Systemic Health and Periodontal Disease.pptx

27 May 2023
Systemic Health and Periodontal Disease.pptx
Systemic Health and Periodontal Disease.pptx
Systemic Health and Periodontal Disease.pptx
Systemic Health and Periodontal Disease.pptx
Systemic Health and Periodontal Disease.pptx
Systemic Health and Periodontal Disease.pptx
Systemic Health and Periodontal Disease.pptx
Systemic Health and Periodontal Disease.pptx
Systemic Health and Periodontal Disease.pptx
Systemic Health and Periodontal Disease.pptx
Systemic Health and Periodontal Disease.pptx
Systemic Health and Periodontal Disease.pptx
Systemic Health and Periodontal Disease.pptx
Systemic Health and Periodontal Disease.pptx
Systemic Health and Periodontal Disease.pptx
Systemic Health and Periodontal Disease.pptx
Systemic Health and Periodontal Disease.pptx
Systemic Health and Periodontal Disease.pptx
Systemic Health and Periodontal Disease.pptx
Systemic Health and Periodontal Disease.pptx
Systemic Health and Periodontal Disease.pptx
Systemic Health and Periodontal Disease.pptx
Systemic Health and Periodontal Disease.pptx
Systemic Health and Periodontal Disease.pptx
Systemic Health and Periodontal Disease.pptx
Systemic Health and Periodontal Disease.pptx
Systemic Health and Periodontal Disease.pptx
Systemic Health and Periodontal Disease.pptx
Systemic Health and Periodontal Disease.pptx
Systemic Health and Periodontal Disease.pptx
Systemic Health and Periodontal Disease.pptx
Systemic Health and Periodontal Disease.pptx
Systemic Health and Periodontal Disease.pptx
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Systemic Health and Periodontal Disease.pptx

Notes de l'éditeur

  1. What causes puberty gingivitis? Puberty gingivitis is most common in preadolescent boys and girls between the ages of 11 and 13. It is typically the result of a combination of elevated hormone levels, which increase the response of gingival tissues to accumulated dental plaque, and poor oral hygiene habits. Symptoms Symptoms of puberty gingivitis are most commonly bleeding and inflammation of the gums. The gum tissue may also become swollen, red, and less firm to the touch. The production of sex hormones (oestrogen and progesterone) increases, then remains relatively constant during the remainder of the reproductive phase.1 Kronman and Loesch2 postulated that anaerobic organisms may use ovarian hormone as a substitute for vitamin K growth factor. During puberty, periodontal tissues may have an exaggerated response to local factors. A hyperplastic reaction of the gingiva may occur in areas where food debris, material alba, plaque and calculus are deposited. The inflamed tissues becomes erythematous, lobulated and retractable.1 During puberty, education of the parent or care giver is a part of successful periodontal therapy. Preventive care, including a vigorous program of oral hygiene, is also vital. Milder gingivitis cases respond well to scaling and root planning, with frequent oral hygiene reinforcement. Severe cases of gingivitis may require microbial culturing, antimicrobial mouthwashes and local site delivery or antibiotic therapy. Periodontal maintenance appointments may need to be more frequent when periodontal instability is noted.3 Treatment You will probably not be too surprised to learn that the best treatment for puberty gingivitis is prevention! As your child gets older, he or she may be less inclined to listen to mom and dad about good oral hygiene practices. However, it’s important to remain firm on this theme to prevent gum disease from developing. Make sure your teen is brushing thoroughly for 2 full minutes at least twice a day, and flossing carefully at least once a day. If a child has already developed gingivitis, it’s best to get it under control as soon as possible, by way of periodontal therapy in the form of scaling and root planing. Mouthwashes containing chlorhexidine can be used to control the infection as well.
  2. Pregnancy gingivitis most commonly develops between months 2 and 8. It may reach a peak during the third trimester. Pregnant women also face an increased risk of both tooth decay and loose teeth. More than 50% of all pregnant women experience some form of pregnancy gingivitis. Pregnancy gingivitis is an hyperplastic reaction to microbial plaque. Elevated estrogen or progesterone levels resulting from hormonal shifts enhance tissue vascularity, which permits an exaggerated inflammatory reaction to plaque. Pregnancy gingivitis produces fiery red, swollen and tender marginal gingiva and compressible and swollen interdental papilla. If pregnancy gingivitis progresses to periodontal disease, it can increase your risk of going into preterm labor.
  3. Fig. 2 patient with a long-term history of type 2 diabetes. (A) Anterior view of the patient’s dental and periodontal condition. (B) Periapical radiographs of the remaining teeth. (C) Clinical photograph of the maxillary premolar area presenting with abscess. (D) Periapical radiograph of the maxillary premolar showing extensive bone loss associated with abscess. Fig. 3 Periodontal abscess in type 1 diabetes. (A) The patient presented with pain and abscess a few weeks after scaling and root planning of the area. (B) severe localized destruction of bone in the area of periodontal abscess. (C) Radiograph of the mandibular right premolar area taken 2 months before the presentation of the abscess.
  4. How does diabetes mellitus cause periodontitis? If diabetes isn't controlled well, higher blood sugar levels in saliva will help bacteria grow. This can cause gum disease. Poor blood sugar control makes it harder for the immune system to fight gum disease. And gum disease may make it harder to control the diabetes. It has been reported that the prevalence of periodontal disease in diabetic patients is >85% (27.3% of patients had gingivitis and 59.5% had periodontitis) whereas the prevalence of periodontitis in the general population is 46% (1,7).
  5. Figure 3 illustrates schematically the mechanisms of interaction between DM and periodontitis. it is well known that diabetic patients present defects in polymorphonuclear leukocyte (PMNL) activity, including chemotaxis, phagocytosis and bactericidal function disorders. Shetty et al. studied PMN functions in 15 diabetic patients with chronic generalized periodontitis, and found that chemotaxis, superoxide production, phagocytosis and killing of Porphy- romonas gingivalis by diabetic PMNs were impaired significantly in comparison with healthy control subjects [58] . Similarly, other studies have shown that diabetic patients with severe periodontitis present reduced chemotaxis in comparison with diabetic subjects with only slight periodontitis, as well as defective apoptosis, which can lead to an increase in PMN retention in the periodontal tissues, which will be accompanied by greater tissue destruction due to continuous MMP and reactive oxygen species (ROS) secretion [56] [57] . A second element for consideration in this two-way relationship is the role of Ad- vanced Glycation End-products (AGEs). AGEs are composites derived from the non- enzymatic, irreversible glycosylation of proteins and lipids that accumulate in plasma, on the walls of blood vessels and tissues in diabetic patients, which are the main element responsible for the development of the micro and macrovascular complications characteristic of DM [59] . It is known that gingival macrophages present receptors with high affinity for AGEs (RAGE), so that they accumulate in the periodontal tissues of diabetics. A study by Schmidt et al. [60] showed that the gingival tissue of adult patients diagnosed with DM who were subjected to surgical periodontal treatment, presented higher quantities of AGEs than that of non-diabetic subjects. This finding is important as the accumulation of AGEs in the periodontal tissues of diabetic patients favors frequent pro-inflammatory episodes. When AGE binds to its receptor, this produces an overproduction of inflammatory mediators such as IL-1b, TNF-a and IL-6 [56] [57] [61] . The formation of these molecules provokes ROS production, which increases oxidative stress, and the consequent cellular changes that take place contribute to the vascular damage involved in many DM complications [62] - [66] . AGEs also increase the respiratory burst of PMNs, which has the potential to increase tissue damage localized in the periodontium. In addition, AGEs have a harmful effect on bone metabolism, producing an alteration to the bone formation and repair mechanisms, together with reduced production of extracellular matrix. Apoptosis may play a role in the increased susceptibility to periodontal diseases among diabetics, and the death of matrix-pro- ducing cells could limit the possibility of repair in inflamed tissues; it is known that AGEs have harmful effects on extracellular matrix formation, in relation to apoptosis of the cells most involved in its formation such as fibroblasts [57] . A third element for consideration is the changes that DM may cause in the composition of subgingival microbiota. Compared with the large number of studies that have investigated the role of inflammatory mechanisms in the relation between DM and periodontal diseases, relatively few have focused on the changes triggered by changes to oral microbiota. The few that exist indicate that in general there are more similarities than differences between diabetic and non-diabetic subjects. Nevertheless, some significant differences have been detected, such as the greater prevalence of Porphyromonas gingivalis [67] and Prevotella intermedia [67] [68] in diabetic subjects. These studies indicate that there are probably subtle differences between diabetics and non-diabetics, although the clinical relevance of these differences is not clear. The origins of these differences could lie in the previously observed effects on periodontal tissues that could favor the growth of more pathogenic species.
  6. Cytokines are regulators of host responses to infection, immune responses, inflammation, and trauma. Some cytokines act to make disease worse (proinflammatory), whereas others serve to reduce inflammation and promote healing (anti-inflammatory). Cytokines are produced in response to invading pathogens to stimulate, recruit, and proliferate immune cells. Cytokines includes interleukins (IL), chemokines, interferons, and tumor necrosis factors (TNF). Cytokines play an important role in normal immune responses, but having a large amount of them released in the body all at once can be harmful. This so-called CYTOKINE STORM happens when the immune system produces too many inflammatory signals. This can can cause serious symptoms that in some cases can lead to organ failure and death
  7. Can bleeding gums be a sign of leukemia? Yes. Your blood platelets help your body stop bleeding. If you have Leukemia, a type of cancer, your platelet count will be low. This makes it harder for you to stop bleeding in different parts of your body, including your gums. Make an appointment with your doctor if your notice symptoms including unusual bleeding of your gums or nosebleeds.
  8. It may be localized to the interdental papilla area (Fig. 8), or it may expand to include the marginal gingiva and partially cover the crowns of the teeth (Fig. 9C and D). GINGIVAL LEUKEMIC INFILTRATION AS THE FIRST MANIFESTATION OF ACUTE MYELOID LEUKEMIA. The leukemic infiltration of the gingival tissue associated or not with gingival enlargement could be the first manifestation of acute leukemia, and it has rarely been reported in the literature.
  9. The Modifiable Risk factors for periodontitis and cancer: Modifiable (smoking, diabetes mellitus, psychological factors, and lifestyle factors - such as diet and alcoholism) and non-modifiable risk factors are host response and genetic factors. Therefore, patients should be encouraged to change their lifestyle and adopt healthy habits (healthy eating, regular physical exercise), eliminate risk factors that may predispose them to cancer (smoking and alcohol), practice good oral hygiene, and visit regularly health professionals. Thus, the health multidisciplinary team must act together to reduce or eliminate potential risks that may affect the oral and systemic overall health of patients.