Multifactorial Etiology of Torus Mandibularis: Study of Twins
Multifactorial Etiology of Torus Mandibularis: Study of Twins
Multifactorial Etiology of Torus Mandibularis: Study of Twins
SUMMARY
Objective. The aim of this study is to investigate the multifactorial etiology of mandibular tori
analyzing the influence of genetics, occlusal overload, various clinical variables and their interactions.
Methods. Overall, plaster casts of 162 twins (81 twin pairs) were analyzed for the presence or
absence of mandibular tori. Atypical wear facets on canine tips or incisors were recorded to diagnose
bruxism. Angle Class, any kind of anterior open bite and positive, negative or flat curve of Wilson
were recorded. Zygosity determination was carried out using a DNA test.
Results. Mandibular tori were found in 56.8% of the cases. In 93.6% of all monozygotic twin
pairs both individuals had or did not have mandibular tori (κ=0.96±0.04; p<0.001), compared to
79.4% concordance of mandibular tori in dizygotic co-twins (κ=0.7±0.12; p<0.001). Prevalence of
mandibular tori was significantly higher in the group of bruxers (67.5%) compared to non-bruxers
(31.3%) (p<0.001). Significant association between mandibular tori and negative or flat curve of
Wilson in the maxillary second premolars and first molars was found (OR=2.55, 95% CI (1.19-5.46),
p=0.016). In all monozygotic bruxers, 97.1% showed concordance of mandibular tori presence in both
co-twins compared to 78.9% dizygotic bruxers, and this difference is statistically significant (p=0.007).
Conclusion. Our results suggest that the mandibular tori are of a multifactorial origin. Mandibular
tori seem to have genetic predisposition, and may be associated with teeth grinding as well as with
negative or flat CW in region of maxillary second premolar and first molar.
Introduction
Torus mandibularis (TM) is a common oral bony of trabecular bone and fibrofatty marrow (1, 2). It is
outgrowth formed by compact bone with small amount mostly found bilaterally in the lingual surface of the
mandible, in the region of canines or premolars (2).
1
Department of Dental and Oral Diseases, Medical Academy, Lithua- Records in the incidence of TM vary inconsistently
nian University of Health Sciences, Kaunas, Lithuania from 0.54% to 64.4% depending on the ethnic group,
2
Department of Prosthodontics, Institute of Odontology, Faculty
of Medicine, Vilnius university, Vilnius, Lithuania
race, or the investigated sample (3). These bony pro-
3
Department of Restorative Dentistry, Periodontology and tuberances are non pathological and usually do not
Endodontology, Center of Oral Health, University produce any symptoms, therefore, the cases of surgical
of Greifswald, Greifswald, Germany removal are rare (4, 5).
4
Clinic of Orthodontics, Medical Academy, Lithuanian University Various possible causes were discussed to explain
of Health Sciences, Kaunas, Lithuania
5
Institute of Biology Systems and Genetics, Veterinary Academy,
the etiology of TM, but the accepted model for the
Lithuanian University of Health Sciences, Kaunas, formation of these bony protuberances is still under
Lithuania question. Historically, the dominant focus is on genet-
ics, and the heredity of TM has been analyzed using
Adomas Auškalnis1 – D.D.S.
Vygandas Rutkūnas2 – assoc. prof., PhD
familial (6, 7), regional studies (8, 9), or comparing
Olaf Bernhardt3 – prof., Dr. med. dent. Habil. ethnic groups (10-12).
Mantas Šidlauskas4 – D.D.S. However, the heredity does not explain all the
Loreta Šalomskienė5 – PhD cases of TM. As stated by Eggen (13), genetic deter-
Nomeda Basevičienė1 – assoc. prof., PhD mination of TM was estimated to be 30%, whereas
Address correspondence to Adomas Auškalnis, Department of Dental 70% of the causes could be explained by influence of
and Oral Diseases, Medical Academy, Lithuanian University of occlusal overload and other clinical variables. In the
Health Sciences, Eivenių str. 2, 50009 Kaunas, Lithuania.
E-mail address: adomas.auskalnis@gmail.com studies analyzing TM etiology, occlusal overload is
Stomatologija, Baltic Dental and Maxillofacial Journal, 2015, Vol. 17, No. 2 35
A. Auškalnis et al. SCIENTIFIC ARTICLES
mostly described as bruxism (14-17) or heavy food DNA analysis. The sample consists of 47 monozygotic
consumption (8, 18). In most of the studies association and 34 dizygotic twin pairs. There were 100 females
between TM and occlusal overload was found. and 62 males in the sample. The age of the subjects
Other clinical variables related with the occlusal ranged from 12 to 51 years (mean age of 20.3±0.9 y.).
characteristics, malocclusion and oromaxillofacial Zygosity determination was carried out us-
function (e. g. Angle class, open bite, buccal overjet, ing a DNA test. The polymerase chain reaction set
curve of Spee etc.) were hypothesized as possibly AmpFℓSTR® Identifiler® (Applied biosystems, USA)
having a role in creating TM (19), but the studies are was used to amplify short tandem repeats and 15
limited. Significant links between TM and Eichner In- specific DNA markers (D8S1179, D21S11, D7S820,
dex, occlusal support at the premolar and molar areas, CSF1PO, D3S1358, TH01, D13S317, D16S539,
occlusal force and presence of TM were found (14). D2S1338, D19S433, vWA, TROX, D18S51, D5S818,
Moreover, number of teeth and adequately developed FGA) and the Amel fragment of the amelogenin gene
jaws were also positively related with the incidence of were used for comparison of genetic profiles. The
TM (20). In the literature, significant relation between zygosity determination using this molecular genetic
TM occurrence and temporomandibular disorders was technique reaches 99.9% accuracy.
reported as well (15, 17). Plaster casts were chosen as a reliable method to
These controversial findings of multifactorial diagnose TM, bruxism, and various occlusal variables
nature give much space for the discussions about (26, 27). Two calibrated observers (periodontologist
the origins of TM. The key to explain multifactorial and general dentist) evaluated the data manually
etiology of TM could be functional matrix hypoth- analyzing the plaster casts and looking for TM. The
esis (21). It is based on Wolff’s law, which state that nodular bone protuberance on the lingual surface of
loading force prompts remodeling and strengthening the mandible in the region of canines or premolars
of the bone (22, 23). According to functional matrix was considered as TM. Bruxism was diagnosed by
hypothesis, compressive stresses may lead to buckling recording the atypical wear facets on incisors and
of the mandible in the mental foramen region, which canine tips or non-functional surfaces. Eccentric wear
has a reduced bone volume. Osteogenic periosteum in facets, arising only during extreme extrusive mandible
these regions is stretched and this tension leads to new movements, were taken as an evidence for teeth grind-
bone formation in the form of tori (19). This functional ing (2, 28-32).
matrix hypothesis considers heredity as well, since Occlusal variables such as Angle Class, any kind
children inherit jaw form from parents (19). However, of anterior open bite in habitual occlusion and positive,
this multifactorial hypothesis of TM occurrence still negative or flat curve of Wilson (CW) on the maxillary
lacks evidence. premolars and molars were recorded. To identify Angle
Therefore, the primary purpose of this research Class, relationship between first molars was recorded.
is to investigate the multifactorial etiology of TM, In a case of Angle Class II subdivision or Angle Class
studying the influence of genetics, occlusal overload III subdivision, when molar relationship was asym-
and other clinical variables taking twins as an investi- metrical and was Class I on the one side and Class II
gation sample. Explanation of the potential causes for or III on the other, the cases were considered as Angle
TM formation may give valuable knowledge about the Class II or Angle Class III (33). CW was considered flat
biomechanical mechanisms improving bone quality when the tips of vestibular and palatal cusps were at the
(24, 25). same level on the both sides of the maxillary premolars
or molars. Patients with negative CW exhibited longer
MATERIAL AND METHODS vestibular cusps compared to palatal cusps, and on the
contrary for the patients with positive CW.
A total 162 pairs of maxillary and mandibular For calibration purposes two examiners were
plaster casts of individuals (81 pairs of twins) were trained for better reliability diagnosing TM, bruxism
examined. The plaster casts were collected using the and occlusal variables. After training, the examiners
database of Orthodontic Department and Scientific evaluated 10 plaster casts, not belonging to the study
Twin Center at the Lithuanian University of Health sample, twice. Recorded Kappa (κ) index for inter-
Science. Plaster models were selected from nationwide rater agreement was >0.8, and intraclass correlation
population-based database randomly. coefficient (ICC) was >0.8 for all parameters.
We used the criteria for inclusion, which were The obtained data were analyzed using the IBM
described as follows: a) subjects have to be with per- SPSS Statistics 22 (SPSS, Inc, Chicago, IL). The inter-
manent dentition; b) no orthodontic treatment has to dependence of qualitative evidence was evaluated by
be performed; and c) zygosity has to be confirmed by Chi-square (χ2) criteria. Risk estimates were calculated
36 Stomatologija, Baltic Dental and Maxillofacial Journal, 2015, Vol. 17, No. 2
SCIENTIFIC ARTICLES A. Auškalnis et al.
RESULTS
Stomatologija, Baltic Dental and Maxillofacial Journal, 2015, Vol. 17, No. 2 37
A. Auškalnis et al. SCIENTIFIC ARTICLES
MZ non-bruxers (91.7%) and DZ non-bruxers (80.0%) Data on TM prevalence in the groups of females
was found as well (p<0.001). and males (60.6% and 50.8% respectively, but no
Multiple logistic regressions analysis did not show statistically significant differences) do not confirm the
significant increase in TM occurrence for the bruxers X chromosome-linked heritability of TM and support
with negative or flat CW in region of maxillary second some previous reports (14, 39). Moreover, our study
premolar and first molar (p=0.089). did not show statistically significant differences of TM
prevalence according to age. These findings differ from
DISCUSSION other reports showing gradual growth of oral bony
outgrowths, which is greater in second or third decade
Prevalence of life (12, 36). Thus, our results may be influenced by
This report demonstrates that TM is dominant oral the young mean age (20.3±0.9 y) of the sample, which
bony outgrowth and has a high incidence (56.8%) in dominates in the database of Scientific Twin Center.
the investigated sample of Lithuanian twins. In the Seeking to evaluate the age dependency on TM preva-
worldwide studies, prevalence of TM has a wide varie- lence more epidemiological studies including various
ty in rates – between 0.54% to 64.4% (3). Higher preva- age groups should be implemented.
lence of TM in our study may be partially explained by
method of data collection. Plaster cast analysis leads to Bruxism
more precise data collection and possibility to calibrate In our study the prevalence of TM is significantly
the examiners, to recalculate and compare the cases correlated with teeth grinding, and these findings are
seeking for maximum accuracy. After training and consistent with other studies (13, 14, 16). The diagnos-
calibration procedure inter-rater agreement (weighted tics of bruxism is controversial and various methods
Kappa) and ICC between researchers diagnosing TM are known (2). In our study bruxism was diagnosed
were 0.82 and 0.97 respectively.
Table 2. Association between TM and different variables
Genetics Variables OR* 95% CI P value
TM dominates in Japanese, Age (>18 years) 1.43 0.77-2.68 0.258
Spanish, Ghanaian populations Gender (women) 1.41 0.74-2.66 0.296
(14,35,36). On the other hand, Ger-
Bruxism 4.58 2.22-9.46 <0.001
man, Norwegian, Croatian, Thai,
Angle Class II Division 1** 1.71 0.64-4.62 0.287
Malaysian populations were re-
ported to have torus palatinus more Angle Class II Division 2** 0.9 0.38-2.13 0.811
commonly (11, 16, 27, 37). Conse- Angle Class III** 0.58 0.24-1.45 0.247
quently, researchers suggest genetics Anterior open bite 1.04 0.48-2.26 0.919
as responsible factor in the etiology Negative or flat CW at first premolar*** 0.65 0.12-3.64 0.621
of TM and other bony protuberances. Negative or flat CW at second premolar*** 2.35 1.11-4.98 0.025
However, until now the influence Negative or flat CW at first molar*** 1.65 0.84-3.24 0.146
of genetics was mostly analyzed Negative or flat CW at second molar*** 3.97 0.45-34.74 0.213
using regional, ethnicity research,
Negative or flat CW at second premolar 2.55 1.19-5.46 0.016
or familial studies (6-8,10-12). The and first molar***
present study gives a new perspec- * Unadjusted odds ratio of logistic regression.
tive since it takes the sample of twins ** Compared to Angle Class I.
as an object to verify the influence *** Compared to positive CW.
In bold – p<0.05. Abbreviations: OR, unadjusted odds ratio; CI, confidence inter-
of genetic factor on the occurrence vals; CW, curve of Wilson.
of TM for the first time. MZ twins
are genetically identical and are ex- Table 3. Concordance values of TM in twin pairs
pressing more similar traits than DZ Concordance values of TM Discordance values of TM
twins. If genes determine the trait, First and second twin with First twin with TM and
agreement between traits (Kappa) TM, or first and second second twin without TM, κ value
in both individuals is close to 1.0 in twin without TM or first twin without TM
MZ twin pair and near to 0.5 in DZ and second twin with TM
twins (38) (0.96 and 0.7 respectively n % n %
in our research). The results of our MZ twins 44 93.6 3 6.4 0.96±0.04
study prove influence of genetic fac- DZ twins 27 79.4 7 20.6 0.7±0.12
tor in TM etiology. Abbreviations: TM, torus mandibularis; MZ, monozygotic; DZ, dizygotic.
38 Stomatologija, Baltic Dental and Maxillofacial Journal, 2015, Vol. 17, No. 2
SCIENTIFIC ARTICLES A. Auškalnis et al.
analyzing plaster casts, because atypical bruxism facets TM between first and second twin in MZ bruxers pair
on plaster casts show a sum of all diurnal and nocturnal indicate multifactorial etiology of TM. Our results
parafunctional activities retrospectively in all life peri- suggest that TM formation could be associated with
ods (26). For this reason, plaster casts analysis is more parafunctional teeth grinding, but genes may play
reliable and objective assessment than self-report of the predisposition role in TM etiology.
grinding activity (29). However, calibration of examin- Higher, but statistically insignificant TM oc-
ers and standard methods for assessment of bruxism currence rates for bruxers with negative or flat CW
has extremely important role in this regard (28). After in the region of maxillary second premolar and first
training and calibration for standard bruxism assess- molar may be explained by multicollinearity. In this
ment inter-rater agreement (Kappa) and ICC between case, two separately significant variables are highly
two examiners were 0.87 and 0.87 respectively. correlated, and are insignificant conducting multiple
Obviously, there are some limitations in this logistic regression analysis (44). In our study high
regard. Tooth wear may not be evident in all cases of multicollinearity between negative or flat CW and
bruxism and depends on the type of bruxism. Atypical, bruxism was proved by Spearman’s rho correlation
eccentric wear facets are usual for teeth grinding. On coefficient (r=0.2, p=0.009), and significant correlation
the other hand, teeth clenching and gnashing may be between the same variables was confirmed by logistic
difficult to recognize evaluating plaster casts. In fact, regression analysis (OR=2.742, 95% CI (1,27-5.92),
our study identifies bruxism only as parafunctional p=0.01). On the other hand, as it was discussed before,
teeth grinding. Therefore, extended studies analyzing negative or flat curvature of CW may provoke lingual
influence of teeth clenching and gnashing on the etiol- buckling of the mandibular teeth in static occlusion or
ogy of TM are necessary. Furthermore, teeth grinding normal group function, and this occlusal overload is
is more common for young people (2) and our study not related to parafunctional teeth grinding.
sample average age was 20.3±0.9 years. The formation of TM seems to be a compensatory
and protective bone reaction to occlusal overload in
Other clinical variables the most vulnerable mandible area. This study leads us
Some authors hypothesized that formation of TM to a discussion about tori removal and their possible
may be related to negative teeth inclination or deep use for autogenous bone grafting for dental implanta-
buccal overjet in Angle II Class. On the other hand, tion (45, 46). Moreover, some authors report recurrent
when direction of the bite force vector is changed growth of TM following their removal due to repetitive
(e.g. in Angle Class III) TM may not be prominent bruxism (26).
(19). Nevertheless, our study does not confirm TM Apparently, gene effects on the morphologic level
dependency on Angle Class. Moreover, our results are pleiotropic (13). Moreover, bruxism becomes al-
show that anterior open bite in habitual occlusion does most habitual function for contemporary patients (47).
not decrease TM incidence rate. Therefore, the search for other clinical and occlusal
However, significant association between nega- variables may play an important role analyzing and
tive or flat CW in the maxillary premolars and first understanding TM etiology. Further clinical investiga-
molars was found. The degree of curvature of the tions, retrospective computer tomography studies or
CW controls the inclination of occlusal guidance and finite-element analysis evaluating correlation of TM
occlusal contact point orientation (40). In case of nega- and other clinical and occlusal variables may give valu-
tive or flat CW inclination, the occlusal guiding path able knowledge for implant angulation, fabrication of
becomes steeper, and it often leads to group function teeth or implant supported posterior restorations, and
and determines greater occlusal load on teeth (40, 41). occlusal adjustment.
In addition, maxillary premolars and molars with the
negative CW usually have negative torque and domi- CONCLUSION
nant occlusal contact in static occlusion on vestibular
slope of vestibular cusps of mandibular premolars (A Our results suggest that the etiology of TM is mul-
contact) (42). This finding supports functional matrix tifactorial. TM seems to have genetic predisposition,
hypothesis (19, 21) as shear load and lingual buckling and may be associated with teeth grinding as well as
of the mandibular teeth initiates TM formation. with negative or flat CW in region of maxillary second
premolar and first molar.
Multifactority
Scholars agree that the potential causes of TM STATEMENT OF CONFLICTS OF INTEREST
are not limited to only one factor (13-15, 43). High
concordance values for the presence or absence of The authors state no conflict of interest.
Stomatologija, Baltic Dental and Maxillofacial Journal, 2015, Vol. 17, No. 2 39
A. Auškalnis et al. SCIENTIFIC ARTICLES
REFERENCES
1. Chi AK, Damm DD, Neville BW, Allen CM, Bouquet J. to mechanical usage: an overview for clinicians. Angle
Oral and maxillofacial pathology. 2008. Orthod 1994;64:175-88.
2. Paesani DA. Bruxism: theory and practice. Quintessence 24. Cortes ARG, Jin Z, Morrison MD, Arita ES, Song J, Tamimi
Publishing; 2010. F. Mandibular tori are associated with mechanical stress and
3. Garcia-Garcia AS, Martinez-Gonzalez JM, Gomez-Font mandibular shape. J Oral Maxillofac Surg 2014;72:2115-25.
R, Soto-Rivadeneira A, Oviedo-Roldan L. Current status 25. Uysal S, Cağirankaya BL, Hatipoğlu MG. Do gender and
of the torus palatinus and torus mandibularis. Med Oral torus mandibularis affect mandibular cortical index? A
2010;15:e353-60. cross-sectional study. Head Face Med 2007;3(1):37.
4. Rocca JP, Raybaud H, Merigo E, Vescovi P, Fornaini C. 26. Grippo JO, Kristensen GJ. The importance of making and
Er:YAG Laser: A New Technical Approach to Remove retaining diagnostic casts. Dent Econ 2015;2:2-4.
Torus Palatinus and Torus Mandibularis. Case Rep Dent 27. Noor MIM, Tajuddin MF, Alam MK, Basri R, Purmal K,
2012;2012:487802. Rahman SA. Torus palatinus and torus mandibularis in a
5. Hassan KS, Alagl AS, Abdel-Hady A. Torus mandibularis Malaysian population. Int Med J 2013;20:767-9.
bone chips combined with platelet rich plasma gel for treat- 28. Marbach JJ, Raphael KG, Janal MN, Hirschkorn-Roth
ment of intrabony osseous defects: clinical and radiographic R. Reliability of clinician judgements of bruxism. J Oral
evaluation. Int J Oral Maxillofac Surg 2012;41:1519-26. Rehabil 2003;30:113-8.
6. Suzuki M, Sakai T. A Familial Study of Torus Palatinus and 29. Dooland KV, Townsend GC, Kaidonis JA. Prevalence and
Torus Mandibularis. Am J Phys Anthropol 1960;18:263-72. side preference for tooth grinding in twins. Aust Dent J
7. Johnson CC, Gorlin RJ, Anderson VE. Torus Mandibularis: 2006;51:219-24.
a genetic study. Am J Hum Genet 1965;17:433-42. 30. Tsiggos N, Tortopidis D, Hatzikyriakos A, Menexes G.
8. Eggen S, Natvig B. Eggen S, Natvig B. Variation in torus Association between self-reported bruxism activity and
mandibularis prevalence in Norway. A statistical analysis occurrence of dental attrition, abfraction, and occlusal pits
using logistic regression. Community Dent Oral Epidemiol on natural teeth. J Prosthet Dent 2008;100:41-6.
1991;19:32-5. 31. Lavigne GJ, Rompré PH, Montplaisir JY. Sleep bruxism: va-
9. Šimunkovic SK, Božic M, Alajbeg IZ, Dulčic N, Boras lidity of clinical research diagnostic criteria in a controlled
VV. Prevalence of Torus Palatinus and Torus Mandibu- polysomnographic study. J Dent Res 1996;75:546-52.
laris in the Split-Dalmatian County, Croatia. Coll Antropol 32. Lobbezoo F, Naeije M. Review: Bruxism is mainly regulated
2011;35:637-41. centrally, not peripherally. J Oral Rehabil 2001;28:1085-91.
10. Sonnier KE, Horning GM, Cohen ME. Palatal tubercles, 33. Staley RN, Reske NT. Essentials of orthodontics. West
palatal tori, and mandibular tori: prevalence and anatomical Sussex, UK: John Wiley & Sons; 2010.
features in a U.S. population. J Periodontol 1999;70:329-36. 34. Altman DG. Practical Statistics for medical research. Chap-
11. Reichart PA, Neuhaus F, Sookasem M. Prevalence of torus man & Hall/CRC; 1991.
palatinus and torus mandibularis in Germans and Thai. 35. Galera V, Moreno JM, Gutierrez E. Oral tori in a sample of
Community Dent Oral Epidemiol 1988;16:61-4. Spanish university students: prevalence and morphology.
12. Al-Bayaty HF, Murti PR, Matthews R, Gupta PC. An epi- Antropologia Portugesa 2004;20/21:281-305.
demiological study of tori among 667 dental outpatients in 36. Bruce I, Ndanu TA, Addo ME. Epidemiological aspects of
Trinidad & Tobago, West Indies. Int Dent J 2001;51:300-4. oral tori in a Ghanaian community. Int Dent J 2004;54:78-82.
13. Eggen S. Torus mandibularis: an estimation of the degree of 37. Haugen LK. Palatine and Mandibular Tori. A Morphologic
genetic determination. Acta Odontol Scand 1989;47:409-15. study in the current Norwegian population. Acta Odontol
14. Yoshinaka M, Ikebe K, Furuya-Yoshinaka M, Maeda Y. Scand 1992;50:65-77.
Prevalence of torus mandibularis among a group of elderly 38. Cummings M. Human Heredity: Principles and issues.
Japanese and its relationship with occlusal force. Gerodon- Cengage Learning; 2014.
tology 2014;31:117-22. 39. Nair RG, Samaranayake LP, Philipsen HP, Graham RGB,
15. Clifford T, Lamey PJ, Fartash L. Mandibular tori, migraine Itthagarun A. Prevalence of oral lesions in a selected Viet-
and temporomandibular disorders. Br Dent J 1996;180:382- namese population. Int Dent J 1996;46:48-51.
4. 40. Slavicek R. Das Kauorgan: Funktionen und Dysfunktionen.
16. Kerdpon D, Sirirungrojying S. A Clinical study of oral tori Klosterneuburg; 2000.
in Southern Thailand: prevalence and the relation to para- 41. Leja W, Hilbe M, Stainer M, Kulmer S. Nicht-Kariose
functional activity. Eur J Oral Sci 1999;107:9-13. Zervikale Lasionen in Relation zum Okklusionstypus und
17. Sirirungrojying S, Kerdpon D. Relationship between Zur Neigung der Individuellen Fuhrungselemente. Dtsch
oral tori and temporomandibular disorders. Int Dent J Zahnarztl Z 1999;54:412-4.
1999;49:101-4. 42. Morikawa O. [Influence of occlusal contacts of implant on
18. Jarvis A, Gorlin RJ. Minor orofacial abnormalities in an adjacent teeth and antagonists displacements]. Kokubyo
Eskimo population. Oral Surg Oral Med Oral Pathol Gakkai Zasshi 2003;70(4):224-33.
1972;33:417-27. 43. Morrison MD, Tamimi F. Oral Tori are associated with lo-
19. Singh GD. On the etiology and significance of palatal and cal mechanical and systemic factors: a case-control study.
mandibular tori. Cranio 2010;28:213-5. J Oral Maxillofac Surg 2013;71:14-22.
20. Eggen S, Natvig B. Relationship between torus man- 44. Der G, Everitt BS. Applied Medical Statistics Using SAS.
dibularis and number of present teeth. Scand J Dent Res CRC Press; 2012.
1986;94:233-40. 45. Barker D, Walls AWG, Meechan JG. Ridge Augmentation
21. Moss ML. The functional matrix hypothesis revisited. 1. Using Mandibular Tori. Br Dent J 2001;190:474-6.
The role of mechanotransduction. Am J Orthod Dentofacial 46. Proussaefs P. Clinical and histologic evaluation of the use
Orthop 1997;112:8-11. of mandibular tori as donor site for mandibular block auto-
22. Reddy MS, Geurs NC, Wang I-C, Liu P-R, Hsu Y-T, Jeffcoat grafts: report of three cases. Int J Periodontics Restorative
RL, et al. Mandibular growth following implant restoration: Dent 2006;26:43-51.
does Wolff's law apply to residual ridge resorption? Int J 47. Slavicek R, Sato S. [Bruxism--a function of the mastica-
Periodontics Restorative Dent 2002;22:315-21. tory organ to cope with stress]. Wien Med Wochenschr
23. Frost HM. Wolff“s Law and bone”s structural adaptations 2004;154:584-9.
Received: 07 04 2014
Accepted for publishing: 25 05 2015
40 Stomatologija, Baltic Dental and Maxillofacial Journal, 2015, Vol. 17, No. 2