyzed 40 patients with KD (30 intravenous immunoglobulin [IVIG] responders and 10 IVIG non-responders), 7 febrile patients with bacterial infections, and 9 normal volunteers. Thirty-three patients with KD were treated with IVIG alone, and remaining seven were treated with IVIG plus prednisolone. We evaluated the rate of platelet-neutrophil aggregates and measured the platelet factor 4 (PF4) and β-thromboglobulin (β-TG) levels in patients with KD. Results: The rate of platelet-neutrophil aggregates was significantly higher in patients with KD than in both patients with bacterial infection and normal volunteers. There was a trend toward increased rate of platelet-neutrophil aggregates within 2 or 3 days after IVIG than before IVIG. The rate of platelet-neutrophil aggregates was significantly higher in patients who showed coronary artery abnormalities (CAA) than in those who showed without CAA and was correlated with PF4 and β-TG levels in patients with KD. Comparing time course analysis, the rate of platelet-neutrophil aggregates was significantly decreased in patients treated with IVIG plus prednisolone than in those treated with IVIG alone. Conclusions: Our findings demonstrate that platelet-neutrophil aggregates play a crucial role in regulating vasculitis, and are involved in the development of CAA. Additional prednisolone treatment in the acute phase of KD might have a potential role in inhibiting amplified reciprocal inflammatory activation by suppressing platelet-neutrophil aggregates.


Author(s):  
Angela Gomez-Simmonds ◽  
Medini K Annavajhala ◽  
Thomas H McConville ◽  
Donald E Dietz ◽  
Sherif M Shoucri ◽  
...  

Abstract Background Patients with COVID-19 may be at increased risk for secondary bacterial infections with MDR pathogens, including carbapenemase-producing Enterobacterales (CPE). Objectives We sought to rapidly investigate the clinical characteristics, population structure and mechanisms of resistance of CPE causing secondary infections in patients with COVID-19. Methods We retrospectively identified CPE clinical isolates collected from patients testing positive for SARS-CoV-2 between March and April 2020 at our medical centre in New York City. Available isolates underwent nanopore sequencing for rapid genotyping, antibiotic resistance gene detection and phylogenetic analysis. Results We identified 31 CPE isolates from 13 patients, including 27 Klebsiella pneumoniae and 4 Enterobacter cloacae complex isolates. Most patients (11/13) had a positive respiratory culture and 7/13 developed bacteraemia; treatment failure was common. Twenty isolates were available for WGS. Most K. pneumoniae (16/17) belonged to ST258 and encoded KPC (15 KPC-2; 1 KPC-3); one ST70 isolate encoded KPC-2. E. cloacae isolates belonged to ST270 and encoded NDM-1. Nanopore sequencing enabled identification of at least four distinct ST258 lineages in COVID-19 patients, which were validated by Illumina sequencing data. Conclusions While CPE prevalence has declined substantially in New York City in recent years, increased detection in patients with COVID-19 may signal a re-emergence of these highly resistant pathogens in the wake of the global pandemic. Increased surveillance and antimicrobial stewardship efforts, as well as identification of optimal treatment approaches for CPE, will be needed to mitigate their future impact.


2017 ◽  
Vol 199 (14) ◽  
Author(s):  
Sujina Mali ◽  
Morgan Mitchell ◽  
Spencer Havis ◽  
Abiodun Bodunrin ◽  
Jonathan Rangel ◽  
...  

ABSTRACT Dormancy is a protective state in which diverse bacteria, including Mycobacterium tuberculosis, Staphylococcus aureus, Treponema pallidum (syphilis), and Borrelia burgdorferi (Lyme disease), curtail metabolic activity to survive external stresses, including antibiotics. Evidence suggests dormancy consists of a continuum of interrelated states, including viable but nonculturable (VBNC) and persistence states. VBNC and persistence contribute to antibiotic tolerance, reemergence from latent infections, and even quorum sensing and biofilm formation. Previous studies indicate that the protein mechanisms regulating persistence and VBNC states are not well understood. We have queried the VBNC state of Micrococcus luteus NCTC 2665 (MI-2665) by quantitative proteomics combining gel electrophoresis, high-performance liquid chromatography, and tandem mass spectrometry to elucidate some of these mechanisms. MI-2665 is a nonpathogenic actinobacterium containing a small (2.5-Mb), high-GC-content genome which exhibits a well-defined VBNC state induced by nutrient deprivation. The MI-2665 VBNC state demonstrated a loss of protein diversity accompanied by increased levels of 18 proteins that are conserved across actinobacteria, 14 of which have not been previously identified in VNBC. These proteins implicate an anaplerotic strategy in the transition to VBNC, including changes in the glyoxylate shunt, redox and amino acid metabolism, and ribosomal regulatory processes. Our data suggest that MI-2665 is a viable model for dissecting the protein mechanisms underlying the VBNC stress response and provide the first protein-level signature of this state. We expect that this protein signature will enable future studies deciphering the protein mechanisms of dormancy and identify novel therapeutic strategies effective against antibiotic-tolerant bacterial infections. IMPORTANCE Dormancy is a protective state enabling bacteria to survive antibiotics, starvation, and the immune system. Dormancy is comprised of different states, including persistent and viable but nonculturable (VBNC) states that contribute to the spread of bacterial infections. Therefore, it is imperative to identify how bacteria utilize these different dormancy states to survive antibiotic treatment. The objective of our research is to eliminate dormancy as a route to antibiotic tolerance by understanding the proteins that control dormancy in Micrococcus luteus NCTC 2665. This bacterium has unique advantages for studying dormancy, including a small genome and a well-defined and reproducible VBNC state. Our experiments implicate four previously identified and 14 novel proteins upregulated in VBNC that may regulate this critical survival mechanism.


1994 ◽  
Vol 21 (2) ◽  
pp. 151-159 ◽  
Author(s):  
Joyce Lilias McComb

Isolated gingival recession may occur in as many as 30 per cent of adolescents, and lead to problems of dentine hypersensitivity, root caries, and gingival inflammation in adult life. This review discusses the prevalence and aetiology of isolated recession, with particular reference to the implications for orthodontic treatment. Consideration is also given to the differing philosophies for management


2015 ◽  
Vol 212 (8) ◽  
pp. 1203-1217 ◽  
Author(s):  
Nan Chiang ◽  
Jesmond Dalli ◽  
Romain A. Colas ◽  
Charles N. Serhan

Endogenous mechanisms that orchestrate resolution of acute inflammation are essential in host defense and the return to homeostasis. Resolvin (Rv)D2 is a potent immunoresolvent biosynthesized during active resolution that stereoselectively stimulates resolution of acute inflammation. Here, using an unbiased G protein–coupled receptor-β-arrestin–based screening and functional sensing systems, we identified a receptor for RvD2, namely GPR18, that is expressed on human leukocytes, including polymorphonuclear neutrophils (PMN), monocytes, and macrophages (MΦ). In human MΦ, RvD2-stimulated intracellular cyclic AMP was dependent on GPR18. RvD2-stimulated phagocytosis of Escherichia coli and apoptotic PMN (efferocytosis) were enhanced with GPR18 overexpression and significantly reduced by shRNA knockdown. Specific binding of RvD2 to recombinant GPR18 was confirmed using a synthetic 3H-labeled-RvD2. Scatchard analysis gave a Kd of ∼10 nM consistent with RvD2 bioactive concentration range. In both E. coli and Staphylococcus aureus infections, RvD2 limited PMN infiltration, enhanced phagocyte clearance of bacteria, and accelerated resolution. These actions were lost in GPR18-deficient mice. During PMN-mediated second organ injury, RvD2’s protective actions were also significantly diminished in GPR18-deficient mice. Together, these results provide evidence for a novel RvD2–GPR18 resolution axis that stimulates human and mouse phagocyte functions to control bacterial infections and promote organ protection.


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