Periodontal Diseases
Lars Granath, William D. McHugh in Systematized Prevention of Oral Disease: Theory and Practice, 2019
Gingivitis and chronic periodontitis are inflammatory diseases, which are thought to be initiated by the influx of antigenic and nonantigenic material from plaque microorganisms. The initial reaction occurs in the marginal gingivae lateral to the sulcus wall and involves an increase in blood flow and in vascular permeability which result in an inflammatory exudate, possibly caused by the release of histamine from mast cells. Cellular responses then become apparent. Neutrophil leukocytes are thought to be the first involved and there is compelling evidence that they are protective in action since, when they are depressed in number as in cyclic neutropenia or in function as in localized juvenile periodontitis, periodontal destruction is more severe.25 It has also been found that certain periodontopathic organisms produce inhibitors of neutrophil chemotaxis and this inhibition of neutrophil function may help to explain how these organisms cause periodontal destruction.
Bacterial Infections of the Oral Cavity
K. Balamurugan, U. Prithika in Pocket Guide to Bacterial Infections, 2019
A positive association was seen between bacterial infections and respiratory infection. In a review, there was a mention of possible mechanism of pathogenesis like bacterial aspiration (P. gingivalis and A. actinomycetemcomitans), modification of respiratory mucosa by enzymes of breakdown products, and cytokines released from periodontal diseases (Scannapieco, 1999). Periodontal and gingival bacterial super infections of individuals affected with HIV was found to present a similar picture to those of individuals who were immune suppressed. In a study done on 31 intact teeth affected by pulp and marginal infections, polymerase chain reaction was used to isolate pathogens like A. actinomycetemcomitans, B. forsythus, Eikenella corrodens, F. nucleatum, P. gingivalis, P. intermedia, and T. denticola (Reichart, 2003). The organisms were present in the chronic apical periodontitis and chronic periodontitis. This was suggestive that any refractory course of endo-perio lesions may be attributed to the endodontic and periodontic pathway of infections (Rupf et al., 2000).
Eosinophil Granule Proteins in Cutaneous Disease
Gerald J. Gleich, A. Barry Kay in Eosinophils in Allergy and Inflammation, 2019
All three patients developed persistent and recurrent pruritic and purpuric papular skin lesions and angioedema of periorbital areas, hands, and feet. Annular erythematous edematous lesions, urticarial plaques, and vesicular lesions occasionally developed. Chronic periodontitis developed in two of the patients without known cause (67). Lesions responded promptly to glucocorticoid therapy but recurred and followed a chronic course. Peripheral blood eosinophilia was variably present (up to 6000/mm3), and erythrocyte sedimentation rate was elevated. No systemic symptoms accompanied the disease, and the patients have been maintained on “burst” and alternate-day glucocorticoid therapy. Follow-up has been for extended times of 24, 18, and 3 years in these patients (67).
Evaluation of serum alanine aminotransferase and aspartate aminotransferase enzyme levels in women patients with chronic periodontitis
Published in Health Care for Women International, 2022
Amir Reza Ahmadinia, Mina Pakkhesal, Mohammad Ali Vakili
Chronic periodontitis is an infection-driven inflammatory disease which may lead to formation of periodontal pockets and ultimately tooth loss by progressive destruction of dental supporting tissues. The main cause of periodontitis is microbial plaque, but environmental factors, social, economic conditions and genetic predisposition affect its development (Damgaard et al., 2015; Han et al., 2016; Nizam et al., 2014; Tamaki et al., 2011). Moreover, Periodontitis have an association with a variety of chronic diseases such as diabetes, respiratory diseases, cardiovascular disease and osteoporosis and conditions affecting general health. It has been stated that chronic periodontitis is effective in the progression of liver diseases, especially nonalcoholic fatty liver (Furuta et al., 2010; Han et al., 2016).
Lycopene solid lipid microparticles with enhanced effect on gingival crevicular fluid protein carbonyl as a biomarker of oxidative stress in patients with chronic periodontitis
Published in Journal of Liposome Research, 2019
Maie S. Tawfik, Khaled A. Abdel-Ghaffar, Ahmed Y. Gamal, Fatma H. El-Demerdash, Heba A. Gad
Chronic periodontitis is an inflammatory condition affecting the supportive structures of the teeth, gingiva, periodontal ligament, alveolar bone, and dental cementum. The primary causative factor of periodontitis is Gram-negative anaerobic or facultative anaerobic bacteria within the subgingival plaque biofilm. Periodontal therapy aims to remove the bacteria using conventional scaling and root planing (SRP). Successful management of periodontitis includes the systemic and local use of antimicrobial agents as adjunct to SRP. However, most of periodontal tissue destruction occurs due to the abnormal host response to pathogenic bacteria including overproduction of reactive oxygen species (ROS) by host defence cells (Meyle and Chapple 2015). Imbalance between ROS production and antioxidant defence system might lead to generation of oxidative stress (Valko et al. 2007), which plays a role in the pathogenesis of periodontal disease (Masi et al. 2011).
Ex vivo anti-inflammatory effects of probiotics for periodontal health
Published in Journal of Oral Microbiology, 2018
Tim Schmitter, Bernd L. Fiebich, Joerg T. Fischer, Max Gajfulin, Niklas Larsson, Thorsten Rose, Marcus R. Goetz
Inflammation of the gingivae (gingivitis) occurs in response to the accumulation of dental plaque on tooth surfaces near the gingival margin. In particular, bacterial lipopolysaccharide (LPS) from Gram-negative bacteria, which increase in number and proportion in plaque as it matures, provokes a non-specific inflammatory immune response [1,2]. This response is mediated by proinflammatory cytokines (e.g. tumor necrosis factor-α [TNF-α] and interleukin [IL]-1β), chemokines (e.g. IL-8) and prostaglandins (e.g. prostaglandin E2 [PGE2]) secreted by gingival epithelial cells, fibroblasts and resident leukocytes [2–4]. These inflammatory mediators influence various cellular processes, including recruitment and chemotaxis of neutrophils, and promote increased vascular dilation and blood flow in the gingiva [5]. Persistent gingival inflammation can progressively exert selective pressure for the development of a dysbiotic and inflammophilic plaque microbiota [6]. In susceptible individuals, these changes can lead to chronic periodontitis, which is characterized by chronic inflammation and irreversible destruction of the supporting tissues of the teeth. Therefore, gingival inflammation should ideally be prevented, or reversed in its early stages.
Related Knowledge Centers
- Aggressive Periodontitis
- Biofilm
- Calculus
- Gingivitis
- Inflammation
- Mouth
- Periodontium
- Periodontal Disease
- Chronic Condition
- Dental Plaque