Evaluation of clinical and microbiological measures to predict treatment response in severe periodontitis

Robertson, Paul B.; Buchanan, S.; Armitage, Gary C.; Newbrun, Ernest; Taggart, Edward J.; Hoover, Charles I.

doi:10.1111/j.1600-0765.1987.tb01576.x

Cited by 13 publications

(8 citation statements)

References 9 publications

(8 reference statements)

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“…Generally, the diagnosis of periodontal disease is based on the presence and extent of gingival inflammation, frequently measured as BOP, 3 PD, 4‐6 CAL, 7,8 and the pattern and extent of alveolar bone loss assessed radiographically. In addition, consideration may be given to age, gingival recession, tooth mobility, medical and dental histories, previous treatment, and signs and symptoms, including pain, ulceration, and microbial deposits 9 .…”

Section: Measurement Of Inflammation Probing Depth (Pd) Clinical Atmentioning

confidence: 99%

Case Definitions for Use in Population‐Based Surveillance of Periodontitis

Page

Eke

2007

Journal of Periodontology

1,222

1,445

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Many definitions of periodontitis have been used in the literature for population-based studies, but there is no accepted standard. In early epidemiologic studies, the two major periodontal diseases, gingivitis and periodontitis, were combined and considered to be a continuum. National United States surveys were conducted in 1960 to 1962, 1971 to 1974, 1981, 1985 to 1986, 1988 to 1994, and 1999 to 2000. The case definitions and protocols used in the six national surveys reflect a continuing evolution and improvement over time. Generally, the clinical diagnosis of periodontitis is based on measures of probing depth (PD), clinical attachment level (CAL), the radiographic pattern and extent of alveolar bone loss, gingival inflammation measured as bleeding on probing, or a combination of these measures. Several other patient characteristics are considered, and several factors, such as age, can affect measurements of PD and CAL. Accuracy and reproducibility of measurements of PD and CAL are important because case definitions for periodontitis are based largely on either or both measurements, and relatively small changes in these values can result in large changes in disease prevalence. The classification currently accepted by the American Academy of Periodontology (AAP) was devised by the 1999 International Workshop for a Classification of Periodontal Diseases and Conditions. However, in 2003 the Centers for Disease Control and Prevention and the AAP appointed a working group to develop further standardized clinical case definitions for population-based studies of periodontitis. This classification defines severe periodontitis and moderate periodontitis in terms of PD and CAL to enhance case definitions and further demonstrates the importance of thresholds of PD and CAL and the number of affected sites when determining prevalence.

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Section: Measurement Of Inflammation Probing Depth (Pd) Clinical Atmentioning

confidence: 99%

Case Definitions for Use in Population‐Based Surveillance of Periodontitis

Page

Eke

2007

Journal of Periodontology

1,222

1,445

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“…Antibody data and data from the treatment of A. actinomycetemcomitans-infected patients with adult or refractory periodontitis provide the most convincing evidence of a possible etiological role of A. actinomyceterncomitans in adult forms of periodontal disease. Thirty-six of 56 adults with destructive periodontal disease examined at multiple time periods at Forsyth Dental Center exhibited an elevated 3,56,58,68,80,119,138,193,224,242,243,245,273,349,351,353,358,380,401,402,415,428,437,442,449,464,465,467 Lower in sites of health or gingivitis and in eden- 56, 169,242,245,327,349,350, 362, 380, 442, tulous subjects 454, 467 Elevated in active lesions 80,81,437 Detected in tissues or cells from lesions 78,320 Elimination resulted in successful therapy 4,64,136,137,170,192,225,276,300,307,359,361,373,379,429,437,459 Recurrent lesions harbored...…”

Section: Suspected Periodontal Pathogensmentioning

confidence: 99%

Microbial etiological agents of destructive periodontal diseases

Haffajee

Socransky²

1994

Periodontology 2000

1,431

1,127

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modulation by Actinobacillus actinomycetemcomitans. I. Chemotaxis, surface receptor expression and F-actin polymerization. J Periodont Res 1992: 27: 264-273. Ashkenazi M, White RR, Dennison DK. Neutrophil modulation by Actinobacillus actinomycetemcomitans. 11. Phagocytosis and the development of respiratory burst. J Periodont Res 1992: 27: 457-465. Ashley FP, Gallagher J, Wilson RE The occurrence of Actinobacillus actinornyceterncornitans, Bacteroides gingiualis, Bacteroides intermedius and spirochaetes in the subgingival microflora in relation to the early onset of periodontitis in a group of adolescents. Oral Microbiol Immunol 1989: 4: 236-238. Asikainen S. Occurrence of Actinobacillus actinomycetemcomitans and spirochetes in relation to age in localized juvenile periodontitis. J Periodontol 1986: 57: Asikainen S, Alaluusua S, Kari K, Kleemola-Kujala E. Subgingival microflora and periodontal conditions in healthy teenagers. J Periodontol 1986: 57: 505-509. Asikainen S, Jousimies-Somer H, Kanervo A, Saxen L. Actinobacillus actinomycetemcomitans and clinical periodontal status in Finnish juvenile periodontitis patients. J Periodontol 1986: 57: 91-93. Asikainen S, Jousimies-Somer H, Kanervo A, Summanen €? Certain bacterial species and morphotypes in localized juvenile periodontitis and in matched controls. J Periodontol 1987: 58: 224-230. Asikainen S, Lai CH, Alaluusua S, Slots J. Distribution of Actinobacillus actinomycetemcomitans serotypes in periodontal health and disease. Oral Microbiol Immunol 1991: 6: 115-118. Astemborski JA, Boughman JA, Myrick PO et al. Clinical and laboratory characterization of early onset periodontitis. J Periodontol 1989: 60: 557-563. Baehni PC, Song M, McCulloch CA, Ellen RP Treponema denticola induces actin rearrangement and detachment of human gingival fibroblasts. Infect Immun 1992: 60: Baehni FI Tsai CC, McArthur W, Hammond BF, Taichman 540-547. 537-541. 3360-3368. Dent Res 1993: 72: 404 (abstr 2407). Bragd L, Dahlen G, Wikstrom M, Slots J. The capability of Actinobacillus actinomycetemcomitans, Bacteroides gingivalis and Bacteroides intermedius to indicate progressive periodontitis; a retrospective study. J Clin Periodontol 1987: 14: 95-99. Bramanti TE, Holt SC. Iron-regulated outer membrane proteins in the periodontopathic bacterium, Bacteroides gingivalis. Biochem Biophys Res Commun 1990: 166: Bramanti TE, Wong GG, Weintraub ST, Holt SC. Chemical characterization and biologic properties of lipopolysaccharide from Bacteroides gingivalis strains W50, W83 and ATCC 33277. Oral Microbiol Immunol 1989: 4: 183-192. Brill CB, Pearlstein LS, Kaplan M, Mancall EL. CNS infections caused by Eikenella corrodens. Arch Neurol 1982: Brondz I, Olsen I. Differentiation between Actinobacillus actinomycetemcomitans and Haemophilus aphrophilus based on carbohydrates in lipopolysaccharide. J Chromatogr 1984: 310: 261-272. Bulkacz J, Newman MG, Socransky SS, Scott DF. Phospholipase A activity of micro-organisms from dental plaque. Microbios Lett 1979: 10: 79-88.

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“…However, the literature contains different definitions of periodontitis. Severe periodontitis has been defined as four or more sites with PPD ≥ 4mm (Robertson et al 1987) or as eight or more teeth with attachment loss of ≥ 5mm (Moore et al 1982). Established periodontitis has been defined as the presence of CAL ≥ 6mm in two or more teeth and one or more sites with PPD ≥ 5mm.…”

Section: Definition Of Periodontitismentioning

confidence: 99%

Bacteraemia due to dental flossing

Crasta

Daly

Mitchell

et al. 2009

J Clinic Periodontology

114

105

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Aims: The aims of this study were to (1) investigate the incidence of bacteraemia following flossing in subjects with chronic periodontitis or periodontal health; (2) identify the micro‐organisms in detected bacteraemias; and (3) identify any patient or clinical factors associated with such bacteraemia. Material and Methods: Baseline blood samples were obtained from 30 individuals with chronic periodontitis (17 M:13 F, 29–75 years) and 30 with periodontal health (17 M:13 F, 28–71 years) following a non‐invasive examination. Each subject's teeth were then flossed in a standardized manner and blood samples obtained 30 s and 10 min. after flossing cessation. Blood samples were cultured in a BACTEC™ system and positive samples subcultured for identification. Results: Forty per cent of periodontitis subjects and 41% of periodontally healthy subjects tested positive for bacteraemia following flossing. Viridans streptococci, which are commonly implicated in infective endocarditis (IE), were isolated from 19% of positive subjects and accounted for 35% of microbial isolates. Twenty per cent of subjects had a detectable bacteraemia at 10 min. post‐flossing. No patient or clinical factors were significantly associated with post‐flossing bacteraemia. Conclusions: Dental flossing can produce bacteraemia in periodontally healthy and periodontally diseased individuals at a rate comparable with that caused by some dental treatments for which antibiotic prophylaxis is given to prevent IE.

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Evaluation of clinical and microbiological measures to predict treatment response in severe periodontitis

Cited by 13 publications

References 9 publications

Case Definitions for Use in Population‐Based Surveillance of Periodontitis

Case Definitions for Use in Population‐Based Surveillance of Periodontitis

Microbial etiological agents of destructive periodontal diseases

Bacteraemia due to dental flossing

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