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Non surgical periodontal treatment in patients with gingivitis and moderate periodontitis.

25/08/2016  |  Tags: Periodontal Treatment, dental laser,
ABSTRACT Objective:  To ascertain in ƀ  ammatory response through interleu- kin 1 ȕ  presence and identify pathogenic microorganisms as pos- sible immunological and microbiological markers in diagnosis and  treatment non-surgical periodontal in patients with gingivitis and  moderate chronic periodontitis in a sample of Mexican population.  Material and methods:  In the present prospective cohort study,  18 patients with signs of gingivitis and 17 patients with moderate  chronic periodontitis were selected. Samples of subgingival bio s  lm  and of crevicular gingival  ƀ  uid were collected.quanti s  ed during the pre-treatment, post-treatment and maintenan- ce phases of the non- surgical periodontal treatment. Continuous  variables were analyzed with the Student test, as well as categorical  variables which were analyzed with the Turkey-Kramer test. For in- dependent groups the Pearson test was used.  Results:  Microbio- logical response variables showed that  Porphyromonas gingivalis Prevotella intermedia, Fusobacterium nucleatum ,  Aggregatibacter  actinomycetemcomitans  significantly decreased in subjects with  gingivitis,  Porphyromonas gingivalis ,  Tannerella forsythia ,  Fuso- bacterium nucleatum ,  Aggregatibacter actinomycetemcomitans  and Actinomyces ssp . decreased in cases. Biochemical response varia- bles showed signi s  cant decrease in IL-1 ȕ  concentration and total  count in individuals with moderate chronic periodontitis in treatment  maintenance phase. The same result applied to clinical response  variables.  Conclusions:  There is a decrease in Interleukine 1 ȕ  le- vels with decrease in micro ƀ  ora. Interleukin 1 ȕ  are sensitive markers  for diagnosis of periodontal disease and assessment of its severity.
Key words:  Non surgical periodontal treatment, Mexican population, gingivitis, moderate periodontitis.
Palabras clave:Tratamiento periodontal no quirúrgico, población mexicana, gingivitis, periodontitis crónica moderada.
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Within  the  scope  of  periodontal  disease  two   entities are distinctive, and they possess clearly  defined phenotypes: gingivitis (G) and periodontitis  (P). These conditions can be clinically observed  through chronic inflammatory processes, although  in one case (periodontitis) this process evolves and  destroys the periodontal attachment apparatus, and  in the other case (gingivitis) the in ƀ  ammatory process  is maintained with no evolution towards destruction. 1-6 This  inflammatory  and  immune  response  is   determined by the presence of periodontal pathogens  which are Gram negative anaerobic bacteria involved  in the subgingival bio s  lm 1,7-11  such as  Porphyromonas  gingivalis ,  Aggregatibacter actinomycetemcomitans (Ac),  Tannerella forsythia  (Tf),  Prevotella intermedia  (Pi),  Fusobacterium nucleatum  (Fn),  Parvimonas  micra   (Pm),   Campylobacter  rectus   (Cr)  and Actinomyces ssp. 11-16  as well by biological modifying  factors such as: systemic factors, genetic factors 17,18 and behavioral factors such as oral hygiene, smoking  habits and stress. 19  In periodontal attachment tissue,  in ƀ  ammatory response comes forth with great amounts  of neutrophil polymorphonuclear leukocytes (PMNs)  and macrophages with phagocytosis and destructive  functions in the sites of bacterial interaction with tissue  surface, inciting the presence of in ƀ  ammatory in s  ltrate,  the activation of the immune system, complement  cascade and the cytokine production system. 10,20,21 Most of the substances released by inflammatory  and  immune  cells  concentrate  in  an  exudate,   characteristic of inflammatory processes observed  in G and moderate chronic periodontitis (MCP). This substance (fluid) is called crevicular gingival fluid  (CGF). In this  ƀ  uid it is possible to identify the following  pro-in ƀ  ammatory cytokines: 1-beta interleukin (IL-1 ȕ )  as well as alpha tumor necrosis factor (TNF- Į ). Both  cytokines are mediators of the in ƀ  ammatory process  because they modulate the extracellular component  of bone and connective tissue. In periodontal disease  they show high CGF levels, therefore they can have  diagnostic interest in G and MCG, since they can be  associated to the active phase of these conditions. 22-25 The aim of the present study was to contribute to the  knowledge of microbial  ƀ  ora in this sample of Mexican  population and assess links between microbial  ƀ  ora and  immunological response in G and its progression to MCP.  A prospective cohorts study was conducted to endeavor  to find differential aspects with respect to etiological  factors and host response. For this purpose quanti s  cation  of IL-1 ȕ  in the CGF was used as immunological marker  and to examine the effect of NSPT at the pre-treatment,  post-treatment and maintenance phases.
18  patients  were  selected  with  clinical  and   radiographic diagnoses of G (evidence of gingival  in ƀ  ammation, volume increase of the gums, redness  and  haemorrhage  when  probing,  without  loss  of   epithelial attachment) and 17 patients with MCP (loss  of insertion in three or more sites in all quadrants,  with pocket depth of 5-7 mm in three or more sites,  radiographic evidence of bone loss at a half of the root  length in three or more sites of all quadrants, bleeding when probing in three or more sites of each quadrant).  These patients attended the San Lorenzo and Tepepan  Stomatological Clinics, attached to the Metropolitan  Autonomous  University,  campus  Xochimilco,  in   Mexico City. All patients granted informed consent,  had not received previous periodontal treatment, and  participated of their own volition in the study. Mean  time between sampling was 12 months.
The clinical parameters in the pre-treatment, post- treatment and maintenance phases, in the SRP in G  and MCP is shown in  tables I and II . NSPT resulted in  signi s  cant reduction in PSD in the G group and PPD  in the MCP group with a p < 0.0001, difference found  among the groups was p  Į  0.03 and CAL in MCP  group p < 0.0001. The PI in G and MCP group with  p < 0.0001 and inter-group comparison was p  Į  0.03.  Gingival Index in group G and MCP with a p < 0.0001  with inter-group difference of p  Į  0.03.