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Revista Facultad de Odontología Universidad de Antioquia

versión impresa ISSN 0121-246X

Rev Fac Odontol Univ Antioq vol.23 no.2 Medellín ene./jun. 2012

 

REVIEW ARTICLE

 

Nonsurgical periodontal therapy

 

 

Leticia Botero Zuluaga1; Alejandro Botero Botero2; Juán Sebastián Bedoya Trujillo3; Isabel Cristina Guzmán Zuluaga4

 

1 Dentist. Specialist in Adult Comprehensive Dentistry. Associate Professor, School of Dentistry, Universidad de Antioquia, Medellín, Colombia
2 Dentist, MA and Ph D Dentistry Sciences. Associate and Emeritus Professor, Dean of the School of Dentistry, Fundación Universitaria Autónoma de las Américas
3 Dentist, Universidad de Antioquia
4 Periodontist, Assistant Professor, School of Dentistry, Universidad de Antioquia, Colombia

 

SUBMITTED: AUGUST 16/2011 - ACCEPTED: FEBRUARY 14/2012

 

Botero L, Botero A, Bedoya JS, Guzmán IC. Nonsurgical periodontal therapy. Rev Fac Odontol Univ Antioq 2012; 23(2): 334-342.

 


ABSTRACT

INTRODUCTION: In the treatment of periodontal diseases, we can rely on nonsurgical periodontal therapy, which has been scientifically proven as its effectiveness has been recognized. The main objective of this article is to demonstrate the usefulness of nonsurgical periodontal therapy, as evidenced in several studies that serve as guidelines, as well as microbiological aspects, effects on tissues and the importance of maintenance therapy after treatment completion.
METHODS: a review was conducted in order to revise this topic considering key periodontal concepts as a guideline.
RESULTS: nonsurgical periodontal therapy (NSPT) is a procedure that cannot and should not be carried out in a few sessions; the time required for its completion is extended as necessary in order to achieve cleaning and adjustment of the roots as completely as possible.
CONCLUSIONS: Several authors have reported that reduction of microbiota remains between 14 and 180 days after therapy. This explains the regular periodontal maintenance appointments. They also indicate that the critical aspect of this therapy is not the choice between a surgical or a nonsurgical procedure, but a detailed and thorough cleaning by the dental professional and the good level of oral hygiene achieved by the patient.

Key words: nonsurgical periodontal therapy, microbiology, clinical parameters, microbiological parameters, periodontitis.


 

 

INTRODUCTION

Nonsurgical periodontal therapy is the multifactorial treatment of periodontal inflammatory lesions, whose main objective is to control and to eradicate such lesions. The therapeutic approach must consider the severity of the disease, the patient's needs and the risk factors, seeking the best possible results.1, 2

The objectives of periodontal treatment are: an immediate goal which consists of preventing and controlling the disease by arresting the pathogenic mechanisms, and an ideal one, which seeks to promote health by restoring the form, function, esthetics, and comfort that have been lost.

Nonsurgical periodontal therapy is indicated in cases of gingivitis, as well as mild to moderate periodontitis, and its main goal is to remove the local irritating factors.3, 4

It is limited in some cases, like in presence of deep periodontal pockets, in cases of bi- and trifurcation involvement, in regions of radicular proximity, in teeth with bad position, and in intra-osseous defects.3

We should also consider the involvement of risk factors such as non-controlled diabetes and tobacco smoking, since they both modify treatment response.5-8

 

CONSIDERATIONS

Dental debridement is the therapeutic action usually known as supragingival/subgingival scaling and radicular planning, which include calculus removal from crown and root, and cementum cleaning, not with the intention of eliminating it, but to normalize it and preserve it.9-12

Supragingival instrumentation is intended to polish the tooth's surfaces as well as the dental materials located outside the gingival margin. It is important to point out that this procedure must especially try to reach those places where hygiene access by the patient is more difficult, in other words, the so-called ''interproximal area''.11, 12 Subgingival instrumentation is performed with both manual (curettes) and power-driven tools (sonic and ultrasonic instruments). 13, 14

The concept of microbiota is used to identify the presence of different species of microorganisms. Subgingival microbiota is divided into three regions of well-defined microorganisms: the ones located on the dental surface, the ones associated with the pockets gap (laxed species) and the ones adhered to the soft wall of the pocket.15 The ones adhered to the dental surface include cocci such as Streptococcus (S. mitis, S. sanguis), Gram positive rods, actinomyces (A. naeslundi, A. viscosus), and species of eubacterium and fusubocterium.16, 17

Non-adhered microbiota is less organized, of a loose appearance, and contains mainly bacteria, Gram negative cocci, and a great number of filaments attached to the adhered plaque; these include: Porphyromonas gingivalis (P. gingivalis), Prevotella intermedia (P. intermedia), Prevotella melaninogenic (P. melaninogenicous) and Peptostreptococcus micros (P. micros), which have the capacity of adhering to the epithelial cells of the latter; strict anaerobes, such as Fusubacterium nucleatum, Selenomona snoxia and Centipeda periodontii, facultative anaerobes, such as Campylobacter, Eikenella corrodens and Haemophilus.16, 17

The mechanism of invasion has been explained as penetration of microorganisms through intercellular gaps, ulcerations in the pocket's epithelium, or direct penetration to the epithelial cell, as the invasion by Aggregatibacter actinomycetemcomitans (Aa), Porphyromona gingivalis (Pg), Treponema denticola (Td), Tannerella forsythia, Capnocytophaga. When making the histological sections of the pocket, some bacteria may be transposed to the soft tissue.18, 19

The presence and participation of viruses in periodontal disease have been reported, especially the human cytomegalovirus (HCMV) in malnourished children among the ages of 3 and 14 years in Nigeria, with necrotizing ulcerative gingivitis, and the Epstein Barr virus, which provoke proliferation and differentiation of immunoglobulin-secreting cells, associated with rapid progression of periodontal disease.20

Several studies have reported the presence of enteric microorganisms in subgingival plaque of patients with periodontal disease in Colombia; for example: Botero et al reported a frequency of 36.2% in Medellín (2008);21 Betancourt et al, 36% in Cali (2006);22 Mayorga de Fayad, Lafaurie et al, 39.2% in Bogotá (2002).23 As for international studies, Barbosa et al found out a prevalence of 32.2% in Brazil and between 14 and 57% in several populations in Europe and the United States.24 All these studies conclude that the most frequently isolated microorganism has been the Escherichia coli, and to a lesser extent Enterobacter, Klebsiella pneumonia, to name just a few. Similarly, they point out the participation of enteric bacteria in the progression of chronic periodontal disease, and they also report the presence of some kind of candida, such as Candida albicans.25, 26

Several studies show that traditional nonsurgical periodontal therapy may control periodontal disease in most of the patients with chronic periodontitis; nevertheless, such therapy has some limitations, such as the difficult adequate instrumentation in hard to reach areas in order to completely remove hard and soft deposits, particularly of the microorganisms that attack soft tissue.27 Recent data suggest that periodontopathic bacteria also inhabit in periodontal pockets as well as in other spots such as supragingival plaque, the mouth, mucus, saliva, and the tonsils, and transmission among these ecological niches may occur, as well as among individuals.28-33

 

EFFECTS OF NONSURGICAL PERIODONTAL THERAPY

The presence of periodontal disease due to loss of connective insertion and periodontal ligament causes the radicular cementum (the hard wall of the pocket) to be exposed to the pocket's gap and thus to be colonized by microorganisms coming from the supragingival region. The changes described are grouped into structural, chemical and toxic.34-36

Some authors recommend the use of acids to ensure radicular detoxification, provided that it takes place after mechanical disinfection. Similarly, instrumentation of the root with the intention of removing all the cementum is not a realistic or a possible goal in clinical terms.10-12

In general, all the authors recommend manual instrumentation after using power-driven instruments to conclude the procedure. The use of fiber optics in power-driven devices seems to improve efficiency of root cleaning.37

Several studies show that the greater the pocket's depth the more residual calculus, and they all state that it is not the same to treat single-rooted teeth than the multi-rooted ones, with bi- and trifurcation involvement or without it.38

A contraction of gingival tissue on the tooth by apically moving towards the gingival margin (marginal retraction) and reconstituting a union of large epithelial adherence between the soft and hard tissues of the dentogingival unit is the effect produced by nonsurgical periodontal therapy on the soft wall of the pocket. Other noticeable effects include bone loss suppression and reorganization of connective tissue in the dentoalveolar unit. This is why clinical parameters such as probing depth, clinical attachment level, bleeding on probing and inflammatory clinical signs are indications of recovery.39

The histopathological processes begin by widening of the epithelial union's intercellular gaps, thus increasing external-internal communication and creating an inflammatory underlying lesion (initial lesion), which is progressively spread, destroying insertion connective tissue of the gingival matter; the epithelial union starts growing towards the connective tissue, apical on the radicular surface without increasing the sulcus' depth but rather the edema accompanying inflammation, thus coronally displacing the gingival margin (early and established lesions). Persistence of the harmful agent makes the lesion advance towards the dentoalveolar unit with destruction of both osseous support and the insertion, thus forming the periodontal pocket.9, 40

The behavior after nonsurgical periodontal therapy ranks from loss of insertion in shallow pockets (1 to 3 mm loss of —0.42 mm) to enlargement of the ones of moderate depth (4 to 6 mm growth +0.55 mm), to even greater enlargement of deep pockets (7 mm or more growth +1.29 mm).

Loss of insertion at the shallow pockets usually occurs at the buccal and lingual sides, in which oral hygiene (brushing) contributes to apical migration of the gingival margin, especially in the presence of thin gingival walls. Similarly, a greater change in the vestibular and lingual sides occurs because of deep defects in the neighboring area, and greater instances occur thus producing tissue leveling. This situation is also explained as effect of pocket instrumentation and is noticeable during the first year after debridement. 39, 41

The clinical parameters of probing depth, clinical attachment level, and bleeding on probing usually improve; only a few spots show poor response, especially in the areas of bifurcations. Most of the studies report the findings as statistical averages, in which some variations in patients and sites are not identified. Long-term evaluation studies of the nonsurgical periodontal therapy demonstrate that a small group of patients (8 to 12%) do not adequately respond to routine therapy; therefore, the therapeutic modality must be chosen depending on the patient and the sites.42

The studies that compare individual results of the diverse (surgical and nonsurgical) therapies in the short and long term did not find significant differences among the clinical parameters that evaluate inflammation.

It is possible that no clinical parameter, either individual or in combination with others, presents high specificity or sensitivity to predict the disease activity in specific sites or to differentiate the response to treatment, except the changes in terms of loss or gain in the levels of insertion, measured in two different times.39, 42

 

REVALUATION

The effect of manual mechanical therapy with curettes and sonic and ultrasonic instruments yields similar results by reducing the total number of mobile Gram negative rods, spirochetes, and colonyforming units.43, 44

This revaluation considers whether it is necessary to perform surgical intervention in those places with inflammatory signs, deep residual pockets, and persistence of periodonto-pathogenic microbiota, and if it is necessary to facilitate visual access for instrumentation.28, 45

It should also be complemented with surgical periodontal therapy in cases that present osseous or mucogingival defects, in order to create a favorable osseous and gingival morphology.4 The cases of bi and trifurcation involvement must be evaluated as they may be treated by means of regenerative procedures with ostoeoconductors, osteoinductors, resorbable and non-resorbable membranes, in order to achieve a guided regeneration of the periodontal ligament.46, 47

Several authors have reported that microbiota reduction remain between 14 and 180 days after therapy. This explains the regular periodontal maintenance appointments.2, 19

They should be followed by support treatment, which includes periodical follow up sessions scheduled according to tissue evolution, and especially to the quality of hygiene by the patient.48-50

 

CONCLUSIONS

There are no clinical or microbiological elements that allow us clearly anticipating the response to a given periodontal treatment, and therefore to select the most efficient therapies for definitely obtaining the best results. Whichever the chosen therapy or its results, it requires a program of periodontal support as well close observance by the patient, both of which are considered as fundamental for treatment success.

 

 

CORRESPONDING AUTHOR

Leticia Botero Zuluaga
Facultad de Odontología
Universidad de Antioquia
Correo electrónico: lbotero@odontologia.udea.edu.co

 

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