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Gingiva and Orthodontic Treatment Vinod Krishnan, R. Ambili, Ze’ev Davidovitch, and Neal C. Murphy Orthodontic appliances, as well as mechanical procedures, are prone to evoke local soft-tissue responses in the gingiva. These effects can either be of positive nature, (physiologic recontouring), helping tooth movement, or negative ones, which should be avoided. The main source of negative outcomes involves orthodontic attachments, which inhibit efficient removal of bacterial biofilms (dental plaque). Undesirable complications are often due to an understandable lack of awareness while the orthodontist focuses on biomechanical matters. While conscientious attention to biomechanical progress justifies this focus, close attention should be paid to infection control and the possibility of iatrogenic side effects. This article considers the issues of ideal orthodontic clinical management as well as those of inadequate patient compliance and infection management. Exactly how therapeutic, prophylactic, and anti-infective issues are assumed or dele- gated by the orthodontist, patient, or the referring dentist is a matter of individual practice style and an integral part of the doctor-patient covenant. This article attempts to provide current information regarding clinical, mi- croscopic, and molecular level effects of orthodontic tooth movement on gingival tissues during fixed appliance therapy, or remedial methods once orthodontic appliances are removed. (Semin Orthod 2007;13: 257-271.) © 2007 Elsevier Inc. All rights reserved. T he periodontium can be divided anatomi- cally between the gingival unit (the soft tissue coronal to the bony crest of the alveolus in health), and the periodontal attachment appara- tus, defined by the cementum, the periodontal ligament (membrane), and the cribriform plate of the alveolus. While gingival disease must precede periodontal infection, not all gingival diseases progress to periodontitis. Because of the unpre- dictable nature of the disease progression, all orth- odontic patients with inflamed gingiva must be considered to be at risk for periodontal damage. For the purposes of syntactical clarity the words “periodontium” and “periodontal diseases” will re- fer to both anatomical elements, unless otherwise specified. Gingival and periodontal diseases are influ- enced by a wide variety of factors, such as host resistance, social and behavioral characteristics, which affect belief values and compliance, re- spectively, compromised systemic resistance (eg, human immunodeficiency virus status), genetic predispositions, tooth level, and finally both quantitative and qualitative compositions of the bacterial biofilm (dental plaque) at the gingival margin. As new discoveries in molecular genetics and the science of virology and bacteriology progress, refinements in concepts of disease risk factors emerge almost annually. 1 Thus, it be- hooves the orthodontists to understand both the physiology and the pathophysiology of the foun- dational tissues, as well as the coronal elements Assistant Professor, Department of Orthodontics, Rajas Dental College, Tirunelveli District, Tamilnadu, India; Senior Lecturer, Department of Periodontics, PMS College of Dental Science and Research, Trivandrum, Kerala, India; Clinical Professor, Depart- ment of Orthodontics, Case Western Reserve University, Cleveland, OH; Associate Clinical Professor, Department of Periodontology, Skeletal Research Center Affiliate, Case Western Reserve University School of Dental Medicine, Cleveland, OH, and Lecturer, Section of Orthodontics, Division of Associated Clinical Specialties, UCLA School of Dentistry, Los Angeles, CA. Address correspondence to Vinod Krishnan, MDS, M. Orth RCS, Gourivilasam, Kudappanakunnu PO, Trivandrum, Kerala State- 695043, India. Phone: 919447310025; E-mail: vikrishnan @yahoo.com © 2007 Elsevier Inc. All rights reserved. 1073-8746/07/1304-0$30.00/0 doi:10.1053/j.sodo.2007.08.007 257 Seminars in Orthodontics, Vol 13, No 4 (December), 2007: pp 257-271
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Page 1: 87490117 8 Gingiva and Orthodontic Treatment

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ingiva and Orthodontic Treatmentinod Krishnan, R. Ambili, Ze’ev Davidovitch, and Neal C. Murphy

Orthodontic appliances, as well as mechanical procedures, are prone to

evoke local soft-tissue responses in the gingiva. These effects can either be

of positive nature, (physiologic recontouring), helping tooth movement, or

negative ones, which should be avoided. The main source of negative

outcomes involves orthodontic attachments, which inhibit efficient removal

of bacterial biofilms (dental plaque). Undesirable complications are often

due to an understandable lack of awareness while the orthodontist focuses

on biomechanical matters. While conscientious attention to biomechanical

progress justifies this focus, close attention should be paid to infection

control and the possibility of iatrogenic side effects. This article considers

the issues of ideal orthodontic clinical management as well as those of

inadequate patient compliance and infection management. Exactly how

therapeutic, prophylactic, and anti-infective issues are assumed or dele-

gated by the orthodontist, patient, or the referring dentist is a matter of

individual practice style and an integral part of the doctor-patient covenant.

This article attempts to provide current information regarding clinical, mi-

croscopic, and molecular level effects of orthodontic tooth movement on

gingival tissues during fixed appliance therapy, or remedial methods

once orthodontic appliances are removed. (Semin Orthod 2007;13:

257-271.) © 2007 Elsevier Inc. All rights reserved.

pdocF“fs

erwshpqbmapfhp

he periodontium can be divided anatomi-cally between the gingival unit (the soft

issue coronal to the bony crest of the alveolus inealth), and the periodontal attachment appara-

us, defined by the cementum, the periodontaligament (membrane), and the cribriform plate ofhe alveolus. While gingival disease must precedeeriodontal infection, not all gingival diseases

Assistant Professor, Department of Orthodontics, Rajas Dentalollege, Tirunelveli District, Tamilnadu, India; Senior Lecturer,epartment of Periodontics, PMS College of Dental Science andesearch, Trivandrum, Kerala, India; Clinical Professor, Depart-ent of Orthodontics, Case Western Reserve University, Cleveland,H; Associate Clinical Professor, Department of Periodontology,keletal Research Center Affiliate, Case Western Reserve Universitychool of Dental Medicine, Cleveland, OH, and Lecturer, Section ofrthodontics, Division of Associated Clinical Specialties, UCLAchool of Dentistry, Los Angeles, CA.

Address correspondence to Vinod Krishnan, MDS, M. Orth RCS,ourivilasam, Kudappanakunnu PO, Trivandrum, Kerala State-95043, India. Phone: �919447310025; E-mail: vikrishnanyahoo.com

© 2007 Elsevier Inc. All rights reserved.1073-8746/07/1304-0$30.00/0

ddoi:10.1053/j.sodo.2007.08.007

Seminars in Orthodontics, Vol 13, No

rogress to periodontitis. Because of the unpre-ictable nature of the disease progression, all orth-dontic patients with inflamed gingiva must beonsidered to be at risk for periodontal damage.or the purposes of syntactical clarity the wordsperiodontium” and “periodontal diseases” will re-er to both anatomical elements, unless otherwisepecified.

Gingival and periodontal diseases are influ-nced by a wide variety of factors, such as hostesistance, social and behavioral characteristics,hich affect belief values and compliance, re-

pectively, compromised systemic resistance (eg,uman immunodeficiency virus status), geneticredispositions, tooth level, and finally bothuantitative and qualitative compositions of theacterial biofilm (dental plaque) at the gingivalargin. As new discoveries in molecular genetics

nd the science of virology and bacteriologyrogress, refinements in concepts of disease riskactors emerge almost annually.1 Thus, it be-ooves the orthodontists to understand both thehysiology and the pathophysiology of the foun-

ational tissues, as well as the coronal elements

2574 (December), 2007: pp 257-271

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258 Krishnan et al

hat have traditionally defined the specialty.ithin these anatomical and disease entities,

ooth anatomy, appliance design, and composi-ion of dental plaque are considered to bearamount local factors, which influence peri-dontal health.2 Among tooth level risk factorsontributing to the etiology of periodontal dis-ases (gingivitis and periodontitis), arch lengtheficiency (crowding) and direct soft-tissue im-ingement are most salient.1-3 The exact mech-nism contributing to disease in any individualatient is still not clearly defined or foreseeable.owever, the malalignment of teeth can ad-

ersely affect gingival health, since the amountf plaque at the gingival margin around teethorrelates rather strongly with gingival inflam-ation and bleeding. It was reported that at

xtremes of oral hygiene, the pathological con-ribution of malocclusion may be eclipsed by

ore profound etiological agents, causing gin-ival or periodontal disease.1,2,4 However, thisorrelation does not necessarily deny the role ofrch length deficiency (ALD), or direct gingivalraumatic impingement, as risk factors in non-xtreme cases. The good news for the practicingrthodontist is that given adequate instruction,ingival infection can be brought under reason-ble control. For example, Addy and coworkerseported that all children who were includedn their study sample and in need of orthodon-ic treatment were plaque free or free fromingival bleeding on probing.4 Yet, in keepingith the concept that ALD may be a risk factor

n non extreme cases, Ashley and coworkerseported that overlapping incisors had a directffect on gingivitis.5 Furthermore, Ainamotated that the degree of oral cleanliness andxtent of periodontal disease were worseround malaligned teeth than around prop-rly aligned teeth.6 Thus, it may be concludedhat a crowded dentition can complicate oralygiene procedures, leading to increasedlaque retention and subsequent gingival in-ammation.

This article attempts to provide current infor-ation regarding clinical, microscopic, and mo-

ecular level effects of orthodontic tooth move-ent on gingival tissues during fixed appliance

herapy, or remedial methods once orthodontic

ppliances are removed. t

linical Changes

he introduction of fixed orthodontic appli-nces into the oral cavity in the form of orth-dontic bands and resin-bonded attachments of-en evokes a local soft-tissue response inconsistentith health or esthetic treatment goals. The prox-

mity of these attachments to the gingival sulcus,laque accumulation, and the impediments theyose to oral hygiene habits further complicate therocess of efficient salutary orthodontic care.7-10

he effects seen clinically following the insertionf orthodontic appliances into the oral cavity canontribute to chronic infection, inflammatory hy-erplasia, gingival recession, irreversible loss of at-

achment (permanent bone loss), and excessiveccumulation of tissue, inhibiting complete extrac-ion space closure. The following discussion ad-resses each of these pathological issues in detail.

nflammatory Changes

rthodontic mechanotherapy is capable of pro-ucing local changes in the oral microbial eco-ystem and altering the composition of the bac-erial plaque qualitatively and quantitatively.enerally, as plaque accumulates, especially sub-ingivally, relatively benign Gram-positive coccicommensal organisms) forms relent to the de-elopment of more pathogenic Gram-negativeods, spirochetes, and motile forms that definehe pantheon of putative pathogens (periodon-opathic bacteria), many of which are unchar-cterized and not culturable for in vitro anal-sis. The development of a stable pathogenicilieu tips the host-parasite homeostasis in favor

f the pathogen and manifests as clinical inflam-ation. This trend is evident by the increased

everity of gingival inflammation observedmmediately after fixed appliance placement.ixed appliances frequently encroach on theingival sulcus, inhibiting effective oral hygieneaintenance.11 Zachrisson and Zachrisson re-

orted that even after maintaining seeminglyxcellent oral hygiene, patients usually experi-nce mild to moderate gingivitis within 1 to 2onths of appliance placement. These infective

hanges are generally quiescent, with no perma-ent damage introduced to tissues, except for0% of adolescents, who might show consider-ble irreversible periodontal attachment appara-

us destruction.7,8 This finding is similar to that
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259Gingiva and Orthodontic Treatment

f Kloehn and Pfeifer, who evaluated pretreat-ent gingivitis in prospective orthodontic pa-

ients with the help of Russell’s periodontal in-ex, and reported a gingivitis prevalence ofpproximately 8%. When an orthodontic appli-nce was placed, there was a sudden drop in theumber of patients who could maintain an ex-ellent oral hygiene from 20% to 6.5%. How-ver, a dramatic improvement in the gingivalondition was observed 48 hours after applianceemoval, as indicated by very low Russell indexcores.9

Clinical studies used various indices for eval-ating gingival inflammation after orthodonticppliance placement. The plaque index, gingi-al index, bleeding on probing, pocket probingepth, Quigley-Hein index (for bonded maxil-

ary and mandibular molars), bonded bracketndex (for bracketed teeth), and a modified gin-ival index, all were used for assessment ofre- and post-treatment gingival conditions.12-17

irtually all studies have reported that orthodon-ic appliances act as protective havens for bacte-ial plaque accumulation, providing an encum-rance to oral hygiene procedures.

ucogingival Problems

he zone of attached gingiva in health is defineds the amount of keratinized tissue from theingival margin apical to the mucogingival junc-ion, minus the depth of the gingival sulcus.ssessment of the mucogingival status is consid-red to be a very important part of the intraoralxamination, if orthodontic treatment is to belanned and rendered. It has been surmised bynecdotal evidence and case studies that ex-reme labial or lingual positioning of teeth maye associated with gingival recession and an

nadequate zone or thickness of attachedingiva.18,19 However, a strong predictive coeffi-ient of correlation has not yet been unequivo-ally demonstrated. Thus, while some recessiongingival dehiscence) may be predicted in orth-dontic cases epidemiologically, the lack oftrong correlation coefficients makes individualatient proclivity so problematic and the emer-ent pathosis so unforeseeable by the practicingrthodontist. This unpredictability is why a pol-

cy of prophylactic soft-tissue grafting and pre-rthodontic periodontal consultation may be

ecommended as prudent for all orthodontic i

atients wherever the attached gingiva is mini-al or thin.20-23

irect Gingival Traumatic Impingement

n patients with a Class II, Division 2 malocclu-ion, functional trauma from incisor impinge-ent on the mandibular soft tissue can result inarginal recession of facial gingiva of mandibu-

ar incisors.24 Similarly, extreme cases of deepite (complete deep bite), direct trauma to theingiva from the incisal edges of mandibularncisors can contribute to gingival recession pal-tal to maxillary incisors.18 Such traumatic dam-ge to gingival tissues might result in the com-lete ablation of the gingival unit providing aortal of entry through which infection couldpread to the subjacent periodontal attachmentpparatus.25 When such a process is allowed toccur, the periodontal status of the patient isompromised, because the depth of the pocketeyond 3 mm inhibits complete bacterial bio-lm removal subgingivally by common homeare techniques, and even professional scalingnd root planning. This of course complicateshe application of orthodontic mechanics, orenders it absolutely contraindicated because, asennstrom and Pini Prato26 have speculated,

ooth movement can convert supragingivallaque subgingivally. However, a prudent orth-dontic treatment plan and a few simple precau-ions can ameliorate or entirely preclude suchnfortunate complications as gingival recessionr periodontal attachment loss11:

. A low profile appliance, which facilitates ac-cess for effective oral hygiene management.

. A complete and explicit informed consentof complications and sequelae before treat-ment commencement, which sets a goal ofgingival health to improve the esthetic rela-tionship of the gingival margin.

. Maintenance of interproximal health, to pre-clude development of papilla loss (black tri-angle phenomenon) when incisor ALD iscorrected.

After full discussion of risks and benefits, therthodontist should allow the well-informed pa-ient to determine whether the benefits of orth-dontic treatment outweigh the side effects oningival health. There is no doubt that the

nsertion of an orthodontic appliance makes
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260 Krishnan et al

aintenance of oral hygiene difficult. Mostatients undergoing fixed appliance treat-ent experience an increased incidence of gin-

ivitis throughout the duration of therapy, but ifhe qualitative nature of the gingival infections noncariogenic, and nonprogressive into theeriodontal attachment apparatus, the perma-ent destructive effects may be minimal, reme-iable, or precluded entirely.

ingival Enlargement

ne of the most common problems with gingi-itis associated with orthodontic treatment isingival overgrowth (Figs 1, 2, and 3). The af-ected tissue is generally edematous, and mayleed when gently probed.14 The first reviewegarding gingival overgrowth appeared in 1933,n volume 3 of The Angle Orthodontist.27 Kloehnnd Pfeifer evaluated in detail the nature andegree of gingival enlargement after orthodon-

ic appliance placement. They reported that theverage incidence of gingival enlargement was 4imes greater around posterior teeth comparedith incisors and canines.9 They listed the fol-

owing causes:

. Mechanical irritation by bands, more on pos-terior than on anterior teeth,

igure 1. This kind of papillary hypertrophy is causedy bacterial biofilm accumulation below the inter-roximal gingival margin. Prolonged presence con-erts hypertrophic tissue to fibrous hyperplasia thatust be removed either during fixed appliance ther-

py to facilitate adjustments or around the debondingppointment. Caution must be exercised to distin-uish between hypertrophy that regresses and perma-ent hyperplasia that may look normal but representsedundant tissue growth covering a portion of thenatomic crown. (Color version of figure is available

nline.) o

. Chemical irritation produced by cementsused for banding,

. Food impaction, because of the proximity ofthe arch wires to the soft tissues, and

. Less efficient oral hygiene maintenance.

Those investigators also reported greater in-idence of gingival enlargement at the interden-al region compared with the facial aspect of theingiva margin. They concluded that as long as aand is in place, it is prone to produce gingival

rritation, leading to enlargement. This situationan be prevented only by properly fitting eachand and making it self-cleansing.9 Those find-

ngs were in contrast to those of Zachrisson, whoound that the mandibular incisor region har-ors the highest risk for the development of

igure 2. Inaccurate placement of elastics can inhibitral hygiene efforts accumulating plaque (arrow) anddding mechanical irritation to the hypertrophiedissue. Black asterisk marks line of erroneous elasticlacement on gingiva and maxillary canines. (Colorersion of figure is available online.)

igure 3. Lip incompetence can contribute to gingi-al enlargement by dehydrating the gingival duringouth breathing. (Color version of figure is available

nline.)

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261Gingiva and Orthodontic Treatment

ingival hyperplasia.7,8 Zentner and coworkersvaluated the proliferative response of cells ofentogingival junction to mechanical stimula-

ion in male rats, and reported that junctionalpithelium rapidly adapts to mechanical stimu-ation by cell proliferation. Their findings wereontradictory to the existing dogma, and theyoncluded that orthodontic tooth movementeed not necessarily produce any detrimentalffect on the stability of the dentogingival junc-ion.28

Published reports indicate that there are def-nite changes in gingival characteristics oncerthodontic appliances are in place. Zachrissoneported consistently higher gingival index val-es and deeper periodontal pockets at inter-roximal surfaces, once orthodontic banding isompleted.7,8 Recent studies have also demon-trated an increase in probing depth after place-ent of orthodontic appliances.13,15,16 Existing

vidence supports the hypothesis that these de-ects may be only pseudo-pockets, which may or

ay not return to a normal topography oncehe appliances are removed. Kloehn and Pfeiferould not find any radiographic evidence of pa-hology in patients with changes in clinicalrown height. They could also demonstrate

dramatic reduction in gingival hyperplasiaithin 48 hours of appliance removal,9 but there

s no definitive proof that “normal” gingival mar-ins will necessarily return to a physiologicallyptimal position at the cemento enamel junc-ion. Normal is a mathematical term meaningmost, median, or arithmetic mean” on a Gauss-an distribution. This definition, however, is notynonymous with optimal health.

ingival Recession and Loss of Attachment

ingival recession is defined as “the exposure ofhe root surface by an apical shift in the positionf gingiva.”29 It depends on the existence of aubjacent alveolar bone dehiscence and is alwayshe result of a loss of attachment.26 To date, noingle causative factor has been identified as aingular etiologic agent, but many predisposingnd precipitating factors have been anecdotallymplicated in its development. The predisposingactors are anatomical, whereas the precipitatingactors consist of trauma or exacerbation of ac-eleration of gingival inflammation, and alveolar

one dehiscences.30 l

An association between orthodontic toothovement and gingival recession has been men-

ioned in both the orthodontic and the peri-dontal literature, with some reports arguing onehalf of a causal connection and others arguinggainst it.31-33 Geiger reported that the inci-ence of gingival recession with fixed orthodon-ic appliances ranges from 1.3% to 10%. It isccepted that a 2-mm-wide attached gingiva isdequate to withstand orthodontic forces andrevent gingival recession. Moreover, it is ar-ued that preexisting mucogingival problemsan be exacerbated with orthodontic force ap-lication.34 Therefore, it seems to be prudentnd useful to identify and localize gingival areast risk, where recession occurs, and advise pa-ients of the anecdotal association, accordingly.

Dorfman suggested that mandibular incisorsay be more prone to recession than any other

eeth.35 He attributed this recession to a thin oronexistent labial plate of bone, inadequate orbsent keratinized gingiva, and labial promi-ence of teeth. When excessive forces are ap-lied, which do not permit repair or remodelingf bone during tooth movement, teeth with in-dequate attached gingiva might show localizedecession. It should be noted, however, that Dor-man explicitly noted that this association wasnpredictable; thus inference of causal connec-ion may be intemperate. An additional predis-osing factor that may be more relevant ishronic marginal gingivitis, or chronic necrotiz-ng ulcerative gingivitis, which may rapidly de-troy the marginal alveolar bone and gingivalttachment, even during application of modestrthodontic forces.34 While this hypothesis isisputed by some,36 research by Aleo and co-orkers37 and others38,39 suggests that bacterialiofilm factors may inhibit cell proliferation nec-ssary to adapt to a repositioning of the dentaloot. Further research demonstrating a lack ofissue proliferation in the presence of marginalental plaque would support such an interpre-ation by compelling in vitro data.

Other biomechanical therapeutic modalitiesssociated with anterior gingival recession logi-ally include transverse expansion and intermax-llary (interarch) springs and elastics. In suchases, a breakdown of fragile gingival attach-ent may occur.40,41 However, despite these re-

orts, the movement of teeth within their alveo-

ar bone envelope was suggested as safe by
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262 Krishnan et al

ennstrom and coworkers.42,43 Those investiga-ors reported that as long as a moving toothemains within the envelope of alveolar boneand presumably the plastic limits of epigeneti-ally determined phenotype), the risk of harm-ul side effects in the gingival tissue is minimal.

ennstrom and coworkers concluded that theareful examination of the quality of the tissue,n addition to merely its linear dimensions, ismportant before applying orthodontic mechan-cs.42,43

Whatever the predisposing or precipitatinggents, a combination of causative factors arearamount; gingival recession can lead to poorsthetics, root sensitivity, loss of periodontal sup-ort, difficulties in maintenance of oral hygiene,nd achieving successful periodontal repair, asell as promoting increased susceptibility to car-

es32 (Figs 4 and 5). However, a number of re-ent studies seem to support the hypothesis thatrthodontic mechanics per se rarely producesingival recession, and that a poor correlationxists between the degree of mandibular incisorroclination and gingival recession. Melsen andllais reported that only 15% of teeth experi-nce either the development or aggravation ofingival recession with orthodontic mechanics.30

hey listed local anatomical factors and the peri-dontal health status of these teeth as predis-

igure 4. Image (A) shows the consequence of fauracket placement, improper removal of adhesiveecession in the mandibular anterior region. Note alttachment loss, gingival recession, and infrabony pocknterior region from the same patient. Note the amourun Sadasivan, MDS, periodontist, Trivandrum, Ker

osing factors to this process. Besides gingival o

ecession, the essential changes during peri-dontal destruction include loss of attachmentnd proliferation of pocket epithelium beyondhe cemento-enamel junction.8 Zachrisson and Al-aes demonstrated loss of attachment in orth-dontic patients, and attributed it to variations

n the gingival condition, the traumatic effect ofncreased thoroughness of tooth brushing, and

echanics by a general practitioner. Note improperresulting in plaque harboring areas, and gingival

e position of molar band, which is prone to inducermation. Image (B) is the radiograph of the maxillaryf bone loss and root shortening. (Picture courtesy ofndia.) (Color version of figure is available online.)

igure 5. Another case of poorly executed orthodon-ic treatment. Note the improper bracket place-

ent, improper removal of adhesive flash resultingn plaque harboring areas, and gingival recession inelation to mandibular anterior. (Picture courtesyf Arun Sadasivan, MDS, periodontist, Trivandrum,erala, India.) (Color version of figure is available

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263Gingiva and Orthodontic Treatment

lacement of orthodontic bands. They found aean attachment loss of 0.41 mm in patientsearing fixed appliances, compared with 0.11m in the control group, and concluded that

his difference was not significant clinically.8

owever, it should be kept in mind that individ-al orthodontists treat individual patients andrithmetic means may have value as generaluidelines to treat and inform patients but haveittle if any predictive (statistical forecasting) ro-ustness for the next patient requiring treat-ent.In other words, although the literature reports

onflicting findings on possible associations be-ween gingival recession and orthodontic mechan-cs, it seems prudent to emphasize the importancef a careful clinical examination, application ofptimal forces, and control over tooth move-ent as a means to avoid or prevent this prob-

em.

he Gingiva and Closure of Extraction Spaces

he application of retraction forces, as well asompressive forces in extraction sites for toothpproximation, often result in accumulation ofingival tissue and enlargement of interdentalapillae. This type of gingival cleft formation islso observed when a couple is applied with theelp of elastic chains for rotation correctionsFig 6). Adjacent to this accumulated tissue, ver-ical invaginations or clefts, of both epitheliumnd connective tissue, are formed on both buc-al and lingual sides.44 It is suggested that trans-

igure 6. Note the accumulation of gingival tissueetween the cuspid and bicuspid (arrow)—gingivalleft formation. This may inhibit tooth movement andurgical excision may be needed after debonding tostablish physiologic soft-tissue contour. (Color ver-

bion of figure is available online.)

eptal fibers may be compressed or displaced,ather than remodeled during tooth movement,nd that the invagination is the result of passiveolding of gingival tissues.45,46 Histological andistochemical studies have shown that hyperpla-ia of epithelium and connective tissues is asso-iated with a loss of collagen and an increase inlycosaminoglycans.44,47 The soft-tissue invagina-ions formed may vary from a shallow groove to aefinite cleft extending to the alveolar bone sur-

ace, exceeding 1 mm in depth. Its presence mayven be augmented with a large osseous defect inhe pressure side of the moving tooth.48 It wasuggested that the anatomical configuration of theccumulated tissue causes difficulty in plaque con-rol, and might also result in extraction space re-pening, as well as relapse.44

ingiva in Systemic Diseases and Drug Intake

ingival enlargement is a common findingssociated with some pathologic conditions. Er-thematous gingival enlargement is often associ-ted with uncontrolled diabetes. Inadequate nu-rition and systemic hormonal stimulation ofteneads to puberty- and pregnancy-associatedingival enlargement, respectively.49 Enlarged,dematous gingiva, soft and tender to touch,hich bleeds easily on mild trauma, is a charac-

eristic feature of acute monocytic, lymphocytic,nd myelocytic leukemia. In addition, throm-ocytopenia and thrombocytopathy can causeingival enlargement and bleeding. All theseonditions may get worse, if oral hygiene main-enance is poor and the rate of plaque accumu-ation is high.50

The literature contains many references sug-esting that some drugs consumed for systemiciseases may contribute to gingival enlarge-ents. Phenytoin sodium, nifedipine, and cyclo-

porine are the most cited drugs contributing tohis type of reaction, that can includeoth interdental papilla and marginal tissue.51,52

ome generalized syndromes are also known toxhibit characteristic gingival enlargement. Thesenclude Rutherford syndrome, Cross syndrome,amon syndrome, and Laband syndrome.53,54 Inll of these conditions, orthodontic attachmentsight act as plaque-harboring areas exacerbating

he predispositions of the general syndrome itself.linicians treating such individuals should always

e aware of the consequences they might face, try
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o minimize appliances that would contribute tolaque retention, and ensure that aggressive infec-

ion control measures are taken by appropriateersonnel.

icrobiological Changes

lacement of an orthodontic appliance in a pa-ient’s mouth is often associated with alterationsn the oral hygiene habits and periodontalealth, as a local change in the oral ecosystemlters the qualitative nature of the local bacterialiofilm. Literature regarding this effect of orth-dontic treatment has outlined the changes inicrobial environment associated with the appli-

nce placement, along with the increase in themount of supra- and subgingival plaque.55-57

pecifically, orthodontic appliances seem to of-er an opportunity to shift plaque compositionrom a predominance of aerobic Gram-positiveocci to more destructive putative pathogens,omprised mainly of facultative and strictly an-erobic Gram-negative species.57,58 This shift re-ults in populating the area with potentialeriodontopathogens such as fusiform bacteriapirochetes, prevotella, and bacteroids. Theseacteria have the potential to produce cytotoxicroducts, which include an array of enzymesapable of hydrolyzing gingival tissues.59

The gingival/microbiologic changes associ-ted with fixed orthodontic appliances can bettributed to the presence of rough-surfacedanding material acting as a “plaque trap” and

rritant to gingival tissues. The plaque-retainingreas created by the orthodontic appliances in-rease the possibility of transforming reversibleingivitis to irreversible and self-perpetuatingeriodontitis.

This exact biochemical process is due to theroduction of endotoxins and lipopolysaccha-ides (LPS) from the cell wall of Gram-negativeacteria on cell death. LPS is demonstrated inubgingival plaque as well as in gingival crevicu-ar fluid of orthodontic patients. LPS is capablef producing inflammatory reactions, which ap-ears to be the predominant mechanism of

issue destruction, leading to periodontal attach-ent loss, alveolar bone loss, and gingival re-

ession. Aside from actively producing destruc-ive processes, the pathologic process can alsonduce several biologic pathways at the same

ime that it inhibits the healing capacity of gin- a

ival tissues. LPS is capable of activating theomplement system and inducing inflammationhrough macrophage release of inflammatory

ediators, such as interleukin (IL)-1, tumor ne-rosis-alpha (TNF-�), IL-6, and IL-8. This activityan, in turn, stimulate bone resorption and in-ibit osteogenesis. Knoernschild and coworkersemonstrated that orthodontic brackets retain anffinity to LPS, which is dependent on bracketaterial composition, surface energy, and surface

orosity.60

Sinclair and coworkers demonstrated anncrease in the percentage of streptococci and

decrease in percentage of actinomyces inubgingival plaque from orthodontic patients.hese findings, which are concordant withther authors, suggest that the increase intreptococcal flora can also lead to a higherncidence of caries. However, their study isncouraging to clinicians, because it failed toemonstrate either an increase in the plaque

evel around the appliances or in the percent-ge of potentially pathogenic Gram-negativerganisms. This observation is consistent withnecdotal evidence that a high level of oralygiene maintenance adopted by the studyubjects can reduce plaque accumulation toeasonable and less pathogenic levels.14 Daviesnd coworkers reinforce this perception in aeport that suggests behavioral factors ratherhan orthodontic appliances, treatment plans,nd force modules per se were responsible forhe degree of oral hygiene and gingival healthn patients wearing fixed orthodontic appli-nces.61

Hagg and coworkers recently evaluated quan-itative and qualitative alterations in the carrierate of candida species, enterobacteria, and as-ociated changes in the plaque index duringrthodontic treatment with fixed appliances.hey could isolate eight coliform species (Kleb-

iella pneumoniae, Enterobacter sakazakii, Enter-bacter cloacae, Enterobacter gergoviae, Pseudomonaseruginosa, Enterobacter agglomerans, Acinetobacter,nd Yersinia species) from clinical study patients.hey could also observe a change of Candidalbicans to a carrier state from a noncarrier state,nce fixed appliances were placed.62

It is clear from the ongoing discussion thatxed appliances retain a direct effect on plaque

ndex and microbiological quantity. The appli-

nce might interfere with oral hygiene practices
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265Gingiva and Orthodontic Treatment

nd an astute clinician should always place anmphasis on strict instructions regarding oralygiene, as well as appliance hygiene, in orth-dontic patients.

istological Changes

ue to inherent problems in planning and con-ucting clinical studies concerning gingival con-itions in humans, a number of researchersave used animal models to perform histologicaltudies that may define actual tissue-level path-genic mechanisms. Histological sections ofrthodontically treated tissues characteristicallyeveal increased numbers of mononuclear infil-rates, along with hyperplasia and proliferation ofocket epithelium. Throughout the duration of

hese studies a dense accumulation of chronic in-ammatory cells occupying large areas of connec-

ive tissue was observed.44,63

Redlich and coworkers outlined the histolog-cal changes at sites of extraction space closure,n the form of papillary epithelial hyperplasia.he newly formed collagen in these regions wasoiled and compressed, in the shape of a “foot-all.”44 There are, however, other reports thattate that the space closure mechanics can leado loss of collagen in the hyperplastic gingiva.64

fter tensile force application in rabbit incisors,an de Velde and coworkers demonstrated

rauma, characterized by tears, ulcerations, anduptures in the gingival epithelium, which canrovide facile access of invasive bacteria andytotoxic products to subjacent bone. Leuko-ytes were present in the histological sections,ttributed to the production of chemoattractionactors following local destruction of tissues.onger periods of tensile force application re-ulted in deeper penetration of leukocytes, withreater degrees of ulcerations and tears. It wasoncluded that these higher levels of damage tohe gingiva occurred as soon as 24 hours afterhe initiation of tooth movement. It is clinicallymportant to note, however, that the gingivaeems to recover by 72 hours after applianceemoval.65

Therefore when gingival inflammation, hy-ertrophy, and incipient periodontitis is immi-ent, temporary removal of an arch wire, to

acilitate flossing and brushing efficacy, may berudent and well within the spectrum of reason-

ble orthodontic treatment planning. In the t

vent of untoward tooth relapse during theourse of treatment, at worst the clinician hasbserved potential relapse. This is a physiologichenomenon, better identified while bracketsre in place even without arch wires. Alterna-ively, relapse after all brackets are removed isften perceived by patients as the end of treat-ent, and the relapse as a sign of treatment

ailure.

iochemical and Vascular Changes

he gingival tissue tolerance to orthodonticanding was evaluated by Cheraskin and Rings-orf, with the help of biochemical tests evaluat-

ng fasting blood glucose levels in humans. Theuthors correlated tissue tolerance to fastinglood glucose levels and stated that subjects whohowed no worsening in blood glucose valuesgrouped around mean) had good tissue toler-nce. In contrast, subjects with poor tissue toler-nce showed blood glucose values widely dis-ersed around the mean values. They suggestedsing fasting blood glucose variability or ho-eostasis as a predicting criterion to assess tissue

olerance of an orthodontic patient.66

Using laser Doppler flowmetry in human gin-iva, Yamaguchi and Nanda measured changesn blood flow after orthodontic force applica-ion. They measured blood flow through thenfraorbital artery, the branch of the maxillaryrtery, and demonstrated an initial reduction inhis parameter within 2 to 3 seconds of forcepplication. There was a gradual recovery inlood flow to the resting level in the attachedingiva when force application was continued,hich was assumed to be the result of indirectlood flow from adjacent capillary loops andetwork of vessels. This flow was possible be-ause of the existence of an open microcircula-ory system in gingival tissues. When the forceas removed, a reactive hyperemia was observed,

he magnitude of which was correlated to theecreased blood flow. The duration of the reac-ive hyperemia was positively correlated to theecreased blood flow observed earlier. That in-estigation illuminates various changes in bloodow associated with orthodontic mechanics, im-lying that force modulation would provide op-

imum force for optimal tooth movement.67
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olecular Level Changes

ollagen fibers, the main structural componentf the extracellular matrix (ECM) of the gingiva,etain a higher turnover rate in the periodontaligament than in the gingival unit, coronal to thelveolar osseous crest. Whenever a force is ap-lied, these fibers are compressed, retracted,r even become hypertrophic.44 Ultrastructuralnalysis with transmission electron microscopyTEM) revealed an increase in the diameter ofollagen fibers in both tension and compressionreas. Degradation of fibers inside the com-ressed papilla can be seen, with longitudinalplits, but without the typical bending pat-ern.44,68

Redlich and coworkers examined the effect ofechanical force on gene expression of colla-

en type 1 (COL-1) and matrix metalloprotein-se-1 (MMP-1) in cultured gingival fibroblasts.hey found that the cells under pressure ex-ressed higher levels of COL-1 and lower levelsf MMP-1 mRNA, compared with the controlells. Assuming that gene expression at gingivalCM components is also affected in vivo, theyerformed another study in dogs. There theybserved no change in mRNA levels of COL-1,issue inhibitor of metalloproteinase (TIMP)-1nd -2, at both pressure and tension regions ofhe gingiva. An interesting finding was the time-ependent regulation of gene expression ofMP-1, and increased activity of this enzyme

ollowing application of force. In the pressureide, a rise in MMP-1 level was observed at day 7,ollowed by a decrease at days 14 and 28,hereas in the tension side, a rise in mRNA levelf MMP-1 was noted at day 3, with a further

ncrease in day 7, followed by a decrease in day4. This pattern was followed by a 10-fold in-rease at day 28. It was concluded that the re-ponsiveness of MMP-1 to force is not only theesult of tissue injury and inflammatory reac-ions, but also of the mechanical stresses them-elves.69

Bolcato-Bellemin and coworkers, through cellultures following application of mechanicaltretch, demonstrated an increase in mRNAene transcription of integrin subunit �1 in gin-ival fibroblasts. Integrin subunit �1 is presentn basal and parabasal cells of the gingival epi-helium, and is involved in the formation of

ocal contacts, where integrin cytoplasmic parts 3

re linked to cytoskeleton components via aridging molecule, focal adhesion kinase (FAK).t was demonstrated that p125FAK, located pri-arily at the cell periphery, is activated by

yrosine phosphorylation on binding of �1-ntegrins to an ECM ligand, triggering signal

echanotransduction. They observed a rise of125FAK in fibroblastic cultures subjected to me-hanical strain, providing a preliminary reportn a potential future research on the role ofingival fibroblasts in tooth movement.70

ong-Term Gingival Effects of Forcepplication

t is clear from the ongoing discussion that orth-dontic treatment has a direct influence on gin-ival health. Glans and coworkers reported on aarked and statistically significant improve-ent in gingival health of patients with initially

rowded dentitions, from 12 weeks after bond-ng until debonding. They attributed this find-ng to leveling of the dentition performed withinhese 12 weeks, making oral hygiene measuresffective, while at the same time evoking patientotivation by creating better esthetics.71 A sim-

lar result was reported by Davies and coworkers,ut they interpreted it as a behavioral change,ather than as the outcome of orthodontic treat-ent per se. They concluded that regular visits

o the orthodontist are the most likely reason forhe improvement in oral hygiene and gingivalealth.61 It may be prudent to secure the sup-ortive comanagement of a periodontist or re-erring dentist where indicated.

anagement or Reduction of the Sideffects of Orthodontic Treatmentn the Gingiva

lthough various methods have been used tomprove oral hygiene, optimum mechanical re-

oval of plaque by brushing and by professionalcaling is considered to be the most importantunction.72-74 End-tufted brushes saturated withactericidal disinfectants such as chlorhexidineluconate, supplemented with floss threaders ortiff plastic floss that can be threaded beneathhe arch wires, are particularly useful. However,equired daily time commitment for effectivelaque abatement is often in the range of 15 to

0 minutes. Thus, family, professional, and staff
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267Gingiva and Orthodontic Treatment

ncouragement for the patient is more helpfulhan repetitious admonitions.

During orthodontic treatment, the impor-ance of a regular brushing routine, as a mea-ure of preventing or reducing gingival disease,hould be emphasized to all patients as an inte-ral and ongoing part of therapy. For this rea-on, a specially designed manual, as well aslectric toothbrushes, for use by orthodontic pa-ients may be effective for some but are a disser-ice when used as a substitute for diligent indi-idual care. An electric toothbrush used as acrutch” can be harmful to oral health by givingalse confidence of gingival health. Trimpeneersnd coworkers compared electric and manualoothbrushes for their efficacy in plaque re-

oval, and concluded that manual toothbrushesre most effective in orthodontic patients.75 Atudy by Kilicoglu and coworkers even foundhat specially designed orthodontic toothbrushesere not superior to classic toothbrushes in

erms of plaque-removing efficacy.15 These re-ults, however, have not remained unchal-enged. In a series of studies that followed, thefficacy of electric toothbrushes, when com-ared with their manual counterparts, wereonstantly superior.15,76-78 Hickmann and co-orkers conducted a detailed evaluation regard-

ng this controversy in 63 patients, with the helpf a plaque index, gingival index, mouth rinseith water, interdental bleeding index, and as-

essment of tissue trauma. The results they ob-ained were in favor of powered toothbrushesith dedicated orthodontic heads.76 All these

tudies point to the importance of oral hygieneeasures rather than just evaluation of different

ypes of tooth brushes—classic, manual orth-dontic, or powered. The factor that is most

mportant clinically is the motivation of the pa-ient to accomplish daily efficient and effectiveemoval of dental plaque, a process for which aeam effort is often necessary and in which allatients should be carefully instructed.

harmaceutical Aids

reventive clinical plaque control methods withhlorhexidine mouthwash have been used inrthodontic patients. In the literature, conflict-

ng results on the efficacy have been reported,ith studies reporting favorable results while

thers report unfavorable results.79-81 Anderson p

nd coworkers evaluated this issue recently andtated that chlorhexidine in addition to regularral hygiene habits was effective in the reductionf plaque and gingivitis in orthodontic patients.hey also assessed the discoloration or staining

n the tooth surface with long-term use of chlo-hexidine and stated that it was neither clinicallyor statistically significant.82

Removal of dental plaque in orthodontic pa-ients with various other measures is also re-orted. Isotupa and coworkers tried polyol gums

n orthodontic patients for plaque control andbserved a reduction in plaque and in Streptococ-us mutans numbers, showing its efficacy.83 Innother study, Othman and coworkers com-ined orthodontic composite resins with benza-

konium chloride, an antimicrobial agent,or bonding orthodontic brackets. The resultsemonstrated effective antimicrobial action byhis compound, without altering the mechanicalroperties of the composite resin.84 The effectf combined application of antimicrobial anduoride varnish to orthodontic patients for theurpose of reducing plaque and gingivitis wastudied by Ogaard and coworkers. They reported

significant reduction in Streptococcus mutansount in plaque during first 48 hours of treat-ent with fixed appliances. They also observed a

ignificant reduction in the amount of plaquend gingivitis in this study sample.85

he Timing of Soft-Tissue Augmentation:rophylactic Versus Therapeutic?

ven though prophylactic management of gin-ival recession in at-risk orthodontic patients re-ains controversial, there were numerous re-

orts that suggest that universal prophylaxis inases of doubt enhances ultimate treatment ef-ciency.20-23,33 Preorthodontic gingival augmen-

ation procedures are indicated in patients withhin gingival tissue and in areas of possible archxpansion, but not if tooth movement is con-trained to the envelope of the alveolar process.he primary therapeutic goal is to increase theuccolingual thickness of the marginal tissuesver teeth that might develop alveolar bone de-iscence during tooth movement. The rationaleehind this procedure is that increasing the gin-ival thickness creates more robust marginal tis-ues, which are less susceptible to trauma or

laque related inflammation and subsequent re-
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ession. The subepithelial free connective tissuerafting for increasing the apicocoronal width oferatinized gingiva and establishing root cover-ge in areas of marginal tissue recession is theost preferred method. The efficacy of this pro-

edure was evaluated by Holmes and coworkersn dogs, and they reported favorable results,hich were stable throughout the orthodontic

reatment period.86

Interdental clefts at the site of extractionpace closure contributing to poor periodontalealth and orthodontic relapse are often treatedy either electrosurgery or conventional surgicalingivectomy.87 Malkoc and coworkers comparedhe efficacy of both techniques and found no sta-istically significantly difference between the re-ults. However, they cautioned against the use oflectrosurgery in patients bearing cardiac pace-akers. They stated that, with proper attention to

afeguards, both techniques can be used effectivelyo remove gingival invaginations and over-rowth—hyperplasia or hypertrophy48 (Fig 7).

he Gingiva After Removalf Orthodontic Appliances

he favorable as well as the harmful effects thatan occur during orthodontic treatment are wellnderstood. The fate of these effects, once theppliance is removed, was addressed by Sallumnd coworkers. They reported a significant re-uction in plaque index, bleeding on probing,nd probing depth, the three most importantarameters indicating clinical gingival health,nce orthodontic appliances are removed. Theemoval of orthodontic appliances, along withrofessional scaling and proper instruction on

igure 7. These two portraits of the same patient dnlargement can add significantly to the esthetic orthogure is available online.)

ral hygiene, leads to significant reduction in p

he periodontopathogens harbored in the oralavity, such as Bacteroides forsythus and Actinoba-illus actinomycetemcomitans, from both supra- andubgingival plaque samples.88

At the molecular level, Redlich and coworkersbserved a gradual increase in both COL-1 andIMP gene expressions concomitant with a de-rease in MMP-1 after removal of orthodonticppliances. These findings indicate progressiveenormalization of collagen metabolism in theingiva, once orthodontic appliances are out ofhe mouth.69

onclusions

his review has attempted to outline all the ef-ects that fixed orthodontic appliances arerone to produce on gingival tissues. It is evi-ent that the mere placement of orthodonticppliances can contribute to undesirable changes,uch as the formation of plaque-harboring areas, ahange in oral ecosystem, a shift from normalora to microbes marked as periodontopatho-ens, gingival inflammation, irreversible gingivalyperplasia, permanent loss of periodontal at-

achment (bone loss), and bony or gingival de-iscence (recession). While these effects can beontrolled by proper oral hygiene measures, fail-ng to adhere to such a regimen might result innitiation of destructive periodontal diseasehrough the breach in natural protective barri-rs. These findings point to the importance oftressing oral hygiene and effective infectionontrol as an integral part of every visit to therthodontist. Repetitive and the “recovery alwaysccompanies . . .” which is “obvious” to theoorly informed, is clearly not supported by

nstrate that attention to and treatment of gingivaltic outcome in total facial esthetics. (Color version of

emodon

eriodontal literature. A thorough, evidenced-

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269Gingiva and Orthodontic Treatment

ased, candid informed consent recruits theatient and parent as collaborative informalcotherapists.” As important and legitimatetakeholders in optimal outcome, they musthare the responsibility for any untoward events,ide effects, or complications that may be per-anently damaging to the underlying soft tissue

nd bone. When a damaging side effect is found,he orthodontist should consider obtaining aonsultation with a periodontist, and removerritating forces, as well as attachments and ap-liances, which may be construed as contribut-

ng factors, so that further destruction is pre-ented.

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4. Addy M, Dummer PM, Griffiths G, et al: Prevalence ofplaque, gingivitis and caries in 11-12 year old children inSouth Wales. Community Dent Oral Epidemiol 14:115-118, 1986

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1. Davies TM, Shaw WC, Worthington HV, et al. The effectof orthodontic treatment on plaque and gingivitis. Am JOrthod Dentofacial Orthop 99:155-161, 1991

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