UPCII M Microbiologia Teórica 25

Apresentação em tema: "UPCII M Microbiologia Teórica 25"— Transcrição da apresentação:

1 UPCII M Microbiologia Teórica 25
2º Ano 2013/2014

2 Sumário Capítulo XX. Doenças Periodontais Definições
O papel da placa bacteriana nas doenças periodontais Teorias da placa Agentes etiológicos das patologias periodontais T25 MJC

3 Saúde Doenças periodontais GEngivite Periodontite Avançada
T25 MJC

4 Periodontite Crónica Localizada Agressiva Necrotizante Peri-implantite
+ comum Associada a factores locais Microbiota variável Progressão lenta Agressiva Severidade independente de factores locais Aumento de A. actinomycemcomitans Progressão rápida Com padrão familiar Leucócitos polimorfonucleares Macrófagos hiper-responsivos (↑Prostaglandinas, ↑ IL1-β). Necrotizante Em indivíduos com outras patologias sistémicas (HIV) trench-mouth Peri-implantite Localizada 1ºs molares e produção aumentada de anticorpos Generalizada Outros dentes e pouca produção de anticorpos T25 MJC

5 Doença periodontal Patologia infecciosa oportunista
Envolve factores do hospedeiro: Genéticos Envolvidos na resposta imune Envolvidos em patologia sistémicas como diabetes Higiene oral Associada às espécies microbianas presentes Hábitos “sociais” Principalmente os que afectam a resposta imunológica como tabaco e alcolismo T25 MJC

6 Placa bacteriana e patologia periodontal
Hipótese da placa não específica (até 70’s) Idade Índices de placa Limiar de resposta Hipótese da placa específica (meio dos 70’s) Excepções ao anterior (por vezes no mesmo paciente) Estudos de cultivo com resultados diferentes Keystone pathogens In the illustration above, the gingival margin (gum line seen at the right of the figure) serves to differentiate two types of plaque: the supragingival plaque seen at the top and the subgingival plaque seen at the bottom of the pocket. Note that the kinds of bacteria (germs) in the two types of plaque are different, with worm-like spirochetes and gram negative rods (G-R) dominating the subgingival plaque. It is these spirochetes and gram negative rods that contribute to periodontal disease, as they release toxins into the gingival (gum) tissue, with a few even penetrating into the tissue, where they are destroyed by host inflammatory cells. Host inflammatory cells are represented in the figure as T cells (T with circle, T-lymphocytes), B cells (B with circle, B-lymphocytes), M cells (M with circle, monocytes/ macrophages) and polymorphonuclear cells (circles with the curved black C-like structure inside). The inflammatory cells cause the gums to redden, swell and bleed, in a process known as inflammation. This inflammatory condition can usually be detected by the dentist or dental hygienist. Clinical studies have shown that the bacteria that cause these inflammatory reactions can be kept at low levels by cleaning or debriding the roots of the teeth by a dental procedure known as scaling and root planing (debridement). This procedure has to be repeated several times during the year in a patient with periodontal pockets. If the pockets are 6 mm or deeper, then debridement is difficult to achieve, and the clinician usually uses a surgical procedure to gain access to the inaccessible plaque and calculus deposits. Certain teeth that are extensively involved are often extracted, as clinical experience indicates that they will not respond to the cleaning procedures. This approach reportedly is successful in about 80 to 85% of patients with advanced forms of periodontal disease, who receive treatment. When the debridement approach fails, as in the so-called refractory patient, these individuals are often given systemic antibiotics. Hipótese ecológica T25 MJC

7 Placa bacteriana e patologia periodontal
Cultura Vs. Técnicas moleculares In the illustration above, the gingival margin (gum line seen at the right of the figure) serves to differentiate two types of plaque: the supragingival plaque seen at the top and the subgingival plaque seen at the bottom of the pocket. Note that the kinds of bacteria (germs) in the two types of plaque are different, with worm-like spirochetes and gram negative rods (G-R) dominating the subgingival plaque. It is these spirochetes and gram negative rods that contribute to periodontal disease, as they release toxins into the gingival (gum) tissue, with a few even penetrating into the tissue, where they are destroyed by host inflammatory cells. Host inflammatory cells are represented in the figure as T cells (T with circle, T-lymphocytes), B cells (B with circle, B-lymphocytes), M cells (M with circle, monocytes/ macrophages) and polymorphonuclear cells (circles with the curved black C-like structure inside). The inflammatory cells cause the gums to redden, swell and bleed, in a process known as inflammation. This inflammatory condition can usually be detected by the dentist or dental hygienist. Clinical studies have shown that the bacteria that cause these inflammatory reactions can be kept at low levels by cleaning or debriding the roots of the teeth by a dental procedure known as scaling and root planing (debridement). This procedure has to be repeated several times during the year in a patient with periodontal pockets. If the pockets are 6 mm or deeper, then debridement is difficult to achieve, and the clinician usually uses a surgical procedure to gain access to the inaccessible plaque and calculus deposits. Certain teeth that are extensively involved are often extracted, as clinical experience indicates that they will not respond to the cleaning procedures. This approach reportedly is successful in about 80 to 85% of patients with advanced forms of periodontal disease, who receive treatment. When the debridement approach fails, as in the so-called refractory patient, these individuals are often given systemic antibiotics. T25 MJC

8 Placa bacteriana e patologia periodontal
Bastonetes (G-) Hipótese da placa específica (meio dos 70’s) Excepções ao anterior (por vezes no mesmo paciente) Estudos de cultivo com resultados diferentes Associação de A.a a periodontite agressiva Bastonetes (G+) Coc-ci (G+) Coc-ci (G-) Facultativos In the illustration above, the gingival margin (gum line seen at the right of the figure) serves to differentiate two types of plaque: the supragingival plaque seen at the top and the subgingival plaque seen at the bottom of the pocket. Note that the kinds of bacteria (germs) in the two types of plaque are different, with worm-like spirochetes and gram negative rods (G-R) dominating the subgingival plaque. It is these spirochetes and gram negative rods that contribute to periodontal disease, as they release toxins into the gingival (gum) tissue, with a few even penetrating into the tissue, where they are destroyed by host inflammatory cells. Host inflammatory cells are represented in the figure as T cells (T with circle, T-lymphocytes), B cells (B with circle, B-lymphocytes), M cells (M with circle, monocytes/ macrophages) and polymorphonuclear cells (circles with the curved black C-like structure inside). The inflammatory cells cause the gums to redden, swell and bleed, in a process known as inflammation. This inflammatory condition can usually be detected by the dentist or dental hygienist. Clinical studies have shown that the bacteria that cause these inflammatory reactions can be kept at low levels by cleaning or debriding the roots of the teeth by a dental procedure known as scaling and root planing (debridement). This procedure has to be repeated several times during the year in a patient with periodontal pockets. If the pockets are 6 mm or deeper, then debridement is difficult to achieve, and the clinician usually uses a surgical procedure to gain access to the inaccessible plaque and calculus deposits. Certain teeth that are extensively involved are often extracted, as clinical experience indicates that they will not respond to the cleaning procedures. This approach reportedly is successful in about 80 to 85% of patients with advanced forms of periodontal disease, who receive treatment. When the debridement approach fails, as in the so-called refractory patient, these individuals are often given systemic antibiotics. Anaeróbios T25 MJC

9 Hipótese ecológica da placa
FC pH Profun-didade e Sangra-mento Profun-didade e Sangra-mento Biological Complexes T25 MJC

10 Implicações na Terapêutica ???
Como é feita actualmente? Como deverá ser feita? T25 MJC

11 T25 MJC

12 T25 MJC

13 Progressão do ecossistema até à doença periodontal
T25 MJC

14 Bibliografia Capítulo 12 até p 261 Capítulo 22-23
Artigos de Keystone pathogens (P.gingivalis e Filifactor allocis) Capítulo 33 T25 MJC