Inflammation represents the body’s protective response to injury and tissue destruction. This response consists of a spectrum of highly coordinated events that occur at the cellular and tissue level. Its purpose is to destroy, dilute, or sequester the injurious agent and the injured tissues in order to permit healing. Inflammation is a defensive mechanism intended to protect the host, but can also be potentially harmful. Clinical signs of inflammation are redness due to open blood vessels, heat due to warmth of blood, swelling due to edema, pain due to stimulation of pain receptors, and loss of function due to edema.
Periodontitis is the inflammation of the periodontium (gingiva and underlying connective tissue) resulting in features such as clinical attachment loss, alveolar bone loss, and periodontal pocketing. In periodontitis, one can see enlargement or recession of the gingivae, bleeding upon probing, increased tooth mobility, drifting of teeth, and/or tooth exfoliation. Chronic periodontitis is a slowly progressing disease process that may occur continuously or in bursts of activity. Historically, the gingival tissue from chronic periodontitis displays junctional epithelium more apical to the cemento-enamel junction, loss of collagen fibers subjacent to the pocket epithelium, bone loss, numerous neutrophils (polymorphonuclear cells (PMNs), and dense inflammatory cell infiltrate with plasma cells, lymphocytes, and macrophages.
Tissue damage in chronic periodontitis is the result of major inflammatory and immunopathologic components activated by the host response. These include alteration of fibroblast function, activation of macrophages to release collagenase and other lytic enzymes, activation of lymphocytes, modulation of fibroblast growth, collagen synthesis, and stimulation of bone resorption. Prostaglandins and cytokines appear to be critically involved in tissue destruction caused by periodontitis.
Concepts of the etiology of periodontitis imply a bacterial infection as the primary cause of the disease. Gingival inflammation is the result of plaque, or bacterial biofilm, which contains gram negative bacteria such as P. gingivalis, B. forsythus, and P. intermedia, amongst many others.2 These bacteria possess complex carbohydrates and proteins on their cell wall, called endotoxins or lipopolysaccharides (LPSs). When these molecules are detected by the host, a protective response ensues, resulting in inflammation, recruitment of white blood cells (WBCs), and release of cytokines and chemical mediators. The chemical mediators that cause the main systemic problems are IL-1, IL-6, and tumor necrosis factor-alpha (TNF-α). The function of IL-1 is to recruit osteoclasts (bone-resorbing cells), which remove bone matrix. The function of IL-6 is to increase fibrinogen, which helps in the clotting mechanism of injured blood vessels. The function of TNF-α is to primarily increase C-reactive proteins (CRPs) which recruit more macrophages to the site of injury. These mediators, although helpful in fighting insult to the body, can be harmful as well.
Richard Nejat, DDS
Dr. Richard Nejat received his Doctorate of Dental Surgery from New York University, where he graduated in the top of his class, receiving the prestigious OKU honors. Following graduation, Dr. Nejat began a three-year residency in periodontics and dental implants at Stony Brook University-State University of New York, where he earned his certificate in periodontics. He is an active instructor in professional continuing education on topics including periodontal medicine, computer-guided and minimally invasive dental implant surgery, and periodontal plastic surgery.
Dr. Nejat is currently involved in numerous clinical research projects involving flapless dental implant surgery, minimally invasive periodontal plastic surgeries, and computer-guided dental implant surgery with immediate function. Dr. Nejat is a Diplomate of the American Board of Periodontology. He maintains private practices in Manhattan, NY and Nutley, NJ.
Daniel Nejat, DMD
Dr. Daniel Nejat graduated magna cum laude from Drew University with a Bachelor of Arts. He continued his education by receiving a Doctorate in Dental Medicine at the University of Medicine and Dentistry of New Jersey Dental School. Presently, Dr. Nejat is completing his postdoctoral periodontal residency at the New York University College of Dentistry.
Morris Nejat, MD
Dr. Morris Nejat graduated cum laude from Drew University in New Jersey and obtained his medical degree from the University of Medicine and Dentistry of New Jersey, New Jersey Medical School. His internship and residency in pediatrics were completed at North Shore University Hospital, Cornell University Medical College. His allergy/immunology fellowship was performed at the R.A. Cooke Institute of Allergy at St. Luke’s/Roosevelt Hospital Center, Columbia University College of Physicians and Surgeons. Dr. Nejat is Board Certified in pediatrics and has received appointments in pediatrics at St. Luke’s/Roosevelt Hospital Center and Bellevue Hospital Center in New York City.
Dr. Nejat is frequently quoted in the media, including NBC news, Fox News, WB11 News, ABC news and numerous consumer publications. He also frequently lectures to physicians and consumers on the topics of allergy, asthma, eczema and food allergies.
Upon completion of this course, the dental professional should be able to:
• Explain the mechanism by which periodontal disease causes production of inflammatory mediators that enter the systemic circulation and affect organ systems in the body
• Explain the mechanism by which inflammatory mediators effect vessel plaque formation and lead to an increased risk of cardiovascular disease
• Explain the mechanism by which periodontal disease mediators worsen the condition in diabetes mellitus
• Describe the association of periodontal disease and the increased risk of development of pneumonia and COPD in the elderly
• Describe the probable association of periodontal disease, tooth loss, and osteoporosis
• Clarify how appropriate treatment of periodontal disease can lead to improvement in outcomes in many of the above disease processes.
CONTINUING EDUCATION CREDIT
The ADAA has an obligation to disseminate knowledge in the field of dentistry. Sponsorship of a continuing education program by the ADAA does not necessarily imply endorsement of a particular philosophy, product or technique.
The ADAA cautions participants taking this course on the hazards of using limited knowledge when integrating new techniques into their practices.
Credits earned upon completion of the course may be used to meet DANB’s Recertification Requirements.
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