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Decision making in the treatment of patients

with malocclusion and chronic periodontitis:


Scientic evidence and clinical experience
Maria L. Geisinger, DDS, MS,1 Ramzi V. Abou-Arraj, DDS, MS,1
Nada M. Souccar, DDS, MS,2 Carolyn M. Holmes, MLIS,3 and
Nicolaas C. Geurs, DDS, MS1
With a marked increase in the number of adult patients seeking corrective
orthodontic care and the high prevalence of destructive periodontal diseases in
the adult population in the United States, the importance of addressing
inammatory periodontal diseases in patients receiving treatment for
malocclusion is critical and timely. Control of initiating etiologic factors should
be a preface to corrective orthodontic treatment of patients with inammatory
periodontal disease. Once these factors have been controlled, the progression
of treatment should be based upon the stability of the periodontal attachment
apparatus, the severity and bony morphology associated with destructive
periodontal disease, and the nature of the orthodontic tooth movement inform
the treatment sequence for patients with malocclusion and concomitant
periodontal disease. In the presence of horizontal bone loss, elimination of
periodontal pockets and other clinical signs of inammation would allow for
immediate progression to corrective orthodontic therapy. Reevaluation of
periodontal conditions after orthodontic tooth movement may then be
followed by denitive periodontal care based upon clinical ndings. Preorthodontic surgical periodontal therapy is appropriate to control periodontal
inammation and/or address deep periodontal defects that may compromise
periodontal stability during orthodontic intervention. Periodontal maintenance
therapy during active orthodontic treatment and post-treatment is critical to
long-term maintenance of orthodontic results and periodontal health. A
staged, interdisciplinary approach can most adequately treat patients to
achieve optimal esthetics, function, and oral health. (Semin Orthod 2014;
20:170176.) & 2014 Elsevier Inc. All rights reserved.

Background
1
Department of Periodontology, University of Alabama at
Birmingham, Birmingham, AL; 2Department of Orthodontics,
University of Alabama at Birmingham, Birmingham, AL; 3Lister
Hill Library, University of Alabama at Birmingham, Birmingham,
AL.
Address correspondence to Maria L. Geisinger, DDS, MS,
Department of Periodontology, University of Alabama at Birmingham, SDB 412, 1530 3rd Ave S, Birmingham, AL 35294-0007.
E-mail: miagdds@uab.edu
Findings: The severity and morphology of periodontal attachment
loss as well as the nature of the orthodontic tooth movement should be
considered when determining the proper treatment sequence and
procedures to be performed for patients with both malocclusion and
periodontal diseases.

& 2014 Elsevier Inc. All rights reserved.


1073-8746/12/1801-$30.00/0
http://dx.doi.org/10.1053/j.sodo.2014.06.006

170

ith recent evidence indicating that up to


50% of American adults have chronic
periodontitis1 and an increasing demand for
orthodontic treatment in esthetic-conscious
adults,2,3 it is important to identify and properly treat patients with periodontitis who are
undergoing orthodontic therapy. Previous
reports have indicated that in the presence of
plaque and gingival inammation, orthodontic
tooth movement can result in further periodontal disease progression and attachment
loss.4,5 Much evidence supports the need for
treatment of active periodontal disease prior to
initiation of orthodontic tooth movement6,7 and
the control of plaque levels during orthodontic

Seminars in Orthodontics, Vol 20, No 3 (September), 2014: pp 170176

Periodontal and orthodontic treatment planning

therapy in periodontally susceptible patients.8


The adjunctive use of orthodontic tooth
movement to correct periodontal infrabony
defects has been demonstrated9,10 but may not
be applicable in all cases. It is thus of critical
importance to select a predictable treatment
sequence for the adult perioortho patient to
allow for treatment and resolution of periodontal
inammation while minimizing treatment time
and surgical intervention and optimizing oral
health and esthetics. A careful evaluation of the
following factors is necessary: (1) patient's overall
health status and periodontal susceptibility, (2)
periodontal diagnosis, (3) malocclusion classication, (4) periodontal bone loss pattern, (5)
periodontal biotype, and (6) oral hygiene levels.

Factors affecting orthodontic and


periodontal treatment outcomes
In clinical practice, achieving optimal oral health
and esthetic results is dependent upon many
patient and treatment factors.

Periodontal conditions
In patients without periodontal disease who
demonstrate good oral hygiene, including
patients with a reduced but healthy periodontium,
proper orthodontic treatment caused no signicant long-term effects on periodontal attachment levels and bone levels4,1114 Conversely, in
patients with clinical signs of active periodontal
disease (i.e., deep PD, BoP, and presence of
subgingival plaque), orthodontic tooth movements can accelerate the disease process, even in
the presence of good oral hygiene.6,13,14 It has also
been well established that certain systemic conditions and ndings are risk factors for disease
progression, including: psychosocial stress,15
tobacco use,1517 systemic immune deciencies,18 diabetes mellitus,19 osteoporosis,20 certain
autoimmune disorders,21,22 and the presence of
putative periodontal pathogens.2325

Periodontal disease severity


Periodontal disease progresses very differently in
individual patients. Even in the absence of dental
care, patients demonstrate various patterns and
rapidity of bone loss.26 In addition, individual tooth
sites may be more at risk for attachment loss based
upon
clinical
ndings
and
anatomical

171

considerations,27 and tooth mortality is associated


with clinical attachment loss, tooth type, and
overall periodontal health of the dentition.28,29

Malocclusion
Depending on the diagnosed malocclusion, differing orthodontic strategies can be utilized to achieve
optimal results. Teeth that have periodontal bone
loss have a more apical center of resistance than
those with a healthy periodontium. Furthermore,
the distance between the center of resistance and
the alveolar bone crest is smaller than that of a tooth
with a healthy periodontium. Therefore, teeth with
periodontal bone loss are more prone to tipping
than bodily movement, and the moment-to-force
values at the bracket level should be increased in
order to achieve translation.30,31 Extraction of severely periodontally involved teeth and tooth movement to treat crowding can yield vast improvements
in oral hygiene.10 Crowding alone has been
reported to increase the risk for gingivitis,
independently from plaque levels.32 In addition,
while tooth rotation can be accomplished fairly
easily, it can be difcult to maintain due to the
slower turnover of the supra-alveolar periodontal
and gingival ber bundles as compared to the
periodontal ligament (PDL) bers.33,34 Severing
these bers to allow for rearrangement has been
accomplished with supracrestal berotomy procedures, which have demonstrated a greater reduction in pure rotational relapse in the maxilla than in
the mandible.35 As denitive periodontal surgery
would also sever these bers, this may be an
additional adjunctive benet of surgical treatment
performed after orthodontic tooth movement.

Periodontal bone loss pattern


Orthodontic movement of teeth into plaqueinduced infrabony pockets has been demonstrated to be possible if the active periodontal
disease has been arrested.13 In addition, extrusive
tooth movement can be used to yield coronal
positioning of connective tissue attachment and
shallowing of one- and two-walled infrabony
defects.3638 On the other hand, intrusion has
been shown to improve the periodontal condition
of healthy reduced periodontal tissues when oral
hygiene and the orthodontic forces are optimal.39,40 Therefore, denitive guided tissue
regeneration and/or osseous surgery in areas
with vertical defects may be best treated after

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Geisinger et al

orthodontic tooth movements as these movements may alter the defect dimensions, if the
patient is able to keep such defects plaque-free
during active orthodontic treatment.

Periodontal biotype
While orthodontic tooth movement is not causative for gingival recession, in patients with thin
periodontal biotype, labial tooth movements can
result in bony dehiscences, which, particularly in
the presence of plaque, can cause subsequent
gingival recession.41,42 However, in patients with
a thick periodontal biotype and/or in patients
receiving lingual movements of labially displaced
teeth, gingival recession is less likely to occur, and
orthodontic treatment may even result in a
reversal of underlying bony dehiscences and
fenestrations.41,4347 A careful assessment of the
patients' overall biotype and the necessary tooth
movement vectors for optimal results is therefore
crucial to determine if surgical gingival augmentation is necessary prior to orthodontic tooth
movement.

Oral hygiene levels


Orthodontic brackets and bands, particularly
placed in the apical third of the tooth crown, can
serve as a plaque-retentive factor and hinder oral
hygiene in patients undergoing orthodontic
tooth movement.48,49 Both qualitative and
quantitative shifts in microbiota toward a more
periodontally pathogenic biolm have been
demonstrated 6 months after the placement of
xed orthodontic appliances.50,51 Oral hygiene
levels, therefore, must be optimal prior to
orthodontic treatment and close maintenance
and monitoring during orthodontic therapy is
warranted.39,52 If periodontal pockets are deep
enough to prevent the patient from maintaining
good oral hygiene, surgical intervention prior to
orthodontic therapy for pocket elimination may
be warranted.

Discussion
The existing scientic literature consistently
emphasizes the importance of oral hygiene and
periodontal maintenance visits during the
orthodontic treatment phase of patients with
chronic or aggressive periodontitis. However,
differences in the treatment sequence of

such cases have been noted due to multiple


considerations.
Orthodontic movement per se has not been
shown to accelerate the destruction of the connective tissue attachment on teeth with healthy
periodontium8,53 or in the presence of debrided
plaque-induced suprabony lesions.7,8 In contrast,
the development of infrabony pockets was noted
on teeth harboring plaque when subjected to
tipping and/or intruding movements.6 Likewise,
bodily movement of teeth with inamed
infrabony pockets was associated with a loss of
connective tissue attachment.7 Conversely, tooth
movement into infrabony defects treated with
open ap debridement or regenerative therapies
had no or improved effect on the attachment
levels.53,54
Therefore, orthodontic treatment must be
preceded by the elimination of plaque-induced
lesions.36 There are exceptions, however, when
the orthodontic therapy is performed early in the
treatment. They include the difculty to
eliminate the periodontal infection due to
unfavorable tooth positions55 and the presence
of periodontally hopeless teeth that could be
used for anchorage purposes but eventually have
to be extracted at the end of the orthodontic phase.
Pathological tooth migration is considered a
common complication in moderate to severe
periodontitis.56 Teeth mostly affected are in the
maxillary anterior sextant and present with a
facial and incisal displacement leading to the
formation of diastemata.57 These teeth are
frequently associated with infrabony defects
due to the disease process. Orthodontic
intrusion was found to be successful in realigning the migrated teeth following surgical
and/or nonsurgical periodontal treatment.10,58
In addition, there is histological evidence of new
cementum and connective tissue attachment
formation when teeth are intruded under good
oral hygiene measures.40 It is hypothesized that
stretching of the periodontal ligament bers
creates a natural barrier against the downgrowth
of epithelial cells along with the increased
turnover rate of these cells due to the orthodontic stimulation.58
Deep infrabony defects, conversely, are often
treated with regenerative periodontal therapies
to help restore the supporting structures of the
tooth. When combined with orthodontic

Periodontal and orthodontic treatment planning

treatment, there is scarce and controversial evidence on the treatment sequence. While it has
been suggested to regenerate the defect prior to
initiation of orthodontic therapy by some
authors,54,59,60 others have proposed tooth
movement following the control of periodontal
inammation but prior to regenerative therapies
in order to create a more suitable defect for that
purpose.61,62
Other modalities of orthodontic movements
such as uprighting of mesially inclined teeth and
orthodontic extrusion have been shown to
reduce deep infrabony pockets and defects.9,63
Tipping the tooth distally minimizes the infrabony defect by widening it while the presence of
furcation involvement may worsen or remain the
same. Orthodontic extrusion has been shown to
lead to a decrease in infrabony defect depth by
coronal positioning the connective tissue
attachment. In addition, teeth with normal
periodontal support that are bodily moved into
an edentulous area with reduced bone height
were found to maintain their connective tissue
attachment and radiographic bone levels.36
Hence, it may be suggested that periodontally
involved teeth could be moved with minimal risks
into edentulous sites demonstrating reduced
alveolar bone height following appropriate
control of periodontal inammation.

Clinical decision matrix


A decision tree is suggested when considering
orthodontic therapy for patients with periodontal
disease (Fig. 1).
Initial periodontal therapy is indicated in all
patients with chronic periodontitis and inammation prior to orthodontic tooth movement.
Improved oral hygiene and nonsurgical or initial
periodontal therapy allow for removal of etiologic factors and reduction of edema and
erythema in the periodontal tissues.
If nonsurgical therapy alone allows for
cleansable defects able to be maintained with
strict periodontal maintenance during and following orthodontic therapy, orthodontic treatment may be started after initial periodontal
therapy.
If adequate plaque control can be maintained
and bleeding on probing can be eliminated in
the presence of residual mild to moderate
periodontal pockets, orthodontic therapy with

173

adequate periodontal maintenance procedures


followed by appropriate Phase II (surgical)
periodontal therapy is warranted.
If access to periodontal pocket depths is not
adequate and bleeding upon probing cannot be
eliminated after initial periodontal therapy,
Open Flap Debridement for access prior to
orthodontic tooth movement should be considered. Access to allow for complete debridement
of root surfaces and reduction of inammation is
imperative prior to initiation of tooth movement.
After orthodontic tooth movement is complete, a
comprehensive periodontal examination should
be performed to determine if further resective or
regenerative periodontal surgical treatment is
warranted or if the patient can be maintained
with regular periodontal maintenance visits. Case
series and case reports have indicated that in
cases where patients are able to maintain plaque
control, regenerative therapy after orthodontic
tooth movement may be effective.61,64
As orthodontic treatment may become challenging due to reduced anchorage possibilities,65
the retention of periodontally hopeless teeth
after initial therapy may be benecial to
maximize anchorage for leveling and aligning
of the maxillary and mandibular arches. These
hopeless teeth will be extracted at the end of
orthodontic treatment, and replacement options
will be considered.
If deep infrabony defects are present as a result
of periodontal attachment loss, regenerative
therapies are indicated prior to orthodontic tooth
movement as cleansability in deep periodontal
defects is not achievable66 and osseous resection
will result in unfavorable crown-to-root ratios and
attachment levels in sites of deep infrabony
defects.67 Pre-orthodontic regenerative therapy
has been shown to be effective, and there have not
been signicant impairments of orthodontic tooth
movement at sites with periodontal regeneration.38,54,59,68 The timing of these procedures is
widely varied in the literature, occurring from 10
days to 6 months prior to initiation of orthodontic
forces. Additionally, bone grafting materials varied widely in the literature and included autografts, allografts, xeonograft, alloplasts, barrier
membranes, and enamel matrix proteins.60
One report of inability to achieve orthodontic tooth movement in an animal model was
associated with hydroxyapatite (HA) graft, but all
other reports demonstrate successful tooth

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Geisinger et al

Figure 1. Proposed decision tree for the management of patients with periodontal disease (PD: probing depth,
BoP: bleeding on probing).

movement.60 Other reports have shown root


resorption associated with orthodontic tooth
movement into grafted sites in animal models.69,70 It is unclear, however, how the prevalence of root resorption in grafted cases may differ
from that in all orthodontic treatment as a whole.71
Strong evidence about the different treatment
options is scarce in the literature. Several case
reports, case series, and reviews have reported on
a multitude of therapies for a combined periodontalorthodontic patient care, and their
methodologies are summarized in the decision
tree. Nonetheless, all approaches agree on controlling the periodontal inammation prior to
any tooth movement. Following this initial therapy, there is a divergence in the sequence of
events based on disease severity, pattern of bone
loss, and type of malocclusion.

Conclusion
The recognition and identication of patients with
periodontal disease in the orthodontic ofce
remains key for a successful treatment and

long-term maintenance of teeth. Similarly, it is


essential for the periodontist to consider orthodontic treatment in combination with periodontal
care for patients with periodontal disease, malocclusion, and optimal oral hygiene and compliance
levels.

References
1. Eke PI, Dye BA, Wei L, Thorton-Evans GO, Genco RJ,
CDC Periodontal Disease Surveillance workgroup. Prevalence of periodontitis in adults in the United States: 2009
and 2010. J Dent Res. 2012;91(10):914920.
2. Proft WR. Contemporary Orthodontics. St. Louis, MO:
Mosby; 2000.
3. Proft WR, Fields HW, Moray LJ. Prevalence of malocclusion and orthodontic treatment need in the United
States: estimates from the NHANES III survey. Int J Adult
Orthod Orthognath Surg. 1998;13(2):97106.
4. Boyd RL, Leggott PJ, Quinn RS, Eakle WS, Chambers D.
Periodontal implications of orthodontic treatment in
adults with reduced or normal periodontal tissues versus
those of adolescents. Am J Orthod Dentofacial Orthop.
1989;96(3):191198.
5. Ong MA, Wang HL, Smith FN. Interrelationship between
periodontics and adult orthodontics. J Clin Periodontol.
1998;25(4):271277.

Periodontal and orthodontic treatment planning

6. Ericsson I, Thilander B, Lindhe J, Okamoto H. The effect


of orthodontic tilting movements on the periodontal
tissues of infected and non-infected dentitions in dogs.
J Clin Periodontol. 1977;4(4):278293.
7. Wennstrm JL, Stokland BL, Nyman S, Thilander B.
Periodontal tissue response to orthodontic movement of
teeth with infrabony pockets. Am J Orthod Dentofacial
Orthop. 1993;103(4):313319.
8. Ericsson I, Thilander B, Lindhe J. Periodontal conditions
after orthodontic tooth movements in the dog. Angle
Orthod. 1978;48(3):210218.
9. Ingber JS. Forced eruption. I. A method of treating
isolated one and two wall infrabony osseous defectsrationale and case report. J Periodontol. 1974;45(4):
199206.
10. Re S, Corrente G, Abundo R, Cardaropoli D. Orthodontic treatment in periodontally compromised patients:
12-year report. Int J Periodontics Restorative Dent. 2000;20
(1):3139.
11. Eliasson LA, Hugoson A, Kurol J, Siwe H. The effects of
orthodontic treatment on periodontal tissues in patients
with reduced periodontal support. Eur J Orthod. 1982;4
(1):19.
12. Artun J, Osterberg SK. Periodontal status of teeth facing
extraction sites long-term after orthodontic treatment.
J Periodontol. 1987;58(1):2429.
13. Sadowsky C, BeGole EA. Long-term effects of orthodontic
treatment on periodontal health. Am J Orthod. 1981;80
(2):156172.
14. Artun J, Urbye KS. The effect of orthodontic treatment on
periodontal bone support in patients with advanced loss
of marginal periodontium. Am J Orthod Dentofacial Orthop.
1988;93(2):143148.
15. Clarke NG, Hirsch RS. Personal risk factors for generalized periodontitis. J Clin Periodontol. 1995;22(2):136145.
16. Bergstrm J, Preber H. Tobacco use as a risk factor. J
Periodontol. 1994;65(5 Suppl):545550.
17. Rivera-Hidalgo F. Smoking and periodontal disease.
Periodontology 2000. 2003;32:5058.
18. Yeung SC, Stewart GJ, Cooper DA, Sindhusake D.
Progression of periodontal disease in HIV seropositive
patients. J Periodontol. 1993;64(7):651657.
19. Emrich LJ, Shlossman M, Genco RJ. Periodontal disease
in non-insulin-dependent diabetes mellitus. J Periodontol.
1991;62(2):123131.
20. Geurs NC, Lewis CE, Jeffcoat MK. Osteoporosis and
periodontal disease progression. Periodontology 2000.
2003;32:105110.
21. Rosenstein ED, Greenwald RA, Kushner LJ, Weissmann G.
Hypothesis: the humoral immune response to oral
bacteria provides a stimulus for the development of
rheumatoid arthritis. Inammation. 2004;28(6):311318.
22. Bartold PM, Marshall RI, Haynes DR. Periodontitis and
rheumatoid arthritis: a review. J Periodontol. 2005;76(11
Suppl):20662074.
23. Newman MG, Socransky SS. Predominant cultivable
microbiota in periodontosis. J Periodontal Res. 1977;12
(2):120128.
24. Socransky SS, Haffajee AD, Cugini MA, Smith C, Kent RL.
Microbial complexes in subgingival plaque. J Clin Periodontol. 1998;25(2):134144.

175

25. Michalowicz BS, Wolff LF, Klump D, et al. Periodontal


bacteria in adult twins. J Periodontol. 1999;70:263273.
26. Le H, Anerud A, Boysen H, Morrison E. Natural history
of periodontal disease in man. Rapid, moderate and no
loss of attachment in Sri Lankan laborers 14 to 46 years of
age. J Clin Periodontol. 1986;13(5):431445.
27. Grbic JT, Lamster IB. Risk indicators for future clinical
attachment loss in adult periodontitis. Tooth and site
variables. J Periodontol. 1992;63(4):262269.
28. Hujoel PP, Le H, Anerud A, Boysen H, Leroux BG. The
informativeness of attachment loss on tooth mortality.
J Periodontol. 1999;70(1):4448.
29. McGuire MK, Nunn ME. Prognosis versus actual outcome. III. The effectiveness of clinical parameters in
accurately predicting tooth survival. J Periodontol. 1996;67
(7):666674.
30. Williams S, Melsen B, Agerbaek N, Asboe V. The
orthodontic treatment of malocclusion in patients with
previous periodontal disease. Br J Orthod. 1982;9
(4):178184.
31. Tanne K, Nagataki T, Inoue Y, Sakuda M, Burstone CJ.
Patterns of initial tooth displacements associated with
various root lengths and alveolar bone heights. Am J
Orthod Dentofacial Orthop. 1991;100(1):6671.
32. Ashley FP, Usiskin LA, Wilson RF, Wagaiyu E. The
relationship between irregularity of the incisor teeth,
plaque, and gingivitis: a study in a group of schoolchildren aged 11-14 years. Eur J Orthod. 1998;20(1):6572.
33. Reitan K. Principles of retention and avoidance of
posttreatment relapse. Am J Orthod. 1969;55(6):776790.
34. Reitan K. Tissue rearrangement during retention and
avoidance of orthodontically rotated teeth. Angle Orthod.
1959;29(2):105113.
35. Edwards JG. A long-term prospective evaluation of the
circumferential supracrestal berotomy in alleviating
orthodontic relapse. Am J Orthod Dentofacial Orthop.
1988;93(5):380387.
36. Thilander B. Infrabony pockets and reduced alveolar
bone height in relation to orthodontic therapy. Semin
Orthod. 1996;2(1):5561.
37. Pontoriero R, Celenza F, Ricci G, Carnevale G. Rapid
extrusion with ber resection: a combined orthodonticperiodontic treatment modality. Int J Periodontics Restorative Dent. 1987;7(5):3043.
38. Diedrich PR. Guided tissue regeneration associated with
orthodontic therapy. Semin Orthod. 1996;2(4):3945.
39. Ong MM, Wang HL. Periodontic and orthodontic treatment in adults. Am J Orthod Dentofacial Orthop. 2002;122
(4):420428.
40. Melsen B, Agerbaek N, Eriksen J, Terp S. New attachment
through periodontal treatment and orthodontic intrusion. Am J Orthod Dentofacial Orthop. 1988;94(2):104116.
41. Wennstrm JL. Mucogingival considerations in orthodontic treatment. Semin Orthod. 1996;2(1):4654.
42. Artun J, Osterberg SK, Kokich VG. Long-term effect of
thin interdental alveolar bone on periodontal health after
orthodontic treatment. J Periodontol. 1986;57(9):341346.
43. Coatoam GW, Behrents RG, Bissada NF. The width of
keratinized gingiva during orthodontic treatment: its
signicance and impact on periodontal status. J Periodontol. 1981;52(6):307313.

176

Geisinger et al

44. Maynard JG. The rationale for mucogingival therapy in


the child and adolescent. Int J Periodontics Restorative Dent.
1987;7(1):3651.
45. Wainwright WM. Faciolingual tooth movement: its inuence on the root and cortical plate. Am J Orthod. 1973;64
(3):278302.
46. Andlin-Sobocki A, Bodin L. Dimensional alterations of
the gingiva related to changes of facial/lingual tooth
position in permanent anterior teeth of children. A 2-year
longitudinal study. J Clin Periodontol. 1993;20(3):219224.
47. Pini Prato G, Baccetti T, Giorgetti R, Agudio G, Cortellini P.
Mucogingival interceptive surgery of buccally-erupted
premolars in patients scheduled for orthodontic treatment.
II. Surgically treated versus nonsurgically treated cases.
J Periodontol. 2000;71(2):182187.
48. Bloom RH, Brown LR. A study of the effects of
orthodontic appliances on the oral microbial ora. Oral
Surg Oral Med Oral Pathol. 1964;17:658667.
49. Diamanti-Kipioti A, Gusberti FA, Lang NP. Clinical and
microbiological effects of xed orthodontic appliances.
J Clin Periodontol. 1987;14(6):326333.
50. Huser MC, Baehni PC, Lang R. Effects of orthodontic
bands on microbiologic and clinical parameters. Am J
Orthod Dentofacial Orthop. 1990;97(3):213218.
51. Quirynen M, Dewinter G, Avontroodt P, Heidbchel K,
Verdonck A, Carels C. A split-mouth study on periodontal
and microbial parameters in children with complete
unilateral cleft lip and palate. J Clin Periodontol. 2003;30
(1):4956.
52. Sanders NL. Evidence-based care in orthodontics and
periodontics: a review of the literature. J Am Dent Assoc.
1999;130(4):521527.
53. Polson A, Caton J, Polson AP, Nyman S, Novak J, Reed B.
Periodontal response after tooth movement into intrabony defects. J Periodontol. 1984;55(4):197202.
54. Ghezzi C, Masiero S, Silvestri M, Zanotti G, Rasperini G.
Orthodontic treatment of periodontally involved teeth
after tissue regeneration. Int J Periodontics Restorative Dent.
2008;28(6):559567.
55. Behr M, Proff P, Leitzmann M, et al. Survey of
congenitally missing teeth in orthodontic patients in
Eastern Bavaria. Eur J Orthod. 2011;33(1):3236.
56. Brunsvold MA. Pathologic tooth migration. J Periodontol.
2005;76(6):859866.
57. Martinez-Canut P, Carrasquer A, Magan R, Lorca A.
A study on factors associated with pathologic tooth
migration. J Clin Periodontol. 1997;24(7):492497.
58. Corrente G, Abundo R, Re S, Cardaropoli D, Cardaropoli
G. Orthodontic movement into infrabony defects in

59.

60.

61.

62.

63.

64.

65.

66.
67.

68.

69.

70.

71.

patients with advanced periodontal disease: a clinical and


radiological study. J Periodontol. 2003;74(8):11041109.
Re S, Corrente G, Abundo R, Cardaropoli D. Orthodontic
movement into bone defects augmented with bovine
bone mineral and brin sealer: a reentry case report. Int J
Periodontics Restorative Dent. 2002;22(2):138145.
Reichert C, Deschner J, Kasaj A, Jger A. Guided tissue
regeneration and orthodontics. A review of the literature.
J Orofac Orthop. 2009;70(2):619.
Passanezi E, Janson M, Janson G, Sant'Anna AP, de Freitas
MR, Henriques JF. Interdisciplinary treatment of localized juvenile periodontitis: a new perspective to an old
problem. Am J Orthod Dentofacial Orthop. 2007;131(2):
268276.
Rotundo R, Nieri M, Iachetti G, et al. Orthodontic
treatment of periodontal defects. A systematic review. Prog
Orthod. 2010;11(1):4144.
Brown IS. The effect of orthodontic therapy on certain
types of periodontal defects. I. Clinical ndings.
J Periodontol. 1973;44(12):742756.
Rabie ABM GR, Boisson M. Management of patients with
severe bone loss: Bone induction and orthodontics. World
J Orthod. 2001;2(2):142153.
Skeggs RM, Benson PE, Dyer F. Reinforcement of
anchorage during orthodontic brace treatment with
implants or other surgical methods. Cochrane Database
Syst Rev 2007:CD005098.
Socransky SS, Haffajee AD. The nature of periodontal
diseases. Ann Periodontol. 1997;2(1):310.
Ammons WF, Smith DH. Flap curettage: rationale,
technique, and expectations. Dent Clin North Am.
1976;20(1):215226.
Cardaropoli D, Re S, Manuzzi W, Gaveglio L, Cardaropoli
G. Bio-Oss collagen and orthodontic movement for the
treatment of infrabony defects in the esthetic zone. Int J
Periodontics Restorative Dent. 2006;26(6):553559.
Kawamoto T, Motohashi N, Kitamura A, Baba Y, Suzuki S,
Kuroda T. Experimental tooth movement into bone
induced by recombinant human bone morphogenetic
protein-2. Cleft Palate Craniofac J. 2003;40(5):538543.
Killiany DM. Root resorption caused by orthodontic
treatment: an evidence-based review of literature. Semin
Orthod. 1999;5(2):128133.
Lupi JE, Handelman CS, Sadowsky C. Prevalence and
severity of apical root resorption and alveolar bone loss in
orthodontically treated adults. Am J Orthod Dentofacial
Orthop. 1996;109(1):2837.

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