01 INFECCIONES INGLES 13/12/05 11:38 Página 111 Bascones Martínez A, Figuero Ruiz E Periodontal diseases as bacterial infection Periodontal diseases as bacterial infection BASCONES MARTINEZ A* Bascones Martínez A, Figuero Ruiz E. Periodontal diseases as FIGUERO RUIZ E** bacterial infection. Av Periodon Implantol. 2005; 17, 3: 111-118. ABSTRACT The periodontal disease is conformed by a group of illnesses affecting the gums and dental support structures. They are caused by certain bacteria found in the bacterial plaque. These bacteria are essential to the onset of illness; however, there are predisposing factors in both the host and the microorganisms that will have an effect on the pathogenesis of the illness. Pe- riodontopathogenic bacterial microbiota is needed, but by itself, it is not enough to cause the illness, requiring the presence of a susceptible host. These diseases have been classified as gingivitis, when limited to the gums, and periodontitis, when they spread to deeper tissues. Classification of periodontal disease has varied over the years. The one used in this work was approved at the International Workshop for a Classification of Periodontal Diseases and Conditions, held in 1999. This study is an overview of the different periodontal disease syn- dromes. Later, the systematic use of antibiotic treatment consisting of amoxicillin, amoxicillin- clavulanic acid, and metronidazole as first line coadjuvant treatment of these illnesses will be reviewed. KEY WORDS Classification, periodontal illnesses, biofilm Publicado en Medicina y Patología Oral 2004; 9 Suppl:S92-107 Acepted for publication: April 2005 INTRODUCTION lis (Pg), Prevotella intermedia (Pi), and Tannerella forsythensis (Tf).These bacteria play an important role in the onset and subsequent development of perio- The term infection is used to refer to the presence and dontitis, participating in the formation of the perio- multiplication of microorganisms in the body (1). dontal pocket, connective tissue destruction, and alve- Periodontal disease is a group of illnesses located in olar bone resorption by means of an immunopathoge- the gums and dental support structures (ligament and nic mechanism. Once periodontitis has been establis- alveolar bone) and are produced by certain bacteria hed, an inflammatory infiltrate is formed consisting of encountered in subgingival plaque (Fig.1). The most different kinds of cells, such as macrophages and important and most prevalent anaerobic gram-negati- lymphocytes that will produce different cytokine ve bacteria in the subgingival area are Actinobaci-llus subtypes, biological mediators responsible for the actinomycetemcomitans (Aa), Porphyromonas gingiva- immunopathology of different illnesses (Table 1) * Catedrático de Medicina Bucal y Periodoncia. Departamento de Estomatología III. Facultad de Odontología. Universidad Complutense de Madrid. ** Licenciada en Odontología. Becaria del Programa Nacional de Formación de Profesorado Universitario del Ministerio de Educación, Cultura y Deporte. Alumna de doctorado. AVANCES EN PERIODONCIA/111 01 INFECCIONES INGLES 13/12/05 11:38 Página 112 Volumen 17 - Nº 3 - Diciembre 2005 TABLE 1.- INFECTIONS TABLE 2.- ORAL FLORA CHARACTERISTICS Polymicrobial (3-6 species) HIGHLY COMPLEX Mixtas (aerobic, facultative, anaerobic) -Heterogeneous -Multiple species ~ 300 species Non specific The same clinical manifestations, -Different ecosystems different aetiology -Abundant - Specific Opportunistic Dental plaque flora -Dynamic OPPORTUNISTIC (Fig.2). Most naturally occurring microorganisms grow on the surfaces in the form of biofilm; dental pla- and plaque control methods were reinstated. que is a good example of this. It is currently known Subsequently, in another longitudinal study carried that the phenotype expressed by the bacteria when out using beagles (dogs), Lindhe (6) (1973) demons- they grow on a surface differs from the phenotype trated experimental periodontitis. Under healthy con- they express when they grow planctonically. This is of ditions, the forces of bacterial aggression and host great clinical relevance, particularly due to the incre- resistance are balanced. When this equilibrium is ase in biofilm resistance to antimicrobial agents (2, 3). upset, be it because of an increase in the number and/ or virulence of the germs or because defences Biofilm is formed in several stages, beginning with are low, the disease emerges. The resulting illnesses the adsorption of host and bacterial molecules onto have therefore been classified as gingivitis, limited to the tooth surface in order to form the so-called acqui- the gum, and periodontitis, when they spread to red film, which allows the microorganisms that have underlying tissues, destroying the insertion of con- been passively transported there to interact by nective tissue to the cement and causing pocket for- means of the forces of attraction of Van der Waals and mation, alveolar bone resorption, tooth mobility and electrostatic forces of repulsion and attraction, the- ultimately leading to the loss of the tooth. When they reby creating a weak bond. This bond is later reinfor- interact with connective tissue, the bacteria provoke a ced by the appearance of strong interactions media- series of inflammatory and immunological reactions ted by specific molecules on the surface of the bacte- in the host that are translated into an accumulation of ria (adhesins) with the complementary receptors of cells associated with the activation of periodontal the dental film itself. Over time, the phenomena of co- destruction processes. Longitudinal studies suggest aggre-gation of new colonizers and multiplication that the disease progresses episodically and is cha- enable the bacteria to adhere firmly to the dental sur- racterized by dormant phases followed by exacerba- face (2, 3). The clinical expression of the different tion, resting during the dormant periods and subse- periodontitis syndromes will depend on the interac- quent tissue destruction during active stages. These tion between host-related factors, the environment periods of periodontal destruction are associated and the microbiological agents. A favourable envi- with various changes in the cell population that con- ronment plus positive genetic factors will determine firms the inflammatory infiltrate located in the sube- an individual_s susceptibility; furthermore the var- pithelial connective tissue (neutrophiles, macropha- ying degrees of severity of the clinical syndromes, ges, lymphocytes, plasma cells, etc.) (7). Starting in rate of progression, relapse, and the random respon- the 90s, the hypothesis has been put forth that predis- se to treatment will also play a key role. posing factors in the host (such as the lack of oral Periodontopathogenic bacterial microbiota is there- hygiene, age, systemic factors such as smoking, dia- fore necessary, but not sufficient on its own for the betes, genetic vulnerability, immunological altera- disease to emerge; a susceptible host must also be tions, etc.) play a key role in the pathogenesis of present (4). Epidemiological studies have demonstra- periodontal illness, as well as microbial factors that ted a significant association between the severity of influence the periodontal pathogenicity of the germs periodontal illnesses, the amount of dental plaque involved (such as specific bacterial adhesion fac- and the degree of oral hygiene, with a cause and tors). At birth, the oral cavity is sterile, although bac- effect relationship between the formation and accu- terial colonization quickly begins, creating the so- mulation of dental plaque and the development of called oral microbial flora or microbiota, where aero- gingivitis. In this regard, Löe_s studies (5) (1965) on bic, strictly anaerobic (65%), saprophytic and patho- experimental gingivitis conducted in Denmark are genic species all coexist. The natural balance (eubio- important. These studies demonstrated a significant sis) can be upset by exogenous or endogenous fac- association between the accumulation of bacterial tors, thereby leading to disease (dysbiosis). Bacterial plaque and gingivitis over the 21 days during which plaque located in the gingival margin (supra and sub- the experiment was carried out. The clinical manifes- gingival) is what triggers the illness; subgingival pla- tations of gingivitis disappeared when oral hygiene que is responsible to a greater degree since it has 112/AVANCES EN PERIODONCIA 01 INFECCIONES INGLES 13/12/05 11:38 Página 113 Bascones Martínez A, Figuero Ruiz E Periodontal diseases as bacterial infection TABLE 3.- CLASSIFICATION OF THE TABLA 4.- CLASSIFICATION WORLD WORKSHOP, 1989 EUROPEAN WORKSHOP, 1993 A. GINGIVITIS A. PRIMARY DESCRIPTORS a. Dental plaque-induced gingival diseas a. Adult periodontiti b. Acute necrotizing ulcerative gingivitis (ANUG). b. Early-onset periodontitis c. Steroid hormone-induced gingivitis. c. Necrotising ulcerative periodontitis d. Drug-induced gingival enlargements. e. Gingivitis associated with blood disorders, nutritional B. SECONDARY DESCRIPTORS a. Tooth distribution. déficits, tumors, genetic factors, viral infections. b. Rate of progression. f. Gingivitis descamativa. c. Treatment response. d. Associated with systemic diseases. B. PERIODONTITIS e. Microbiological characteristics. a. Adult periodontitis. f. Ethnicity. b. Early-onset periodontitis: g. Other factors. i. Prepuberal periodontitis: 1.1. Localized hough they present a series of shortcomings. For 2.2. Generalized example, in the classification