References

Socransky SS. Relationship of bacteria to the etiology of periodontal disease. J Dent Res. 1970; 49:203-222
Socransky SS, Haffajee AD. The bacterial etiology of destructive periodontal disease: current concepts. J Periodontol. 1992; 63:322-331
Grossi SG, Genco RJ, Machtei EE, Ho AW, Koch G, Dunford R Assessment of risk for periodontal disease. II. Risk indicators for alveolar bone loss. J Periodontol. 1995; 66:23-29
Clarke NG, Hirsch RS. Personal risk factors for generalized periodontitis. J Clin Periodontol. 1995; 22:136-145
Page RC, Sims TJ, Geissler F, Altman LC, Baab DA. Defective neutrophil and monocyte motility in patients with early onset periodontitis. Infect Immun. 1985; 47:169-175
Tal M. Periodontal disease and oral hygiene. Described by Antonic van Leeuwenhoek. J Periodontol. 1980; 51:668-669
Socransky SS, Haffajee AD, Smith C, Dibart S. Relation of counts of microbial species to clinical status at the sampled site. J Clin Periodontol. 1991; 18:766-775
Haffajee AD, Socransky SS. Microbial etiological agents of destructive periodontal diseases. Periodontol 2000. 1994; 5:78-111
Socransky SS, Haffajee AD, Cugini MA, Smith C, Kent RL Microbial complexes in subgingival plaque. J Clin Periodontol. 1998; 25:134-144
Ali RW, Skaug N, Nilsen R, Bakken V. Microbial associations of 4 putative periodontal pathogens in Sudanese adult periodontitis patients determined by DNA probe analysis. J Periodontol. 1994; 65:1053-1057
Grant DA, Flynn MJ, Slots J. Periodontal microbiota of mobile and non-mobile teeth. J Periodontol. 1995; 66:386-390
Mombelli A, Casagni F, Madianos PN. Can presence or absence of periodontal pathogens distinguish between subjects with chronic and aggressive periodontitis? A systematic review. J Clin Periodontol. 2002; 29:10-21
Duarte PM, Bastos MF, Fermiano D, Rabelo CC, Perez-Chaparro PJ, Figueiredo LC, Faveri M, Feres M. Do subjects with aggressive and chronic periodontitis exhibit a different cytokine/chemokine profile in the gingival crevicular fluid? A systematic review. J Periodontal Res. 2015; 50:18-27
Chapple IL, Genco R. Working Group 2 of Joint EFP/AAP Workshop. Diabetes and periodontal diseases: consensus report of the Joint EFP/AAP Workshop on Periodontitis and Systemic Diseases. J Clin Periodontol. 2013; 40:106-112
Angelopoulos AP, Goaz PW. Incidence of diphenylhydantoin gingival hyperplasia. Oral Surg Oral Med Oral Pathol. 1972; 34:898-906
Seymour RA, Thomason JM, Ellis JS. The pathogenesis of drug-induced gingival overgrowth. J Clin Periodontol. 1996; 23:165-175
Ellis JS, Seymour RA, Steele JG, Robertson P, Butler TJ, Thomason JM. Prevalence of gingival overgrowth induced by calcium channel blockers: a community-based study. J Periodontol. 1999; 70:63-67
Calsina G, Ramón JM, Echeverría JJ. Effects of smoking of periodontal tissues. J Clin Periodontol. 2002; 29:771-776
Martinez-Canut P, Lorca A, Magán R. Smoking and periodontal disease severity. J Clin Periodontol. 1995; 22:743-749
Breivik T, Thrane PS, Murison R, Gjermo P. Emotional stress effects on immunity, gingivitis and periodontitis. Eur J Oral Sci. 1996; 104:327-334
Armitage GC. The complete periodontal examination. Periodontol 2000. 2004; 34:22-33
Miller SC.Philadelphia: P Blakiston's Son & Co Inc; 1938
Hamp SE, Nyman S, Lindhe J. Periodontal treatment of multirooted teeth. Results after 5 years. J Clin Periodontol. 1975; 2:126-135
Davies SJ, Gray RJ, Linden GJ, James JA. Occlusal considerations in periodontics. Br Dent J. 2001; 191:597-604
Armitage GC, Cullinan MP. Comparison of the clinical features of chronic and aggressive periodontitis. Periodontol 2000. 2010; 53:12-27
Armitage GC. Periodontal diagnoses and classification of periodontal diseases. Periodontol 2000. 2004; 34:9-21
Armitage GC. Development of a classification system for periodontal diseases and conditions. Ann Periodontol. 1999; 4:1-6

Diagnosis and management of chronic and aggressive periodontitis part 1: periodontal assessment and diagnosis

From Volume 44, Issue 4, April 2017 | Pages 306-315

Authors

Despoina Chatzistavrianou

DDS MFDS RCSEd, MClinDent Pro, MPros RCSEd

Specialist in Prosthodontics, Specialty Registrar in Restorative Dentistry, Birmingham Dental Hospital and University of Birmingham School of Dentistry, Birmingham Community Healthcare NHS Trust, Birmingham, UK

Articles by Despoina Chatzistavrianou

Fiona Blair

BDS, LDS, FDS(Rest) RCPS, MSc, DRD, MRD

Consultant in Restorative Dentistry, Birmingham Dental Hospital, St Chad's Queensway, Birmingham B4 6NN, UK

Articles by Fiona Blair

Abstract

Periodontal disease remains one of the most common diseases that affect the oral cavity. The differential diagnosis between chronic and aggressive periodontitis can be complex for some clinicians and the correct diagnosis is a key element in disease management. The three-part series will review periodontal clinical assessment and diagnosis, periodontal management and finally will discuss two clinical cases. This paper will focus on periodontal disease pathogenesis, periodontal clinical assessment and diagnosis.

CPD/Clinical Relevance: This paper aims to provide the general dental practitioner with an understanding of periodontal disease pathogenesis and to highlight elements in the clinical assessment which will help to establish the diagnosis.

Article

Periodontal disease is a complex inflammatory disease that affects the periodontal structures, including the gingiva, cementum, periodontal ligament and alveolar bone.1 Both chronic and aggressive periodontitis are plaque-related diseases initiated by bacteria (Figure 1).2 The host response, genetic predisposition and environmental risk factors do not initiate periodontal disease, however, can influence the extent and severity of periodontal disease (Table 1,Figure 2).3,4,5,6

Subgingival plaque consists of a large and complex bacterial mixture of 400 or more species; certain bacterial combinations, under specific circumstances, can promote periodontal tissue breakdown.7 The bacterial species involved in the initiation and progression of periodontal disease have been classified based on their pathogenicity and grouped into complexes (Figure 3).8

Register now to continue reading

Thank you for visiting Dental Update and reading some of our resources. To read more, please register today. You’ll enjoy the following great benefits:

What's included

  • Up to 2 free articles per month
  • New content available