Nueva Clasificación de enfermedades periodontales y periimplantarias PDF

Nueva Clasificación de enfermedades periodontales y periimplantarias 01. Salud periodontal y gingivitis Orientación para clínicos El sistema de clasificación de 1999 fue el primero en reconocer la necesid...

Nueva Clasificación de enfermedades periodontales y periimplantarias 01. Salud periodontal y gingivitis Orientación para clínicos El sistema de clasificación de 1999 fue el primero en reconocer la necesidad de clasificar las enfermedades y condiciones gingivales, pero su enfoque contenía muchos defectos. No definía “salud” y la descripción de la gingivitis era innecesariamente compleja. La Nueva Clasificación del World Workshop de 2017 ofrece una definición clara, tanto histológica como clínica, de salud periodontal. También simplifica la definición de gingivitis, agrupándola en dos categorías: gingivitis inducida por biofilm de placa bacteriana y enfermedades gingivales no inducidas por biofilm de placa bacteriana. La salud gingival clínica es definida tanto en un periodonto intacto como en un periodonto reducido, mientras que la salud/estabilidad es definida para un paciente con periodontitis tratado con éxito. Fecha de publicación: Marzo 2019 (documento original en Inglés) Fecha de publicación: Julio 2019 (documento traducido a Español) Traducido por: European Federation of Periodontology © European Federation of Periodontology  Nueva Clasificación de enfermedades periodontales y periimplantarias 01. Salud periodontal y gingivitis Orientación para clínicos El sistema de clasificación de 1999 fue el primero en reconocer la necesidad de clasificar las enfermedades y condiciones gingivales, pero su enfoque contenía muchos defectos. No definía “salud” y la descripción de la gingivitis era innecesariamente compleja. La Nueva Clasificación del World Workshop de 2017 ofrece una definición clara, tanto histológica como clínica, de salud periodontal. También simplifica la definición de gingivitis, agrupándola en dos categorías: gingivitis inducida por biofilm de placa bacteriana y enfermedades gingivales no inducidas por biofilm de placa bacteriana. La salud gingival clínica es definida tanto en un periodonto intacto como en un periodonto reducido, mientras que la salud/estabilidad es definida para un paciente con periodontitis tratado con éxito. Autor Iain Chapple + info en www.sepa.es Orientación para clínicos 3  Nueva Clasificación de enfermedades periodontales y periimplantarias Introducción Las enfermedades periodontales humanas abarcan un amplio espectro de condiciones. Algunas de ellas están relacionadas con el biofilm de placa bacteriana mientras que otras aparecen independientemente del acúmulo de biofilm y pueden ser modificadas por el biofilm o no ser influidas por él. El sistema de clasificación de 1999 fue el primero en reconocer una necesidad de clasificar las enfermedades gingivales. Pero tenía muchos defectos. Dentro de su clasificación de las condiciones gingivales se encuentran algunas rarezas, como la “gingivitis asociada a diabetes mellitus” y la “gingivitis por déficit de ácido ascórbico”, que inducen a error (la “gingivitis por déficit de ácido ascórbico”, por ejemplo, no existe – en realidad, se refiere al escorbuto o ulceraciones gingivales causadas por déficit de ascorbato). En este sistema no se intentó definir “salud”, lo que claramente es un factor crítico al intentar establecer definiciones de caso de una enfermedad. Y la descripción Una decisión de la gingivitis era innecesariamente compleja, ya que integraba tanto factores fundamental predisponentes como modificadores en el diagnóstico. está relacionada En el contexto de estas limitaciones de la clasificación de 1999, el Grupo de con el concepto Trabajo 1 del World Workshop de 2017 decidió crear una definición clara de salud periodontal, tanto a nivel histológico como clínico. Asimismo, adoptó una de salud metodología reduccionista para permitir definir gingivitis según únicamente dos “prístina” categorías principales: (1) gingivitis inducida por biofilm de placa bacteriana dental y (2) enfermedades gingivales no inducidas por biofilm de placa bacteriana. versus “clínica” Definiendo la salud periodontal Un factor crítico a la hora de definir la salud fue reconocer que puede existir salud periodontal a nivel localizado y a nivel de boca completa, así como en un periodonto intacto o reducido. Un periodonto intacto es aquel que no presenta pérdida de inserción clínica (PIC/CAL) o pérdida ósea, mientras que un periodonto reducido puede aparecer en dos situaciones independientes: bien en un paciente sin periodontitis (por ejemplo, pacientes con alguna forma de recesión gingival o después de una cirugía de alargamiento coronario) o en un paciente con antecedentes de periodontitis. Por ello, se establecieron definiciones de caso de salud y gingivitis para las tres situaciones, en los términos descritos a continuación. Otra decisión fundamental está relacionada con el concepto de salud “prístina” versus “clínica”. Dado que en Medicina la normalidad es definida como el encaje del 95% de la población con esa definición, y que el 95% de los adultos tienen uno o más puntos de sangrado en sus bocas, el término “salud” tiene que aceptar algunas zonas localizadas con inflamación ligera. La literatura ha evidenciado que se producen cambios histológicos en la microvasculatura gingival casi inmediatamente después de la erupción dentaria y que existe un infiltrado inflamatorio evidente como parte de un sistema de defensa inmunológico normal. Lo mismo es aplicable a signos clínicos inflamatorios sutiles en zonas aisladas como parte de la “salud clínica”. La salud prístina, por tanto, puede ser considerada como algo excepcional y limitado en gran medida a los libros de texto ( 25 g,105,121,122 with the average maximum probing force re‐ on the full‐mouth evaluation of all sites available for examination. ported to be in the 50‐ to 70‐g range,122 such differences in force magnitude have been shown to result in consistent but moderate Biomarkers in oral fluids changes in BOP prevalence. For example, the mean BOP response when a 25‐ and a 50‐g probing force were applied varied by 3 to 16 With increasing knowledge of gingivitis pathophysiology, specific bio‐ percentage points, depending on patient status (pre‐ or post‐treat‐ markers detected in oral fluids have emerged as potential candidates ment, high or low BOP tendency) and study.117‒119 The lack of infor‐ to help characterize and thus define a GC. Among the most promising mation in the literature on the prevalence of patients who fall within biomarkers are inflammatory cytokines, indicators of the inflamma‐ a particular mean BOP range given a specific probing force applied, tory host response, which can be recovered from GCF and saliva.142,143 combined with the fact that the aforementioned studies were based on a limited number of participants (10 to 12), makes it difficult to GCF proteomics fully ascertain the true impact of the probing force on the catego‐ Although several studies have investigated GCF proteomics under rization of patients based on their BOP response. Nevertheless, conditions of gingival inflammation, most of them concentrated on further review of the data reported from patients with optimal oral the healthy‐inflamed transition at specific sites. Proteomic analyses hygiene118,119 suggests that use of a 25‐g force results in a majority conducted on GCF obtained from healthy sites (i.e., sites with GI = 0, (∼70%) of these patients having a BOP response of ≤10%. PD ≤ 3 mm, attachment loss ≤1.5 mm) of periodontally healthy sub‐ jects showed that GCF proteomics is rather complex, consisting of Methods to assess gingival bleeding: full‐mouth vs. partial‐ approximately 200 distinct proteins, 57% of which were identified mouth assessment also in plasma and 43% were apparently not plasma related.144 This Although a comprehensive periodontal examination is generally clearly indicates that even though serum contributes to GCF com‐ based on the examination of all teeth at mesio‐buccal, mid‐buccal, position, GCF is an oral fluid with a distinctive proteomic profile. disto‐buccal, mesio‐lingual, mid‐lingual, disto‐lingual (MB‐B‐DB‐ Moreover, this quantitative analysis of GCF showed that the domi‐ ML‐L‐DL) surfaces,132 a partial mouth examination protocol (based nant proteins in conditions of periodontal health were intracellular on a minimum number of selected quadrants, teeth and sites repre‐ and nucleotide proteins (25%) and hydrolytic enzymes (19%).144 sentative of the entire dentition) would be highly desirable for both Under experimental gingivitis conditions, the GCF proteomic pro‐ patients and oral health professionals. file of inflamed sites showed substantial changes when compared to At present, however, the everyday clinical application of a par‐ that observed in periodontal health. In particular, only 28 proteins tial‐mouth examination protocol in defining the extent of gingival out of 186 identified at inflamed sites were found to be common inflammation remains limited by the following issues: 1) Available with those detected at healthy sites.145 validation data are not sufficient to identify the most accurate par‐ More recently, there has been a further attempt to character‐ tial‐mouth examination protocol. Although the level of agreement ize the GCF profile of a patient with gingivitis (i.e., a patient with a between partial‐mouth and full‐mouth examination protocols in given amount of gingival inflammation and no attachment/bone loss) TA B L E 3 Studies comparing GCF biomarker levels in gingivitis and other periodontal conditions (i.e., health and periodontitis) S54 | Year of Sites for GCF Periodontal health (H): Gingivitis (G): case Periodontitis (P): case Authors publication Population assessment case definition definition definition Main results Ulker 2008 Recruited at the Faculty In the G group, GCF Not reported Not reported – No significant differences in the et al.146 of Dentistry, University of samples were levels of cystatin C, TNF‐α, and Gazi, Turkey collected from four IL‐1b between G and H. (G = 10, H = 25) maxillary upper incisors that were affected by gingivitis. Perozini 2010 Recruited at the Two randomly selected According to AAP 1999 According to AAP 1999 According to AAP 1999 In G, IL‐1b concentration was et al.147 University of Taubatè, teeth in each patient (systemically healthy (clinical signs of (clinical signs of inflamma‐ significantly lower compared to P Brazil with no history of inflammation without tion with attachment loss) and similar to H. ALP levels in G (P = 12, G = 12, H = 12) periodontal disease) attachment loss) were significantly lower than P and higher than H. Hardan 2011 Recruited at Temple 4 sites (1 per quadrant) No CAL loss No CAL loss ≥ 4 teeth (≥ 1 tooth in each GCF levels of hydrophobic et al.148 School University, US The sites were the most < 5 sites with GI = 2 ≥ 5 sites with GI = 2 quadrant) with ≥ 1 site aminoacids showed a significant (P = 23, G = 18, H = 32) representative of with CAL≥ 4 mm increase from healthy to G each condition. condition. No difference in GCF levels of sulfur compounds between H and G. Becerik 2012 Recruited at the School of Mesio‐buccal aspects of PD ≤3 mm Varying degrees of Aggressive P: IL‐11 total amount was significantly et al.149 Dentistry, Ege two anterior teeth No gingival recessions gingival inflammation CAL ≥5 mm and PD≥ 6 mm higher in Chronic P compared to University, Izmir, attributable to CAL ≤2 mm at ≥90% of on ≥8 teeth, at least 3 of G. No significant differences in Turkey periodontitis sites those are other than total amounts of IL‐1b, IL‐6, (Aggressive P = 20, CAL≤ 2 mm at ≥90% of Radiographic distance central incisors or first OSM, and LIF between G and Chronic P = 20, G = 20, sites between the CEJ and molars either P or H. H = 20) BOP score < 10% bone crest ≤3 mm Radiographic bone loss G had elevated OSM concentration Radiographic distance at > 90% of the ≥30% of the root length when compared to H, and between the CEJ and proximal tooth sites on affected teeth; significantly higher LIF concen‐ bone crest ≤3 mm Chronic P: tration than Aggressive P. No at > 90% of the CAL ≥5 mm and PD ≥6 mm significant differences in proximal tooth sites in multiple sites of all four concentration of IL‐1b, IL‐6, and quadrants of the mouth. IL‐11 between G and either P or Moderate‐to‐severe H. alveolar bone loss present on radiographs Gokul 2012 Recruited at the Not reported Clinically healthy Clinical signs of Clinical signs of inflamma‐ TNF‐α levels in G were significantly et al.150 Department of periodontium with inflammation with no tion with attachment loss higher than H, and similar to P. Periodontics, no evidence of evidence of attach‐ and radiographic bone Priyadarshini Dental disease ment loss and loss College & Hospital, (Ramfjord's Periodontal radiographic bone loss (Ramfjord's Periodontal Chennai, India Disease Index = 0) (Ramfjord's Periodontal Disease Index = 4–6) (P = 20, G = 20, H = 20) Disease Index = 1–3) TROMBELLI et al. (Continues) TA B L E 3 (Continued) Year of Sites for GCF Periodontal health (H): Gingivitis (G): case Periodontitis (P): case Authors publication Population assessment case definition definition definition Main results Ertugrul 2013 Recruited at the Faculty 4 sites in 4 Ramfjord No CAL > 2 mm BOoP score > 50% Aggressive P: IN G, CCL28, IL‐8, IL‐1b and TNF‐a TROMBELLI et al. et al.151 of Dentistry, Yuzuncu teeth in H and G No PD > 3 mm Radiographic distance 16–30 years of age levels Yil University, Turkey subjects BOP score < 15% between the CEJ and ≥ 20 natural teeth Were significantly higher compared (Aggressive P = 21, 4 BOP+ sites in 4 Radiographic distance bone crest < 3 mm ≥ 6 incisors and/or first to H and significantly lower Chronic P = 21, G = 21, Ramfjord teeth in G between the CEJ and at > 95% of the molars with ≥ 1 site with compared to Chronic P and H = 21) subjects bone crest < 3 mm proximal tooth sites PD and CAL > 5 mm Aggressive P. 4 BOP+ sites in 4 teeth at > 95% of the ≥ 6 teeth other than first showing the deepest proximal tooth sites molars and incisors with pockets in the ≥ 1 site with PD and chronic and CAL > 5 mm aggressive P subjects Chronic P: Inflammation in the gingiva Vertical and horizontal bone loss on radiographs PD≥ 5 mm in ≥ 6 sites of at ≥ 4 single‐rooted teeth with CAL≥ 4 mm Kinney 2014 Recruited at the Michigan Mesiobuccal aspect of 8 CAL < 3 mm CAL < 3 mm ≥ 4 sites with CAL > 3 mm GCF biomarkers associated with et al.152 Center for Oral Health sites. No PD > 4 mm No PD > 4 mm ≥ 4 sites with PD > 4 mm stable and progressing cases were Research clinic, Ann Site selection was BOP score ≤ 20% BOP score > 20% ≥ 4 sites with radiographic evaluated. Arbor, Michigan based on group No radiographic No radiographic alveolar bone loss (P = 44, G = 24, H = 15) classification (in alveolar bone loss bone loss patients without periodontitis, sites with PD less than 4 mm and/or CAL less than 3 mm were ranked higher; in patients with gingivitis, sites were ranked even higher if they had BOP). Huynh 2015 Patients attending the The sites chosen were PD≤ 3 mm BOP score > 5% ≥ 2 sites with PD≥ 5 mm Forty‐two proteins were considered et al.153 Royal Dental Hospital of the most representa‐ BOP score≤ 5% mGI≥ 1 BOP score≥ 5% to have changed in abundance. Of Melbourne and staff at tive of each condition. mGI < 1 PI ≥ 20% mGI≥ 1 note, cystatin B and cystatin S the Melbourne Dental PI < 20% No radiographic bone PI I≥20% decreased in abundance from H to School, Australia. loss radiographic bone loss G and further in P. Complement proteins demonstrated an increase from H to G followed by a decrease in P. | S55 (Continues)  S56 | TROMBELLI et al. (Table 3).146‒155 Overall, these studies indicate that the GCF pro‐ ALP: alkaline phosphatase; BOP: bleeding on probing; CAL: clinical attachment level; CCL28: mucosa‐associated epithelial chemokine; CEJ: cementum‐enamel junction; mGI: modified gingival index; IL‐1ß: interleukin 1ß; IL‐6: interleukin 6; IL‐8: interleukin 8; IL‐11: interleukin 11; IL‐35: interleukin 35; IL‐37: interleukin 37; LIF: leukemia inhibitory factor; OSM: oncostatin M; PD: probing depth; PI: Plaque Index; between G and either H or P. IL‐37 The IL‐37 total amount was similar IL‐35 levels in G were significantly teomic profile of gingivitis subjects is qualitatively and quantitatively lower in P compared to G and H. concentration was significantly lower than H and similar to P. different from that of periodontal health; more specifically, a greater number of proteins have been found in gingivitis compared to peri‐ odontal health.153 Moreover, the amount of some proteins (e.g., IL‐1b, ALP, complement factors, MMP‐9, fibronectin, lactotrans‐ ferrin precursors, alpha‐actinin) is higher in gingivitis compared to Main results periodontal health,147,153 while other proteins (e.g., cystatin‐B, cys‐ tatin‐S) are present in lower amounts in gingivitis.153 Despite these reported GCF proteomic differences between periodontal health and gingivitis, the overall paucity of data on the ≥ 50% alveolar bone loss in ≥ 50% alveolar bone loss in PD≥ 5 mm, CAL≥ 4 mm ≥ 4 teeth in each jaw with ≥ 4 teeth in each jaw with GCF proteomic profile of gingivitis subjects, along with the hetero‐ PD ≥ 5 mm and CAL ≥ Periodontitis (P): case geneity between studies in terms of GC definition (Table 3), site se‐ BOP score > 80% lection for GCF sampling, and GCF sampling methods, as well as the BOP score > 50% ≥ 2 quadrants ≥ 2 quadrants practical limitations in performing such an assessment chairside in daily practice, currently eliminate the possibility to use the GCF pro‐ definition 4 mm teomic profile as the basis for GC definition. Salivary proteomics between the CEJ and Radiographic distance Whole mouth saliva (WMS) is not only composed of major and minor bone crest≤ 2 mm Gingivitis (G): case salivary gland secretions but also contains mucosal transudates from BOP score≥ 20% BOP score≥ 20% all surfaces of the mouth, lymphoid tissues, oropharynx, and GCF. No CAL loss PD < 4 mm PD≤ 3 mm Saliva, a hypotonic aqueous solution that contains proteins, pep‐ definition tides, enzymes, hormones, sugars, lipids, growth factors and a va‐ riety of other compounds, has a complex composition.156 Proteomic studies on human saliva revealed > 1,000 proteins and peptides.143 between the CEJ and Periodontal health (H): Radiographic distance Some studies have characterized the salivary proteomic profile bone crest≤ 2 mm BOP score < 20% BOP score < 20% of gingivitis (i.e., a patient with a given amount of gingival inflamma‐ case definition tion and no attachment/bone loss) compared to periodontal health No CAL loss PD≤ 3 mm (Table 4).146,154,155,157‒160 The analyses showed that gingivitis was PD < mm associated with significantly increased amounts of blood proteins (serum albumin and hemoglobin), immunoglobulin peptides and ker‐ atins,158 PGE2 and MIP‐1α,160 and more than double the amounts of GI≥ 2 and PD≤ 3 mm; GI≤ 1 and PD≤ 3 mm; GI≥ 2 and PD≥ 5 mm selected according to In G: BOP+ sites with multirooted tooth. In P: BOP+ sites with In H: BOP‐ sites with the baseline clinical MMP‐8, MMP‐9, and IL‐6.157 In periodontal health, salivary cystatins 2 non‐adjacent sites 2 sites in 1 single‐ appeared to be more abundant.158 Similarly to GCF proteomics, the measurements rooted and 1 Sites for GCF use of salivary proteomics to identify a patient with gingivitis has assessment substantial limitations, mainly due to the heterogeneity in gingivitis definition among studies (Table 4), as well as the methodology used for proteomic profiling. Recruited at the Faculty (P = 20, G = 20, H = 20) (P = 20, G = 20, H = 20) Faculty of Dentistry, Izmir Katip Cxelebi of Dentistry, Izmir, Microbiologic markers University, Izmir, Periodontology, Department of Recruited at the From the earliest studies of Löe and coworkers, which established Population Turkey Turkey the bacterial etiology of gingivitis in the 1960s, 2,3 to investigations reported in the late 1990s,161‒165 the microbiological assessment TNF‐α: tumor necrosis factor α. of gingivitis (and periodontitis) was based on bacterial culture, and (Continued) morphological, biochemical and other targeted analyses of col‐ publication lected plaque samples. These studies identified several Gram‐posi‐ Year of 2015 2015 tive anaerobes (e.g., Actinomyces viscosus, Parvimonas micra (formerly Micromonas and Peptostreptococcus micros)), Gram‐positive facul‐ TA B L E 3 tative species (Streptococcus spp), and Gram‐negative anaerobes Köseoğlu et al.154 et al.155 Authors Saglam (e.g., Campylobacter gracilis, Fusobacterium nucleatum, Prevotella intermedia, Veillonella parvula) as associated with gingivitis,166 with TA B L E 4 Studies investigating salivary biomarker levels in gingivitis and other periodontal conditions (i.e., health and periodontitis) Year of Periodontal health (H): Gingivitis (G): Periodontitis (P): Authors publication Population case definition case definition case definition Main results 146 Ulker et al. 2008 Recruited at Faculty of Dentistry, University Not reported Not reported – No significant differences in cystatin C, TROMBELLI et al. of Gazi, Turkey TNF‐α and IL‐1ß levels between G and H (G = 10, H = 25) Ramseier 2009 Recruited at the Michigan Center for Oral CAL < 3 mm CAL < 3 mm ≥4 sites with G showed levels of MMP‐8 and MMP‐9 that et al.157 Health Research clinic, Ann Arbor, PD > 4 mm PD > 4 mm CAL > 3 mm were intermediate between H and P Michigan, US BoP score ≤20% BoP score > 20% ≥4 sites with (P = 49, G = 32, H = 18) No radiographic bone loss No radiographic PD > 4 mm bone loss ≥4 sites with radiographic bone loss Da R. 2011 Recruited at the School of Dentistry, Federal BOP score < 10% No CAL loss – G was associated with increased amounts of Goncalves University of Espirito Santo, Brazil PD < 3 mm BOP score > 50% serum albumin and hemoglobin, immuno‐ et al.158 (G = 10, C = 10) PD > 3 mm globulin peptides and keratins. Cystatins in > 50% of were more abundant in H sites Kinney 2011 Recruited at the Michigan Center for Oral CAL < 3 mm CAL < 3 mm ≥4 sites with Same cohort as Ramseier et al. 2009157. The et al.159 Health Research clinic, Ann Arbor, No PD > 4 mm No PD > 4 mm CAL > 3 mm paper focuses on the association of salivary Michigan, US No radiographic bone loss No radiographic ≥4 sites with biomarkers and periodontal disease (P = 41, G = 23, H = 15) BOP score ≤20% bone loss PD > 4 mm progression. BOP score > 20% ≥4 sites with radiographic bone loss Köseoğlu 2015 Recruited at the Department of No CAL loss No CAL loss ≥ 4 teeth in each jaw IL‐35 levels in G were significantly lower et al.154 Periodontology, Faculty of Dentistry, PD ≤3 mm PD ≤3 mm with PD ≥ 5 mm, than H and significantly higher than P Izmir Katip Cxelebi University, Izmir, BOP score < 20% BOP score ≥20% CAL ≥ 4 mm Turkey ≥ 50% alveolar bone (P = 20, G = 20, H = 20) loss in ≥ 2 quadrants BOP score > 50% Saglam 2015 Recruited at the Faculty of Dentistry, Izmir, PD < 4 mm PD < 4 mm ≥ 4 teeth in each jaw Similar levels of IL‐37 between H, G, and P et al.155 Turkey (G = 20, H = 20) BOP score < 20% BOP score≥20% with PD ≥ 5 mm Radiographic CEJ‐bone Radiographic and CAL ≥ 4 mm crest ≤ 2 mm CEJ‐bone BOP > 80% crest ≤2 mm ≥ 50% alveolar bone loss in ≥ 2 quadrants Syndergaard 2014 Recruited at the University of Kentucky No CAL ≥2 mm No CAL≥ 2 mm – Concentrations of MIP‐1α and PGE2 were et al.160 College of Dentistry, Kentucky, US PD ≤4 mm PD≤ 4 mm significantly (G = 40, H = 40) BOP score < 20% BOP score≥ 20% Higher (2.8 times) in G compared to H | BOP: bleeding on probing; CAL: clinical attachment level; CEJ: cementum‐enamel junction; IL‐1ß: interleukin 1ß; IL‐6: IL‐35: interleukin 35; IL‐37: interleukin 37; MIP‐1α: macrophage inflammatory protein 1α; MMP‐8: matrix metalloproteinase 8; MMP‐9: matrix metalloproteinase 9; PD: probing depth; PGE2: prostaglandin E2; TNF‐α: tumor necrosis factor α. S57 S58 | TROMBELLI et al. the flora becoming more diverse with time and the development inflammation were evaluated for their relationship with CRP levels 167 and progression of gingivitis. Efforts to identify microbiologic in serum. While in some studies CRP levels were found to be signifi‐ differences among persons with a stronger or weaker gingival in‐ cantly positively correlated with papillary bleeding index186 or GI,184 flammatory response to plaque accumulation did not find significant other authors failed to find an association between CRP levels and differences.161 Although quantitative differences were consistently GI,185 BOP,185,187 or the number of sextants with at least one BOP+ identified for targeted species among sites characterized by gingivi‐ site.188 Certain factors may have contributed to the heterogeneity 162‒164 tis and periodontitis or health, none of the associated bacterial among these findings. First, criteria for GC definition varied greatly species were unique to gingivitis and, therefore, their presence can‐ among studies. Second, control of potential confounders through not be considered pathognomonic. adequate statistical analyses (e.g., multivariate models) was applied The introduction in the late 90s of open‐ended molecular meth‐ only in some studies.187,188 Overall, the above mentioned findings ods and their application to the detection of microbes broadened seem to demonstrate that the inflammation of marginal gingival tis‐ significantly the spectrum of bacterial species associated with peri‐ sues determines an increase in systemic inflammation, assessed in odontal diseases, with many previously unidentified and/or unculti‐ terms of CRP levels. However, other studies have failed to demon‐ 168‒171 vated bacteria linked with periodontitis. In the last few years, strate potentially relevant systemic effects during gingivitis devel‐ these molecular techniques have been applied, along with novel sta‐ opment.189 Therefore, the relationship between severity of gingival tistical approaches, to the study of the biofilm associated with gingi‐ inflammation and severity of systemic inflammation in patients with vitis and compared to health and periodontitis.172‒177 These studies gingivitis remains unclear. have demonstrated that the transition from health to disease follows the principles of primary ecological succession, with change in abun‐ Genetic markers dances of indigenous species, rather than acquisition of newer organ‐ isms. Even as these studies identified previously unrecognized species Two specific pieces of information suggest that susceptibility to in gingivitis, they confirmed that the biofilms associated with gingivitis gingivitis may be genetically controlled.190,191 The first line of evi‐ and periodontitis share most species (albeit with quantitative differ‐ dence comes from studies of patients with Down syndrome. Despite ences). Emerging evidence suggests that clusters of bacteria, rather no differences in plaque accumulation rates, patients with Down than individual species, might be of use as diagnostic markers for each syndrome, compared to age‐ and sex‐matched genetically healthy disease; and that bacterial functions (e.g., proteolysis, flagellar assem‐ controls, exhibit more extensive gingival inflammation and at much bly, bacterial motility) may be a more robust discriminant of disease earlier times.192 The second line of evidence comes from studies on than species. While these early novel findings support a gene‐cen‐ twins. Michalowicz et al.193 studied monozygous and dizygous adult 178‒182 tric rather than a species‐centric approach to disease causation, twin pairs and reported that, based on ratios of within‐pair variances further studies are required to better characterize such bacterial clus‐ or heritability estimates, there was a significant genetic component ters and gene functions and to validate their potential use both as a for gingivitis and other clinical parameters. For gingivitis, in particu‐ diagnostic tool and as response to treatment monitoring tool.183 lar, they estimated from reared‐apart monozygous twins that 82% of the population variance may be attributed to genetic factors.193 These findings provide strong support for the role of genetic make‐ Systemic inflammation markers (CRP) up in gingivitis susceptibility. As for other chronic inflammatory diseases, the relationship be‐ Recent evidence is available evaluating whether genetic charac‐ tween periodontal diseases (including gingivitis) and systemic levels teristics, in general, and gene polymorphisms, in particular, may con‐ of inflammatory markers has been evaluated. The biologic mecha‐ tribute to exacerbated gingival inflammation in response to plaque nisms supporting the plausibility of this association rely on the entry accumulation. Since the host immune response is a dominant gene of pathogenic bacteria from the biofilm of periodontally diseased expression pathway during the onset and resolution of gingival in‐ sites into the blood stream and on the entry into the circulation of flammation, with several genes being significantly up‐ or downreg‐ excess local levels of host‐derived inflammatory mediators. ulated,194 particular emphasis has been placed upon evaluating the Among the investigated biomarkers, particular attention has potential association between cytokine gene polymorphisms and been paid to C‐reactive protein (CRP), which is produced in response gingival inflammation in either observational, cohort studies195‒200 to many forms of trauma or diseases and contributes to host defense or experimental gingivitis trials. 201‒204 Although the available evi‐ as part of the innate immune response. Studies that evaluated the dence suggests a role for some gene polymorphisms in determining association between gingivitis and serum levels of CRP universally the susceptibility to plaque‐induced gingival inflammation, defini‐ identified gingivitis as a condition characterized by serum CRP lev‐ tive associations between ≥1 genetic indicators and the severity of els which are intermediate between those measured in periodontal gingival inflammation are not yet available, in part because of the health and periodontitis, although differences in serum CRP levels limited number of gene loci investigated and the small number of observed between gingivitis and the other periodontal conditions subjects included in pertinent studies. 205 To date, a limited number 184‒186 did not consistently reach statistical significance in all studies. of studies have attempted to investigate the genetic profile of gin‐ In subjects with gingivitis, the severity and extent of gingival givitis and healthy cases (Table 5).197,200,206‒208 However, large‐scale  TROMBELLI et al. TA B L E 5 Case‐control studies investigating the association between gene polymorphisms and gingivitis (versus healthy controls) Year of Periodontal health (H): case Gingivitis (G): case Investigated gene Authors publication Population definition definition polymorphisms Main results 206 Dashash et al. 2006 248 whites Healthy gingiva Clinical evidence of IL‐10 ‐1082 The GCC/GCC genotype, which has been Aged 8 to 12 years And no evidence of bleeding gingivitis assessed by IL‐10 ‐819 associated with increased production of IL‐10, (G = 164, H = 84) on probing or clinical signs gingival and bleeding IL‐10 ‐592 was significantly more frequent in H than in G. of inflammation on probing indices Dashash et al.197 2007 146 whites Healthy gingiva and had Presence of IL‐1RN Significant association between IL‐1Ra genotype Aged 8 to 12 years Neither evidence of bleeding Bleeding on probing at and periodontal status (H vs G). The IL‐1RN*2 (G = 98, H = 48) on probing nor clinical signs any site, as deter‐ allele (A2) was significantly more frequent in H, of inflammation mined by gingival and and the carriage of A2 seemed to be protective papillary bleeding on against gingivitis. probing indices Holla et al. 207 2008 455 whites GI = 0 Total sum of GI values at IL‐6‐174 Significant differences in haplotype frequencies Aged 11 to 13 years At all 24 examined sites 24 examined sites≥ 4 IL‐6‐572 between G and H. The CGA haplotype was (G = 272, H = 183) IL‐6‐597 significantly more frequent in G than in H. The IL‐6 – 174C allele was more frequent in G than in H, and allele C remained a risk factor for G regardless of plaque or gender. Vokurka et al. 200 2009 298 whites GI = 0 Total sum of GI values at MMP‐9‐1562 The prevalence of MMP‐9‐1562 alleles was Aged 11 to 13 years At all 24 examined sites 24 examined sites≥ 4 IL‐18‐607 significantly higher in G compared to H. A highly (G = 147, H = 151) significant association of the composite genotype (formed by the variants of both genes) with G was found. Garlet et al. 208 2012 608 whites and BOP score < 10% BOP > 70% IL1B‐3954 Positive associations were found for IL6‐174, Afro‐American/ PD > 3 mm ≤ 1 tooth per sextant IL6‐174 IL10 ‐592 and TLR4‐299 Mulatto subjects CAL > 1 mm with CAL loss ≤1 mm TNFA‐308 (P = 197, G = 193, No history of tooth loss IL10 ‐592 H = 218) due to periodontitis TLR4‐299 a BOP: bleeding on probing; CAL: clinical attachment level; gingival index; IL‐1: interleukin 1; IL‐1RA: interleukin 1 receptor antagonist; IL‐6: interleukin 6; IL‐10: interleukin 10; MMP‐9: matrix metallopro‐ teinase 9; TNF: tumor necrosis factor. | S59 S60 | TROMBELLI et al. genome‐wide association studies hold promise for the identification perception of a condition‐specific (CS) impact was limited to 27.1% of genetic variations that are significantly associated with severe of subjects. Specificity with respect to individuals with no CS‐impact gingival inflammation. 209 among periodontally healthy subjects was 0.83. Similarly, in a sam‐ Emerging evidence indicates that the inflammatory response ple of 1,100 12‐year old and 871 15‐year old Thai children, 1 mm) upon the obser‐ A recent systematic review 2 reported clinical observations sug‐ vation of the periodontal probe visible through the gingiva. This gesting that sites with minimal or no gingiva associated with intra‐ method was found to have a high reproducibility by De Rouck et sulcular restorative margins are more prone to gingival recession al, 22 showing 85% inter‐examiner repeatability (k value = 0.7, P‐ and inflammation. The authors concluded that gingival augmen‐ value = 0.002). The authors scored GT as thin, medium, or thick. tation is indicated for sites with minimal or no gingiva that are Recently, a color‐coded probe was proposed to identify four gin‐ receiving intra‐crevicular restorative margins. However, these gival biotypes (thin, medium, thick and very thick). 23 conclusions are based mainly on clinical observations (low level of evidence). Keratinized tissue width is easily measured with a periodontal probe positioned between the gingival margin and the mucogingival The impact of orthodontics junction. There is a possibility of gingival recession initiation or progres‐ Although bone thickness assessment through CBCT has high di‐ sion of recession during or after orthodontic treatment depend‐ agnostic accuracy12,13,24 the exposure to radiation is a potentially ing on the direction of the orthodontic movement. 30,31 Several harmful factor. authors have demonstrated that gingival recession may develop during or after orthodontic therapy. 32‒36 The reported prevalence is spanning 5% to 12% at the end of treatment. Authors report an Gingival recession increase of the prevalence up to 47% in the long‐term observation Gingival recession is defined as the apical shift of the gingival margin (5 years). However, it has been demonstrated that, when a facially with respect to the cemento‐enamel junction (CEJ);1 it is associated positioned tooth is moved in a lingual direction within the alveolar with attachment loss and with exposure of the root surface to the process, the apico‐coronal tissue dimension on its facial aspect oral environment. Although the etiology of gingival recessions re‐ will increase in width. 37,38 A recent systematic review 2 concluded mains unclear, several predisposing factors have been suggested. that the direction of the tooth movement and the bucco‐lingual thickness of the gingiva may play important roles in soft tissue Periodontal biotype and attached gingiva alteration during orthodontic treatment. There is a higher prob‐ A thin periodontal biotype, absence of attached gingiva, and re‐ ability of recession during tooth movement in areas with 1 mm. En relación el biotipo periodontal en 2 tipos: biotipo fino, compuesto a esto último, un reciente estudio realizado por Sharma por encía fina, festoneada, de apariencia delicada y trans- et al.11 , mediante el uso de un calibrador de Vernier modi- lúcida, asociada a dientes de forma cónica y triangular, ficado estableció que la encía adherida presenta un grosor y biotipo grueso, caracterizado por una encía voluminosa, de 0,56 a 1,02 mm, siendo las mujeres quienes presentaban abultada, con festoneado plano de apariencia densa y fibró- menores grosores. En el último tiempo, el tamaño en las tica, asociada a dientes con predominio del ancho sobre diferentes zonas de la mucosa masticatoria, así como el gro- el largo coronario1. La inspección visual consiste en eva- sor gingival, han provocado gran interés desde el punto de luar la arquitectura de los tejidos periodontales para definir vista epidemiológico y terapéutico5. Numerosos estudios3,5,9 si pertenecen a un biotipo delgado o grueso, siendo un han concluido que el espesor de encía juega un rol funda- método subjetivo, ya que depende de la observación de mental en el desarrollo de patologías mucogingivales y el cada clínico3. Eghbali et al.4 evaluaron la precisión de este éxito de la terapia periodontal. Müller et al.8 observaron método con distintos operadores, encontrando que solo la que pacientes con enfermedad periodontal y biotipo grueso mitad de ellos lograron determinar el biotipo periodontal presentaban sacos periodontales de mayor profundidad que de forma certera, con mayor porcentaje de error en pacien- los pacientes con biotipo fino, quienes, a diferencia de los tes que presentaban un biotipo fino4,5. La determinación del primeros, presentaban recesiones gingivales. Lee et al.5 biotipo gingival a través de la transparencia de la sonda evaluaron el biotipo a través de modelos tridimensiona- dentro del surco gingival es el método más utilizado hoy les. Utilizaron el escaneo de modelos de yesos en 133 en día, puesto que ha demostrado ser sencillo y eficaz al pacientes midiendo el área vestibular de la papila inter- momento de evaluar el espesor gingival3. Kan et al.9 postu- dental, la superficie facial de los 2 incisivos centrales laron que la visualización de la sonda a través del margen superiores, el ancho y el ángulo de papila interdental. Sus gingival indicaba un biotipo delgado, y si este no era visible, conclusiones apuntan a que la suma de las áreas de las super- se asociaba a un biotipo grueso. Además, se reportó que este ficies papilares de canino a canino es la mejor forma para 194 M. Navarrete et al. Figura 1 Biotipo periodontal medido mediante parámetros visuales: a) biotipo grueso; b) biotipo fino. determinar el biotipo gingival, aseverando incluso que este Odontología de la Universidad Andrés Bello sede Viña del método es más apropiado que el propuesto por Kan et al.9. Mar, que cursaron cuarto, quinto o sexto año durante 2013. Fu et al.6 utilizaron cone-beam para clasificar el biotipo gin- La selección de los pacientes se efectuó por conveniencia, gival, concluyendo que no existen diferencias significativas en base a los siguientes criterios de inclusión: profundi- al determinarlo clínica o radiográficamente. Además, obser- dad de sondaje ≤ 3 mm, sin pérdida de inserción, índice varon que la tomografía computarizada era un método fiable de higiene oral ≥ 80%, sangrado al sondaje ≤ 15% y presen- y exacto en la medición del biotipo, ya que mide tejido cia de al menos 6 dientes anterosuperiores. Toda persona blando por alteración del contraste de la imagen y tejido incluida en este estudio firmó un consentimiento informado, duro, representado por hueso alveolar6. Posteriormente el cual fue aprobado por el Comité de Ética e Investiga- Cook et al.7 evaluaron mediante cone-beam diferencias en ción de la Universidad Andrés Bello, sede Viña del Mar. el grosor de la cortical vestibular de biotipos periodontales Las mediciones fueron realizadas por un solo clínico, cali- clasificados como finos o gruesos, concluyendo que el biotipo brado previamente por un especialista, mediante el índice gingival se relaciona con la posición de la cresta ósea, el gro- kappa (␬), cuya fuerza de concordancia fue de 0,66 intere- sor de cortical vestibular y el ancho de tejido queratinizado. xaminador y 0,70 (␬) en la calibración intraexaminador. Los Estos resultados respaldan los datos reportados por Fu et al.6 instrumentos utilizados se calibraron de la siguiente forma: respecto a presentar al cone-beam como un método certero en la regla milimetrada se constató que entre reglones exis- en la determinación del biotipo gingival7. Por otra parte, se tiera 1,00 mm, mediante pie de metro digital; la sonda han utilizado dispositivos ultrasónicos para clasificar bioti- Florida® posee un sistema de calibración electrónica, el cual pos gingivales, siendo escasos los estudios al respecto. Uno se activa previo a su uso; lima de endodoncia tipo K #20 de ellos fue realizado por Müller et al.8 , quienes mediante (Dentsply, Maillefer EE. UU.), calibrada mediante nomencla- un dispositivo de medición ultrasónica denominado SDM® tura ISO, y sonda periodontal Fox Williams (American Eagle, determinaron el espesor de la encía masticatoria. La vali- Montana, EE. UU.), calibrada por el fabricante. Siete días dez y la reproducibilidad de las medidas mostraron ser del previos a la medición de las variables se realizó instruc- 95%, comportándose como un método poco invasivo y fiable. ción de higiene oral, y los datos obtenidos se registraron Sin embargo, el instrumento presenta limitaciones respecto en una ficha clínica. Las variables medidas fueron: género, a no entregar información si el grosor de encía adherida edad y biotipo gingival mediante distintos métodos. Al uti- supera los 2,5 mm. Además, los resultados pueden ser alte- lizar parámetros visuales se asignó a los pacientes una de rados si la angulación del aparato es incorrecta y su costo es las siguientes categorías: biotipo gingival festoneado fino, elevado4,5. Finalmente, teniendo en cuenta que la correcta al presentar apariencia delicada, es decir, encía delgada, clasificación del biotipo es importante en el diagnóstico y frágil y prácticamente traslúcida, y biotipo gingival plano el tratamiento de patologías orales y sus secuelas, junto a grueso, caracterizado por una apariencia de encía densa y la falta de consenso respecto a las dimensiones adecuadas fibrótica (fig. 1). La determinación del biotipo utilizando la de tejidos gingivales para determinar el biotipo, surge la transparencia de la sonda periodontal se realizó mediante el necesidad de investigar, teniendo como objetivo comparar sondaje del surco gingival en la zona media vestibular de los distintos métodos de evaluación del biotipo gingival y corre- dientes 1.1, 1.2 y 1.3, con sonda periodontal Fox Williams lacionarlos con la medición directa de grosor y ancho de (American Eagle, Montana, EE. UU.). La denominación bio- encía adherida en zona estética del maxilar superior. tipo fino se estableció al observar el contorno de la sonda subyacente a través de la encía, y biotipo grueso cuando Material y método no se observó dicho contorno (fig. 2), parámetros descritos por Kan et al.9. Para evaluar el ancho de encía adherida Se realizó un estudio descriptivo tipo serie de casos donde primero se midió la distancia comprendida entre el margen se examinaron 30 alumnos pertenecientes a la Facultad de gingival y la unión mucogingival, en la zona media de la Correlación entre biotipo gingival, ancho y grosor de encía adherida 195 Figura 2 Biotipo periodontal medido mediante transparencia de la sonda: a) biotipo grueso, no se observa contorno de la sonda subyacente al margen gingival; b) biotipo fino, se observa contorno de la sonda subyacente al margen gingival. cara vestibular de los dientes 1.1, 1.2 y 1.3, utilizando una 6 regla milimetrada, y luego a esta medida se le restó la pro- Ancho de encía adherida fundidad de sondaje obtenida mediante sonda Florida®. La 5 unión mucogingival fue determinada de manera visual por medida en mm la diferencia de color existente entre la encía queratinizada 4 y la mucosa alveolar, al traccionar el labio10. Finalmente, para evaluar directamente el grosor de encía adherida se 3 midió la distancia entre la superficie epitelial y el periostio del hueso subyacente3 , anestesiando al paciente desde el 2 diente 1.1 al 1.3, mediante técnica infiltrativa. El grosor de encía adherida fue determinado en 3 puntos: 0,5 mm hacia 1 coronal a la unión mucogingival, punto intermedio del ancho Fino Grueso total de la encía adherida y 0,5 mm hacia apical del fondo 1,1 ancho EA 1,2 ancho EA 1,3 ancho EA del surco gingival. Para esto, se usó una lima de endodon- cia tipo K #20 (Dentsply, Maillefer, EE. UU.), estéril, la cual, Biotipo periodontal se introdujo en dirección perpendicular a la tabla vestibu- lar. La distancia se midió desde el tope de goma a la punta Figura 3 Distribución del ancho de encía adherida según bio- de la lima, utilizando una regla de endodoncia, magnifica- tipo periodontal mediante transparencia de la sonda en dientes ción con lupa, y fue expresada en milímetros, aproximando 1.1, 1.2, 1.3. a los 0,5 mm más cercanos, para luego obtener el prome- Datos expresados en milímetros. EA: encía adherida. Se observa dio de las 3 mediciones. En el análisis de datos se utilizó que el ancho promedio de la encía adherida fue mayor en el test chi-cuadrado Pearson para variables cualitativas como biotipo grueso que en el biotipo fino, donde el incisivo central evaluación mediante parámetros visuales, transparencia de mostró la mayor diferencia y el canino la menor diferencia de la sonda y género del paciente. La prueba t de Student se ancho entre biotipos. utilizó para relacionar variables cualitativas como biotipo mediante transparencia de la sonda y parámetros visuales con cuantitativas como ancho y grosor de encía adherida. la sonda, ancho y grosor de encía adherida (figs. 3 y 4), El test de McNemar se empleó para analizar concordan- el 53,33% de los pacientes presentaron biotipo grueso y el cia entre ambos métodos diagnósticos; el test de regresión 46,67% biotipo fino, siendo este último más prevalente en lineal, para relacionar ancho y grosor de encía adherida, y el mujeres (62,5%). En relación con el género, 17 sujetos se test Shapiro Wilk, para evaluar la distribución de variables. ajustaban a la definición de biotipo fino (56,67%), de los cua- El nivel de significación empleado fue del 95%, utilizando un les 4 eran hombres (28,57%) y 13 mujeres (81,25%). Por otra valor p de 0,05. parte, 13 pacientes fueron clasificados como biotipo grueso (43,33%), de los cuales 10 eran hombres (71,43%) y 3 mujeres (18,75%), siendo esta diferencia estadísticamente significa- Resultados tiva (test chi-cuadrado de Pearson, p = 0,004). Al evaluar el biotipo mediante transparencia de la sonda, las diferencias De los 30 sujetos examinados, 14 eran hombres (46,67%) y entre el género masculino y el femenino no fueron significa- 16 mujeres (53,33%). La edad promedio fue 23 años (± 2,3), tivas (test chi-cuadrado de Pearson p = 0,063). Al relacionar con un rango de 22-30 años, y las variables tuvieron dis- los resultados obtenidos por transparencia de la sonda y tribución normal (test Shapiro Wilk). Al evaluar el biotipo parámetros visuales, el test de simetría demostró que no periodontal mediante parámetros visuales, transparencia de hay diferencias estadísticamente significativas (p = 0,375) 196 M. Navarrete et al. 2 Tabla 2 Valores obtenidos para el ancho promedio de encía adherida al medir el biotipo periodontal mediante transpa- Grosor de encía adherida rencia de la sonda medida en mm 1,5 Diente Biotipo n Promedio ± DE T p 1.1 Fino 14 2,57 ± 1,02 1,350 0,1880 1 Grueso 16 3,13 ± 1,21 1.2 Fino 14 2,79 ± 0,97 0,529 0,6012 Grueso 16 3,00 ± 1,21 1.3 Fino 14 2,64 ± 0,84 1,107 0,9158 ,5 Grueso 16 2,69 ± 1,35 Fino Grueso Promedio 1.1 Promedio 1.2 DE: desviación estándar; n: número de casos; T: resultado del Promedio 1.3 test. Biotipo periodontal Promedio expresado en milímetros; test T no pareado; p < 0,05. Figura 4 Distribución del grosor de encía adherida según bio- tipo periodontal mediante transparencia de la sonda en dientes Tabla 3 Grosor promedio de encía adherida al medir el 1.1, 1.2, 1.3. biotipo periodontal mediante transparencia de la sonda Datos expresados en milímetros. Se observa que el grosor pro- Diente Biotipo n Promedio ± DE T p medio de la encía adherida fue mayor en el biotipo grueso. Al igual que en el ancho promedio, el incisivo central mostró la 1.1 Fino 14 1,08 ± 0,31 1,015 0,3188 mayor diferencia de grosor entre ambos biotipos y el canino Grueso 16 1,20 ± 0,31 la menor diferencia. 1.2 Fino 14 1,00 ± 0,20 1,169 0,2522 Grueso 16 1,10 ± 0,28 entre ambos métodos (test de McNemar), con una sensi- 1.3 Fino 14 0,96 ± 0,23 0,264 0,7940 bilidad del 92,86% y una especificidad del 75%, resultados Grueso 16 0,99 ± 0,29 expuestos en la tabla 1. Con respecto a la medición directa DE: desviación estándar; n: número de casos; T: resultado del del ancho