Objective: 

To investigate the prevalence of distinguishable soft tissue scarring after the removal of temporary anchorage devices (TADs) such as orthodontic miniscrews and to analyze the factors associated with scar formation.

Materials and Methods: 

The prevalence of soft tissue scarring in 66 patients (202 miniscrew removal sites) was clinically investigated at least 1 year after miniscrew removal. To determine the clinical factors associated with soft tissue scar formation, miniscrew stability; host factors including age, gender, and gingival biotype; and miniscrew-related factors such as insertion site, vertical position, and insertion period were evaluated.

Results: 

The prevalence of a distinguishable scar remaining at least 1 year after miniscrew removal was 44.6%. Patients with flat gingiva showed a significantly higher prevalence of soft tissue scar formation than did those with pronounced scalloped gingiva (P < .05). Maxillary buccal removal sites showed a significantly higher prevalence of soft tissue scar formation than did those in the mandible or palatal slope (P < .05). Miniscrew sites at the alveolar mucosa showed a significantly lower prevalence of soft tissue scar formation than did those in the mucogingival junction or the attached gingiva (P < .01).

Conclusion: 

The prevalence of distinguishable scarring after miniscrew removal was fairly high. On the basis of our results, patients with flat gingiva and buccal interdental gingival insertion sites are more susceptible to scar formation.

Temporary anchorage devices (TADs) such as orthodontic miniscrews are now accepted in contemporary orthodontics as effective orthodontic appliances. During miniscrew insertion, the threads of the miniscrew penetrate the soft tissue, cortical bone, and cancellous bone to provide stability, and the head structure is commonly exposed to the oral cavity. However, unlike dental implants, TADs are by definition temporary devices, which are removed after use. Most clinicians use one simple universal removal scheme, manual turning of the miniscrew in the opposite direction of insertion, assuming that the site will naturally heal over time.

The removal of a miniscrew leaves a transient open wound in the oral cavity that penetrates the soft tissue and the underlying alveolar bone and has a sulcular epithelium component at the wound margin, similar to a tooth-extraction site. Therefore, the healing process after miniscrew removal is assumed to follow the classical healing cascade of an alveolar socket after tooth extraction.1,2  In clinical dentistry, it is commonly accepted that intraoral wounds heal more rapidly with less scar formation than skin wounds,36  and the most favored sites for miniscrew insertion, such as the attached gingiva or the palate, are considered safe zones regarding scar formation.5,6 

However, clinically distinguishable soft tissue scars are frequently noted after miniscrew removal even years later. In general, the scar tissue is localized to the removal site, has a clear margin and a protuberant appearance similar to a small lump or a wart, and is distinguished from the adjacent tissue by a whitish color (Figure 1A,B). A histological study with Beagle dogs reported that the epithelial lining and inflamed soft tissue surrounding the failed miniscrew due to root touching may not resolve, suggesting the possibility of irreversible soft tissue changes after miniscrew removal.7  However, the natural course of soft and hard tissue healing, let alone the clinical possibilities of incomplete healing after miniscrew removal, have not been documented in the orthodontic literature.

Figure 1.

Typical soft tissue scar detected after miniscrew removal. (A, B) Development of a typical soft tissue scar at identical miniscrew removal sites (black arrow) just after debonding and miniscrew removal (A) and 18 months after removal (B). (C, D) Scarless healing of identical miniscrew removal sites (black arrow) just after debonding and miniscrew removal (C) and 12 months after removal (D). Note the presence of distinguishable, whitish, lumplike soft tissue scarring in (B) compared with scarless healing in (D).

Figure 1.

Typical soft tissue scar detected after miniscrew removal. (A, B) Development of a typical soft tissue scar at identical miniscrew removal sites (black arrow) just after debonding and miniscrew removal (A) and 18 months after removal (B). (C, D) Scarless healing of identical miniscrew removal sites (black arrow) just after debonding and miniscrew removal (C) and 12 months after removal (D). Note the presence of distinguishable, whitish, lumplike soft tissue scarring in (B) compared with scarless healing in (D).

Close modal

Therefore, the primary objective of this study was to investigate the overall prevalence of soft tissue scarring after the removal of orthodontic miniscrews. The objectives were (1) participants: adult orthodontic patients (>18 years old); (2) outcome: prevalence of scar formation; and (3) time: 1 year or more after miniscrew removal. In addition, our secondary objective was to retrospectively analyze factors associated with scar formation.

Subjects

To calculate the overall prevalence of scarring after miniscrew removal, a prospective study was designed. First, an assessment period (July 2012–May 2013) was set. During the assessment period, all adult subjects (>18 years old) who came in for posttreatment checkups and had used orthodontic miniscrews during treatment at the Department of Orthodontics, Gangnam Severance Hospital, were evaluated for the presence of scarring at miniscrew removal sites.

Wound regeneration including maturation and remodeling usually continues up to 12 months8,9 ; thus, scars detected after 1 year can be considered irreversible. Therefore, subjects examined had completed orthodontic treatment that included the use of miniscrews, and the miniscrews had been removed for at least 1 year (range, 12–58 months) prior to the assessment. Institutional Review Board approval was obtained.

The study cohort consisted of 66 adult subjects: 52 women (mean age, 28.5 ± 10.02 years) and 14 men (mean age, 28.9 ± 8.87 years). Two types of self-drilling miniscrews—the cylindrical type (1.5 mm in diameter, 7 mm in length; ACR OAS-T1507, Biomaterials Korea, Seoul, Korea) or combined cylindrical and tapered type (1.8 mm in diameter, 7 mm in length; Orlus Classic 1O18107, Ortholution, Seoul, Korea)—were used, and all miniscrew heads were exposed to the oral cavity. Orthodontic forces were loaded immediately and directly using elastomeric modules for en masse retraction or molar intrusion. The miniscrews were removed manually using the same hand driver used for insertion. Saline irrigation was performed without any medication after the removal.

Investigation of the Presence of Scar Tissue and Its Prevalence

The examiner clinically assessed the removal sites to determine the presence of scarlike tissue that was distinguishable from the adjacent tissue by its color, morphology, and texture. Scar tissue was defined as present when the removal site showed the following specific features: (1) whitish color distinguishable from the adjacent reddish-pink gingiva or the oral mucosa; (2) small, elevated, lumplike morphology localized to the removal site matching the size of the miniscrew diameter; and (3) firm texture upon palpation compared with the adjacent tissue (Figure 1A,B). Scar tissue was defined as not present when the removal site was indistinguishable from the neighboring tissue (Figure 1C,D). After the clinical evaluation, intraoral photographs were taken. The second examiner reconfirmed the presence of the distinguishable scarlike tissue using intraoral photographs, and interrater reliability was calculated. Of the 66 subjects, 13 had their second visit during the evaluation period (36 sites out of 202 sites). During the second visit, which was in general after 6 months of the primary assessment, the subjects were reexamined by the same examiner, and the intrarater reliability was calculated. The kappa values for the inter- and intrarater reliability were both 1.00, indicating 100% agreement on judging the presence of scars.

Analysis of Factors Associated With Scar Formation

The clinical records of the enrolled subjects were retrospectively collected. Candidate-influencing factors were selected based on previous reports. Miniscrew stability was selected since histological changes were reported following the removal of failed miniscrews, suggesting possibilities of scarring.7  Host factors such as age and gingival biotypes may influence soft tissue response during healing1012 ; thus, they were raised as candidate factors. Miniscrew insertion factors such as location were selected because differences in anatomical structures were reported to show differences in healing.1,3,5 

Miniscrew Stability

Removal sites of clinically stable miniscrews, which showed no sign of mobility and were used successfully until removal, were classified into the success group. Removal sites that had a history of early removal because they were clinically unacceptable for anchorage due to miniscrew mobility were classified into the failure group.1316 

Host Factors: Gender, Age, and Gingival Biotypes

Subjects were subdivided into age groups for comparison. Using initial photographs, anatomical crown length (CL; Figure 2, arrow), the distance between the gingival margin and the incisal edge of the crown, and the crown width (CW; Figure 2, dotted arrow), the distance between the approximal tooth surface of the borderline between the portion of the cervical and middle third of the of the maxillary right central incisor were measured, and the crown form ratio (CW/CL) was calculated to determine the pronounced scalloped and flat gingival biotypes as mentioned previously.10  Of the 66 subjects, the highest and lowest 20% (13 subjects) of each tail in terms of CW/CL ratio were classified into the flat gingival biotype (CW/CL, 0.61 ± 0.097) or the pronounced scalloped gingival biotype (CW/CL, 0.81 ± 0.0759), respectively (Figure 2A,B). In general, the pronounced scalloped gingival biotype is characterized by a long, slender crown form; long interdental papilla; thin buccal marginal gingiva; and narrow attached gingiva, while the flat gingival biotype indicates a relatively short and wide crown form, short interdental papilla, thick buccal marginal gingiva, and wide attached gingiva.10,11,17 

Figure 2.

The determination of gingival biotypes. Crown length (CL, arrow), the distance between the gingival margin and the incisal edge of the crown and the crown width (CW, dotted arrow), and the distance between the approximal tooth surface of the borderline between the portion of the cervical and middle third of the of the maxillary right central incisor were measured, and the crown form ratio (CW/CL) was calculated to determine the pronounced scalloped and flat gingival biotypes. Flat gingival biotype (A) indicates a higher anatomical crown width/crown length ratio than pronounced scalloped gingival biotype (B).

Figure 2.

The determination of gingival biotypes. Crown length (CL, arrow), the distance between the gingival margin and the incisal edge of the crown and the crown width (CW, dotted arrow), and the distance between the approximal tooth surface of the borderline between the portion of the cervical and middle third of the of the maxillary right central incisor were measured, and the crown form ratio (CW/CL) was calculated to determine the pronounced scalloped and flat gingival biotypes. Flat gingival biotype (A) indicates a higher anatomical crown width/crown length ratio than pronounced scalloped gingival biotype (B).

Close modal

Miniscrew-Related Factors

The buccolingual insertion sites, vertical position, and insertion period were investigated using clinical records including intraoral photographs. The buccolingual insertion sites were divided into the maxillary buccal (including labial), mandibular buccal (including labial), palatal slope, and midpalatal regions. One subject was excluded from the statistical comparison because only one miniscrew was removed from the midpalate. For miniscrews placed in the maxillary or mandibular buccal regions in the vertical position were additionally evaluated and subdivided into three groups: within the attached gingiva, at the mucogingival junction, or within the alveolar mucosa. The palatal slope and midpalatal areas were not classified according to vertical position because these areas are evenly composed of thick, keratinized gingiva. The insertion period was calculated from the date of miniscrew insertion to its removal.

Statistical Analysis

The percentage of distinguishable scars per total sites was calculated. To clarify the relationship between the prevalence of scarring and the clinical factors, the chi-square test was performed and the relative risk was calculated. An independent t-test was performed for continuous variables. SAS (Statistical Analysis System, SAS Institute, Cary, NC) software was used for statistical analysis. The significance level was set at P < .05.

Prevalence of Distinguishable Scarring After Miniscrew Removal

Of the 66 subjects, 43 had one or more distinguishable scars at the miniscrew removal sites. Of the 202 miniscrew removal sites, 90 presented distinguishable scarring, indicating an overall prevalence of 44.6%.

Of the 202 miniscrews evaluated, 186 were clinically stable until their removal (success group), and the other 16 were removed because they were clinically unacceptable for anchorage due to mobility (failure group). The overall success rate of the 202 miniscrews evaluated was 92.1%. The prevalence of scarring in the success and the failure groups was 45.2% and 37.5%, respectively. The prevalence of scarring was not significantly different between the two groups (Table 1).

Table 1. 

Prevalance of Scar Formation (%)a

Prevalance of Scar Formation (%)a
Prevalance of Scar Formation (%)a

Association Between Host Factors and the Prevalence of Scarring

Gender and age

Of the 52 female subjects, 37 had one or more soft tissue scar sites. For men, 6 of 14 had one or more soft tissue scar sites. The prevalence of scarring was 48.2% (81 of 168) for women and 26.5% (9 of 34) for men. The prevalence of scarring according to gender was not statistically significant (Table 2). Statistical significance was not indicated between the different age groups (Table 3).

Table 2. 

Prevalance of Scar Formation According to Gendera

Prevalance of Scar Formation According to Gendera
Prevalance of Scar Formation According to Gendera
Table 3. 

Prevalance of Scar Formation According to Agea

Prevalance of Scar Formation According to Agea
Prevalance of Scar Formation According to Agea

Gingival biotypes

In the pronounced scalloped biotypes, 5 of 13 patients had at least one soft tissue scar. In the flat gingival biotypes, 10 of 13 had one or more soft tissue scars. The prevalence of scarring was 18.8% (6 of 32) for pronounced scalloped biotypes and 46.7% (21 of 45) for the flat gingival biotypes. The flat gingival biotypes had a significantly higher prevalence of scarring than did the pronounced scalloped biotypes (P < .05; Table 4).

Table 4. 

Prevalance of Scar Formation According to Gingival Biotypes

Prevalance of Scar Formation According to Gingival Biotypes
Prevalance of Scar Formation According to Gingival Biotypes

The relative risk of scarring in the flat gingival biotypes was 2.5 (95% confidence interval [CI], 1.13–5.46), indicating a risk of scarring 2.5 times higher than the pronounced scalloped biotypes.

Association Between the Miniscrew-Related Factors and the Prevalence of Scarring

Insertion sites and vertical position

The prevalence of distinguishable scarring in the maxillary buccal, mandibular buccal, and palatal slope regions was 56.6% (69 of 122), 27.4% (17 of 62), and 23.5% (4 of 17), respectively. The maxillary buccal region had a significantly higher prevalence of scarring compared with the mandibular buccal or palatal slope regions (P < .05; Table 5). The relative risk of scarring in the maxillary buccal region was 2.1 times that of the mandibular buccal region (95% CI, 1.34–3.18) and 2.4 times that of the palatal region (95% CI, 1.01–5.74).

Table 5. 

Prevalence of Scar Formation According to Insertion Sitesa

Prevalence of Scar Formation According to Insertion Sitesa
Prevalence of Scar Formation According to Insertion Sitesa

The prevalence of scarring in the attached gingiva, mucogingival junction, and alveolar mucosa was 58.3% (28 of 48 sites), 50.5% (49 of 97 sites), and 23.1% (9 of 39 sites), respectively. The alveolar mucosa showed a significantly lower prevalence of scarring compared with the attached gingiva or the mucogingival junction (P < .05; Table 6). The relative risk of scarring in the attached gingiva was 2.5 (95% CI, 1.36–4.70) and in the mucogingival junction was 2.2 (95% CI, 1.19–4.01), indicating a 2.5 and 2.2 times higher risk of scarring than the alveolar mucosa, respectively.

Table 6. 

Prevalence of Scar Formation According to Vertical Insertion Positiona

Prevalence of Scar Formation According to Vertical Insertion Positiona
Prevalence of Scar Formation According to Vertical Insertion Positiona

Insertion Period

The mean insertion period of the miniscrews was 11.7 ± 9.13 months in subjects with distinguishable scars and 11. 2 ± 9.03 in subjects without distinguishable scars. The insertion period was not significantly different between the two groups (Table 7).

Table 7. 

Comparison of Insertion Periods Between Subjects With and Without Scarringa

Comparison of Insertion Periods Between Subjects With and Without Scarringa
Comparison of Insertion Periods Between Subjects With and Without Scarringa

A scar is a fibroproliferative lesion caused by an imbalance between the synthesis and degradation of the extracellular matrix during remodeling after inflammation or trauma.18  Skin scars with an elevated, firm surface limited to the inflammation or trauma site where the continuity of epithelium was destroyed are classified as hypertrophic scars.19  The scar remaining after miniscrew removal has similar characteristics as hypertrophic scars of the skin.20,21  The prevalence of hypertrophic scars in various skin regions is reported to be about 60–63%.12,22  It is generally accepted that intraoral wounds are less likely to scar than skin wounds.4,5  Accordingly, we observed that the prevalence of scarring at miniscrew removal sites was 44.6%, lower than skin lesions but not so low as to be ignored.

During the wound-healing process, primary closure of the wound, minimal mechanical stimuli, and sufficient vascularization are essential for favorable healing.23  In addition, the shallower the wound depth, the better the prognosis for healing.4,24,25  Because commercially available miniscrews are less than 2 mm in diameter, the current removal schemes do not necessarily recommend primary closure using sutures after miniscrew removal.26  Even though the regions used for miniscrew insertion (such as the attached gingiva and the palate) are known as the safe zone for scar formation,46  there are several conditions that are unfavorable for scarless healing of miniscrew removal sites regardless of stability. Continuous mechanical stimulation is unavoidable due to mastication and phonation, and the wound penetrates deep into the cancellous bone, which may limit the healing process.

Intrinsic individual characteristics are known to affect the scarring process of wounds.27  Our results indicate that patients with a flat gingival biotype are more susceptible to scarring than are those with the pronounced scalloped biotype. Individuals with flat gingiva are known to have a lower risk of gingival recession than those with pronounced scalloped gingiva.10  On the other hand, gingival regrowth is more evident following surgical procedures in the thick flat gingival biotypes compared with the scalloped thin gingival biotypes regardless of age and gender.11,28  Judging from these findings, patients with flat gingiva may have a more active synthetic process or may be more resistant to degradation. Therefore, during the healing process after miniscrew removal, patients with flat gingiva may synthesize excessive collagen compared with those with pronounced scalloped gingiva, which easily results in hypertrophic scars.

Of the miniscrew-related factors, insertion sites in the alveolar mucosa showed less scar formation than did those in the attached gingiva or the mucogingival junction. Histologically, the alveolar mucosa consists of nonkeratinized epithelium, loose connective tissue with abundant vascularization, and many more elastic fibers than collagen.11  These histological features might contribute to more favorable wound healing. Maxillary buccal insertion sites are more likely to have detectable scarring compared with those in the mandible. Since the maxillary buccal region has wider attached gingiva compared with the mandible, more miniscrews might have been inserted into the attached gingiva of the maxilla, thereby increasing the risk of scarring. Alternatively, the differences in bone composition between the maxilla and mandible may have caused the significant differences in scarring in these regions. Differences in the presence of food debris, which is reportedly more prevalent in the extraction sockets of the maxilla, may also hinder healing after miniscrew removal.1 

Clinically, some patients are conscious of the abnormal appearance of the scar tissue and question whether it will disappear over time. Although there is no pain on palpation, esthetic issues may arise when scarring is present in the anterior region. It also creates differences in tactile sensations of the tongue during intraoral functions, especially when located in the palatal region. Most importantly, unexpected and unwanted scarring can reduce patient satisfaction with the treatment outcome.

The gingival biotype may be helpful for predicting the susceptibility to scarring after miniscrew removal, but regulation of intrinsic characteristics is far beyond our treatment scope. On the other hand, regulation of miniscrew-related factors such as insertion sites is more feasible. However, the most favorable and common miniscrew insertion site, the maxillary buccal interdental region within the attached gingival zone,2932  turned out to be the most susceptible site for scarring.

Therefore, to solve this clinical dilemma, the development of appropriate postoperative/removal care to promote favorable healing may be necessary. One action may be to provide primary closure of the removal site with sutures or to use pressure garments to inhibit excess proliferation of fibroblasts, protect against irritation, and reduce the scar size as with skin lesions.20,33,34 

Although miniscrew failure per se did not increase the risk of scarring, our study was cross-sectional, and the course of initial healing was not evaluated. Since infection and persistent inflammation after removal may cause incomplete healing and result in scarring,7  the natural course of healing after miniscrew removal and factors influencing initial healing should be further evaluated in the future.

  • The overall prevalence of distinguishable scarring after miniscrew removal was 44.6%.

  • The flat gingival biotype and insertion sites in the maxillary buccal interdental region are susceptible for scarring.

This research was supported by the Faculty Research Grant 6-2013-0179, College Dentistry, Yonsei University.

1.
Pietrokovski
J
,
Massler
M
.
Ridge remodeling after tooth extraction in rats
.
J Dent Res
.
1967
;
46
:
222
231
.
2.
Amler
MH
.
The time sequence of tissue regeneration in human extraction wounds
.
Oral Surg Oral Med Oral Pathol
.
1969
;
27
:
309
318
.
3.
Szpaderska
AM
,
Zuckerman
JD
,
DiPietro
LA
.
Differential injury responses in oral mucosal and cutaneous wounds
.
J Dent Res
.
2003
;
82
:
621
626
.
4.
Wong
JW
,
Gallant-Behm
C
,
Wiebe
C
,
et al.
Wound healing in oral mucosa results in reduced scar formation as compared with skin: evidence from the red Duroc pig model and humans
.
Wound Repair Regen
.
2009
;
17
:
717
729
.
5.
Mak
K
,
Manji
A
,
Gallant-Behm
C
,
et al.
Scarless healing of oral mucosa is characterized by faster resolution of inflammation and control of myofibroblast action compared to skin wounds in the red Duroc pig model
.
J Dermatol Sci
.
2009
;
56
:
168
180
.
6.
Larjava
H
,
Wiebe
C
,
Gallant-Behm
C
,
Hart
DA
,
Heino
J
,
Hakkinen
L
.
Exploring scarless healing of oral soft tissues
.
J Can Dent Assoc
.
2011
;
77
:
b18
.
7.
Chen
SSH
,
Chang
HH
,
Chen
YH
,
et al.
Tissue reaction surrounding miniscrews for orthodontic anchorage: an animal experiment
.
J Dent Sci
.
2012
;
7
:
57
64
.
8.
Bond
JS
,
Duncan
JA
,
Sattar
A
,
et al.
Maturation of the human scar: an observational study
.
Plast Reconstr Surg
.
2008
;
121
:
1650
1658
.
9.
Gurtner
GC
,
Werner
S
,
Barrandon
Y
,
Longaker
MT
.
Wound repair and regeneration
.
Nature
.
2008
;
453
:
314
321
.
10.
Olsson
M
,
Lindhe
J
.
Periodontal characteristics in individuals with varying form of the upper central incisors
.
J Clin Periodontol
.
1991
;
18
:
78
82
.
11.
Lindhe
J
,
Karring
T
,
Lang
NP
.
Clinical Periodontology and Implant Dentistry
. 4th ed.
Oxford, UK
:
Blackwell
;
2003
.
12.
Kim
JH
,
Sung
JY
,
Kim
YH
,
et al.
Risk factors for hypertrophic surgical scar development after thyroidectomy
.
Wound Repair Regen
.
2012
;
20
:
304
310
.
13.
Papageorgiou
SN
,
Zogakis
IP
,
Papadopoulos
MA
.
Failure rates and associated risk factors of orthodontic miniscrew implants: a meta-analysis
.
Am J Orthod Dentofacial Orthop
.
2012
;
142
:
577
595
e577
.
14.
Motoyoshi
M
,
Matsuoka
M
,
Shimizu
N
.
Application of orthodontic mini-implants in adolescents
.
Int J Oral Maxillofac Surg
.
2007
;
36
:
695
699
.
15.
Chaddad
K
,
Ferreira
AF
,
Geurs
N
,
Reddy
MS
.
Influence of surface characteristics on survival rates of mini-implants
.
Angle Orthod
.
2008
;
78
:
107
113
.
16.
Kim
JS
,
Choi
SH
,
Cha
SK
,
et al.
Comparison of success rates of orthodontic mini-screws by the insertion method
.
Korean J Orthod
.
2012
;
42
:
242
248
.
17.
Olsson
M
,
Lindhe
J
,
Marinello
CP
.
On the relationship between crown form and clinical features of the gingiva in adolescents
.
J Clin Periodontol
.
1993
;
20
:
570
577
.
18.
Tredget
EE
.
Pathophysiology and treatment of fibroproliferative disorders following thermal injury
.
Ann N Y Acad Sci
.
1999
;
888
:
165
182
.
19.
Tuan
TL
,
Nichter
LS
.
The molecular basis of keloid and hypertrophic scar formation
.
Mol Med Today
.
1998
;
4
:
19
24
.
20.
Urioste
SS
,
Arndt
KA
,
Dover
JS
.
Keloids and hypertrophic scars: review and treatment strategies
.
Semin Cutan Med Surg
.
1999
;
18
:
159
171
.
21.
Niessen
FB
,
Spauwen
PH
,
Schalkwijk
J
,
Kon
M
.
On the nature of hypertrophic scars and keloids: a review
.
Plast Reconstr Surg
.
1999
;
104
:
1435
1458
.
22.
Mahdavian Delavary
B
,
van der Veer
WM
,
Ferreira
JA
,
Niessen
FB
.
Formation of hypertrophic scars: evolution and susceptibility
.
J Plast Surg Hand Surg
.
2012
;
46
:
95
101
.
23.
Slemp
AE
,
Kirschner
RE
.
Keloids and scars: a review of keloids and scars, their pathogenesis, risk factors, and management
.
Curr Opin Pediatr
.
2006
;
18
:
396
402
.
24.
Dunkin
CS
,
Pleat
JM
,
Gillespie
PH
,
Tyler
MP
,
Roberts
AH
,
McGrouther
DA
.
Scarring occurs at a critical depth of skin injury: precise measurement in a graduated dermal scratch in human volunteers
.
Plast Reconstr Surg
.
2007
;
119
:
1722
1732
.
25.
Monstrey
S
,
Hoeksema
H
,
Verbelen
J
,
Pirayesh
A
,
Blondeel
P
.
Assessment of burn depth and burn wound healing potential
.
Burns
.
2008
;
34
:
761
769
.
26.
Park
YC
,
Kim
JK
,
Lee
JS
.
Atlas of Contemporary Orthodontics
.
Vol III. Seoul, Korea
:
Shinheung International
.
2005
.
.
27.
Brown
JJ
,
Bayat
A
.
Genetic susceptibility to raised dermal scarring
.
Br J Dermatol
.
2009
;
161
:
8
18
.
28.
Pontoriero
R
,
Carnevale
G
.
Surgical crown lengthening: a 12-month clinical wound healing study
.
J Periodontol
.
2001
;
72
:
841
848
.
29.
Kuroda
S
,
Sugawara
Y
,
Deguchi
T
,
Kyung
HM
,
Takano-Yamamoto
T
.
Clinical use of miniscrew implants as orthodontic anchorage: success rates and postoperative discomfort
.
Am J Orthod Dentofacial Orthop
.
2007
;
131
:
9
15
.
30.
Cheng
SJ
,
Tseng
IY
,
Lee
JJ
,
Kok
SH
.
A prospective study of the risk factors associated with failure of mini-implants used for orthodontic anchorage
.
Int J Oral Maxillofac Implants
.
2004
;
19
:
100
106
.
31.
Deguchi
T
,
Takano-Yamamoto
T
,
Kanomi
R
,
Hartsfield
JK
Jr,
Roberts
WE
,
Garetto
LP
.
The use of small titanium screws for orthodontic anchorage
.
J Dent Res
.
2003
;
82
:
377
381
.
32.
Deguchi
T
,
Nasu
M
,
Murakami
K
,
Yabuuchi
T
,
Kamioka
H
,
Takano-Yamamoto
T
.
Quantitative evaluation of cortical bone thickness with computed tomographic scanning for orthodontic implants
.
Am J Orthod Dentofacial Orthop
.
2006
;
129
:
721
.
e727
712
.
33.
Fulton
JE
Jr.
Silicone gel sheeting for the prevention and management of evolving hypertrophic and keloid scars
.
Dermatol Surg
.
1995
;
21
:
947
951
.
34.
Kischer
CW
,
Shetlar
MR
,
Shetlar
CL
.
Alteration of hypertrophic scars induced by mechanical pressure
.
Arch Dermatol
.
1975
;
111
:
60
64
.