Dental Hypotheses

: 2020  |  Volume : 11  |  Issue : 1  |  Page : 16--23

Genetic Consideration of the Relationship Between Determinants of Occlusal Morphology, the Articular Eminence and Internal Derangement of the Temporomandibular Joint

Richard G Standerwick 
 Private Practitioner, Langley BC, Canada

Correspondence Address:
Richard G Standerwick
Private Practice, 20159 88th Ave., Langley BC Canada V1M0A4.


Introduction: The articular eminence and condyle-fossa relationship reflects a secondary growth site and the morphology appears to be influenced by determinants of occlusal morphology which are subject to genetic variation of dentoalveolar bone metabolism. The Hypothesis: the articular eminence of the TMJ inclination is a function of sagittal, vertical and transverse determinants of occlusal morphology and therefore it may be possible to influence modeling of the articular eminence with orthodontic treatment at least in a transient way. Evaluation of the Hypothesis: The morphology of the articular eminence, dentoalveolar bone remodeling rates associated with IL-Beta and determinants of occlusal morphology are considered with respect to the etiology of articular disc displacement and internal derangement of the temporomandibular joint.

How to cite this article:
Standerwick RG. Genetic Consideration of the Relationship Between Determinants of Occlusal Morphology, the Articular Eminence and Internal Derangement of the Temporomandibular Joint.Dent Hypotheses 2020;11:16-23

How to cite this URL:
Standerwick RG. Genetic Consideration of the Relationship Between Determinants of Occlusal Morphology, the Articular Eminence and Internal Derangement of the Temporomandibular Joint. Dent Hypotheses [serial online] 2020 [cited 2020 May 24 ];11:16-23
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Dentoalveolar bone is a dynamic connective tissue which influences the relationship of the dental articulations during function and growth by supporting individual teeth. The teeth and dentoalveolar bone appear to display an interdependent relationship with the ginglymo-arthrodial type temporomandibular joint (TMJ) through function, growth and development by connection through the mandible. Further, the articular eminence of the temporomandibular joint (AE) displays a developmental and functional relationship to the variation of sagittal, vertical and transverse determinates of occlusal morphology (DOM) during growth and it is postulated that this relationship is influenced by genetic haplotype of the dentoalveolar bone through inflammatory cytokines such as Interleukin 1-β (IL-1β). [1],[2]

Growth pattern of the AE more closely resembles that of the viscerocranium, even though it is part of the neurocranium.[3] The roof of the glenoid fossa appears to deepen by modeling while more significant sagittal and vertical growth is achieved by deposition at the top of the tubercle which implies application of pressure at the articular surfaces must be transient as the cambium layer of a dense fibrous connective tissue covering the mandibular condyle and AE are periosteal-like in nature and unsuited to grow against a pressure gradient.[2],[4],[5] TMJ development may be less a function of pressures exerted but rather a reflection of the aponeurotic sling connecting the mandible to the cranium,[6] where the articular eminence and condyle-fossa relationship is a secondary growth complex influenced by the sagittal, vertical and transverse DOM.[1],[2]

Growth results in a steeper slope of the AE which appears to take place in three phases associated with development of determinants of occlusal morphology (DOM) through the eruption of the central incisors, the permanent first molars and the permanent second molars.[7] Determinants of occlusal morphology would include sagittal, vertical and transverse determinants such as condylar guidance/angle of the articular eminence, anterior guidance/overbite and overjet, tooth inclinations, posterior cusp heights, plane of occlusion, the curve of Spee, lateral translation, distance from the rotating condyle, distance from the midsagittal plane and intercondylar distance.[8]

Considerable growth of the AE occurs prior to the complete eruption of the primary molars and on completion of primary dentition eruption the AE displays mature morphology and greater than 50% its mature size.[3],[9] Delays in morphologic development occur around 12 to 18 months of age and may be related to the establishment of a functional occlusion as facial skeletal growth shifts from primary to secondary growth mechanisms; the mandibular synchondrosis fuses and the posterior palatal synchondrosis converts to a fibrous suture.[1]

Articular eminence height is half of the adult height at 2 years of age which correlates with reduced anterior guidance and cusp heights of the primary dentition compared to the permanent dentition with primary dentition displaying dimensions approximately half that of the permanent dentition.[1],[10] Average primary incisor overbite is 1 mm compared to the 3 mm overbite displayed by completely erupted permanent incisors, and the overbite of primary canine and premolar teeth are 1 mm less (at least half) than the permanent canine and premolar vertical relationships.[11] As the permanent maxillary incisors erupt, there is hint of AE change progressively around 7 or 8 years of age while the maxillary lateral incisors begin to erupt and central incisor roots progressively lengthen to stabilize anterior guidance. If a subcondylar fracture resulting in resorption of a mandibular condyle were to occur at these ages displaying significant growth, assuming normal function of an interocclusal relationship is maintained, a new mandibular condyle has been shown to form.[2]

Vertical growth of the AE occurs at a very high rate until the age of 7, in conjunction with the period of deciduous dentition development and function and by 10 years of age the AE is 70%–72% of an adult dimension, after which AE growth slows around 11 years of age. The decrease in growth may result from difficult function during the mixed dentition due to exfoliation of the succedaneous teeth.[12]

Not until the maxillary canine erupts is final AE shape attained although still immature in size; it is notable that the intra-arch second molar eruption is temporally similar to canine and second premolar eruption.[10],[13] The transition from the juvenile to an adult chewing pattern appears to develop in conjunction with eruption of the permanent canines about the age of 12.[14],[15] and the inability to achieve normal canine function can result in a lack of chewing pattern transition observed with adults who display severe anterior open bites and retain a juvenile chewing pattern.[14] Similarly, wide lateral excursion observed in children[16] may be due to the lack of significant anterior and lateral guidance,[14] contributing to immature AE morphology.[17]

Association of AE inclination to overbite and overjet both in both protrusive and laterotrusive excursions (anterior guidance),[18] and working-side occlusal interference have an immediate significant effect on working-side/ipsilateral condylar movement where the magnitude of condylar rotation or displacement is correlated with the magnitude of occlusal alteration.[19] Correlation between AE slope and the inclination of the anterior teeth (47.6 and 42.7 degrees, respectively) suggests a functional relationship[20] and is a common consideration of occlusal rehabilitation.[8],[21]

Growth continues to approximate the somatic growth curve and by 20 years of age the AE is 90% to 94% of full height, achieving full inclination by approximately 30 years of age.[3],[22],[23] As with development of the dentition, AE modeling follows the demise of the dentition displaying reductions height loss as teeth are affected by attrition, loss, and declines in muscularity and connective tissue resilience during the fourth decade,[4],[21],[24],[25],[26] Continued progression through to edentulism is associated with AE flattening, however AE contour can be maintained by restoration with complete dentures.[27]

Articular eminence inclination and internal derangement

Disc displacement (DD) is a commonly accepted condition within internal derangement (ID) of the TMJ, a subset of temporomandibular disorders. It appears that DD is less likely to be found in joints with a shallow AE; not only the protrusive condylar pathway angulation but also the lateral condylar pathway steepness may be important for development of DD/ID.[8],[28],[29],[30],[31],[32] Eminectomy has been advocated as effective treatment for disc displacement, however fracture of mini-plates, used for internal osseous fixation is an issue.[31],[33] A biomechanical theory of DD postulates that with a steep eminence, there is tendency for the disc to rotate farther forward than normal on the condyle as the disc-condyle assembly rotates forward within the glenoid fossa during mouth opening. Meanwhile there is a stabilizing force produced by the masseter and temporalis, which if combined with a steeper AE places a greater relative distalizing force relative to the disc.[34],[35] This might also result in permanent stretching and laxity of the ligaments attaching the articular disc to the condyle.[36],[37],[38] The disc articulating against a steep AE during mouth opening would gradually achieve a more anterior position relative to the condyle predisposing the disc to anterior displacement.[34]

As well, there may be an effect on the lubrication of the joint as the disc is forced along the AE. Increase in friction due to increased AE inclination could force the disc anteriorly a greater distance than normal exhausting the effect of weeping lubrication during mandibular rotation with opening resulting in DD.[39]

A third consideration could be the establishment of posterior occlusal support through the hydraulic mechanism provided by the teeth and dentoalveolar bone. The more support provided by the posterior teeth could reduce the strain experience by the articular disc during intense jaw muscle contraction.[40]

Prevalence of internal derangement

The glenoid fossa of the youngest infants is flat and the diminutive AE reflects the minimal risk of disc displacement under the age of 5.[41] With increasing age and AE development, the prevalence of DD increases to 11.8% for children 8 to 15 years of age,[42] and a peak incidence of symptomatic DD occurs during puberty for both sexes as permanent canine teeth begin to influence the dental occlusion.[43] Development of painful DD in the teenaged years is 4 times greater than the risk later in life and displays a greater female expression relative males (3.3:1, Isberg; 4.25:1 Katzberg).[43],[44] Another peak incidence is seen with female individuals during the third and fourth decade and believed linked to hormonal factors.[43] Disc displacement is frequently found with pre-orthodontic adolescents[45] and may indicate a need for early correction of predisposing factors that are susceptible to orthodontic and orthopedic treatment.

Disc displacement is common in asymptomatic individuals (21-34%) and highly correlated in individuals with TMD (77-86%).[44],[46],[47]

Interestingly, the peak incidence of TMD in general is between 20 and 40 years of age[48]; basically associated with non-growing individuals prior to the age related loss of connective tissue resiliency and decreased muscle growth. Approximately 50% of asymptomatic patients display a sign or symptom of “TMD”,[8],[48] a proportion leaning toward the influence of Medellin genetics. Understanding a genetic aspect with regard to TMD and DOM may explain why occlusal parameters alone cannot provide a complete understanding since they are dynamic and insufficiently “prime” variables.

The Hypothesis

Hypothesized is that the AE inclination is a function of sagittal, vertical and transverse DOM and therefore it may be possible to influence modeling of the AE with orthodontic treatment at least in a transient way. These dental relationships are developed through dentoalveolar compensations linked to a genetic haplotype modulating tooth eruption, dentoalveolar hydraulics and plasticity, muscle, connective tissue and TMJ development, function and pathology. Within this definition, incisor relationships of overbite and overjet influence growth and development of the TMJ and manifestations of DD as an aspect of ID/TMD.

Evaluation of the Hypothesis

The genetic haplotype of an individual is expected to influence the developmental processes of growth and functional occlusal morphology by influencing 3-dimensional tooth position through the inflammatory process of tooth movement.[1] For example, it is known that individuals with the interleukin 1-β allele-1 haplotype (IL- β allele-1) display a predisposition toward external apical root resorption (EARR),[1],[2],[49] a decreased catabolic osseous remodeling and less compliant dentoalveolar bone resulting in increased anchorage and slower rates of tooth movement.[2],[50],[51] Conversely, individuals with IL-1β allele-2 (related to periodontal disease) display increased catabolic osseous remodeling,[1],[2] increased tooth movement rates, decreased relative bone anchorage value and increase plasticity of dentoalveolar bone.[2],[50],[52] Dentoalveolar bone haplotype in conjunction with soft tissue forces can therefore influence tooth positions and DOM which are associated with temporomandibular joint modeling in a way associated with ID of the TMJ. Individuals with a genetic predisposition toward increased dentoalveolar modeling,[50],[51] may display teeth that are more compliant to movement possibly resulting in positional change such as increase spacing of teeth or fremitus (dentoalveolar flexion and hydraulics) while lack of adaptation may be associated with tooth fracture, dental attrition, periodontal damage, root resorption or intracapsular derangements of the TMJ.[53],[54] When considering the lack of attrition associated with contemporary refined diets,[55],[56] there is a possibility that an individual with an unfavorable genetic dentoalveolar compensation could be prone to ID. Individuals with the genetic predisposition toward increased dentoalveolar bone modeling (IL-1β allele 2) may display greater DOM accommodation, which may explain the great variation in response to TMD treated with therapeutic DOM compensations in combination with the genetically determined adaptability of the TMJ.[57] Facial growth rotation of the maxilla and mandible along with divergence of the jaws are compensated by tooth eruption, and as the teeth erupt, they create their supporting bone and gingival tissues which are immature in mineral density and collagen content respectively.[1],[2],[58],[59] In addition to the dentoalveolar genetic predisposition, the decreased bone mineral density and gingival collagen content at younger ages may allow greater adaptation through mechanisms such as tooth tipping as enlarging muscles place pressure on the teeth.[2] The tooth positions are also influenced by the combination of the relatively pliable muscle and rigid supporting connective tissue which has been shown to increase in density and thickness with age.[6],[60] Orthodontic or restorative occlusal adjustment for “non-growing” individuals might be a consideration and it would seem preferable to alter the occlusion to be contiguous with the musculoskeletal stable position, except it is important to remember that there is significant mesial dental migration and vertical dental eruption with late adult “growth” adaptation of the orofacial capsular matrix as well as issues of parafunction or sleep apnea which place the occlusal relationship in a constant state of flux.[61],[62]

Dentoalveolar compensations relative to mandibular growth regarding intramatrix rotation as observed with the different growth patterns for europrosopic versus leptoprosopic individuals would be affected by variation in bone remodeling rates [Figure 1] and [Figure 2].[63],[64],[65],[66],[67],[68] Application of dentoalveolar haplotype adaptation would also be expected to display a predictable relationship with dentoalveolar compensation with Class 2 orthopedic treatment [Figure 2] and [Figure 3] For example, an untreated Class II growth pattern with mandibular dentoalveolar retrusion relative to pogonion (the most anterior point of the mandible on a cephalogram) would be expected to display a genetic haplotype for more compliant bone and therefore should display a similar condylar position to a Class 1 growth pattern because the dentoalveolar bone metabolism would allow the mandible to grow forward with less restriction relative to the dentoalveolar component [Figure 3].[69],[70] Moreover, it has been observed that the more forward growth of the mandible relative to the maxilla, the greater the forward movement of the dentition relative to the maxilla, and the greater the backward movement of the dentition relative to the mandible when the occlusal interface was locked in an untreated Class 2 malocclusion.[69],[71] For this reason the anterior-posterior position of the dentition and curve of Spee relative to the mandibular condyle and AE must be considered since it is associated with posterior tooth cusp heights and inclinations.[8] A curve of Spee and dentition more distally/dorsally positioned will be able to accommodate steeper posterior tooth cusps but may also result in a steeper articular eminence inclination and higher predisposition toward internal derangement.[8]{Figure 1}{Figure 2}{Figure 3}

Class II mandibular growth without dentoalveolar retrusion relative to pogonion would be expected to display transient restriction of condylar growth (smaller mandible) followed by a return to growth (slower) and a more posteriorly positioned condyle-fossa position.[72] The lack of dentoalveolar retrusion relative to pogonion may indicate an individual with a genetic type for decreased compliance/bone modeling (e.g. IL-1β Allele-1).

These differences on the Class 2 dentoalveolar compensations could also influence the position of maxillomandibular rotation at the molars, premolars or incisors [Figure 1].

Orthodontic manipulation of teeth and TMJ modeling

Hypothesized is that the articular eminence inclination is a function of sagittal, vertical and transverse DOM and therefore it may be possible to influence modeling of the glenoid fossa with orthodontic treatment at least in a transient way. It is problematic that the modeling of fossa form has begun in the mixed dentition and largely complete by the time the maxillary canines are erupting (and the permanent second molars) but this roughly correlates with the recommended time for functional appliance treatment. It would seem counterintuitive that that teeth should determine the shape of the glenoid fossa as tooth position is adaptive to soft tissue forces,[2],[73],[74],[75],[76] however the dentoalveolar region is most symmetrical aspect of the viscerocranium as compensatory changes occur to minimize the effects of underlying skeletal asymmetry in order to allow for a functional occlusion.[77] It must be remembered that functional forces affecting the TMJ are heavy but transient heavy forces.[2],[4]This position also seems to reflect dental restorative theories as condylar guidance is considered with respect to anterior guidance, posterior tooth cusp heights and inclinations, antero-posterior positioning of the dentition relative to the AE and occlusal plane orientation.[8],[21]

Modelling the AE with interceptive orthodontic treatment may reduce the risk of internal derangement of the TMJ.[30],[34],[78],[79] TMJ adaptation to late adolescent treatment is expected to occur by 2 years on average in sync with reestablishment of normal chewing seen after unilateral condylar fracture, and after progressive condylar resorption following orthognathic surgery.[80],[81] Interceptive treatment would be of little value in the primary dentition as deciduous teeth occlude less tightly with each other than those of the permanent dentition due to cusp heights. [82]

Skeletal divergency as related to the gonial angle must be considered since a large gonial angle is related to a shallow articular eminence, while the opposite is also true, and a decreased gonial angle is related to a steep articular eminence.[83] Also, repositioning of the condyle with Class 2 orthopedic correction place the condyle more anteriorly in the glenoid fossa which should cause modeling of the AE resulting in height and inclination reduction.[83],[84] Therefore, repositioning with functional appliances may be of clinical value although modeling effect might not be expected for approximately 2 years.

Consequences of the hypothesis

It is recommended that the functional aspect of the dentoalveolar process be viewed as a possible controlling or associated factor in TMJ ontogeny, which in cases, may influence a clinician toward early orthodontic treatment to minimize the impact of determinants of occlusal morphology associated with internal derangement of the TMJ. It is quite possible that there is a genetic basis for the occlusal variation within internal derangement of the TMJ. The understanding of underlying genetic factors could create research opportunities and testing of TMD-related genetic haplotypes and understanding dentoavleolar compensations during growth and development.

Financial support and sponsorship


Conflicts of interest

There are no conflicts of interest.


1Roberts WE, Hartsfield JK Jr. Bone development and function: genetic and environmental mechanisms. Seminars in Orthodontics 2004;10:100-22.
2Roberts W. Bone physiology, metabolism, and biomechanics in orthodontic practice, in Orthodontics: Current Principles & Techniques, Graber TM, Vanarsdall RL, Vig KWL, editors. 2005, Elsevier Mosby: St. Louis, Mo. p. 221-92.
3Katsavrias EG. Changes in articular eminence inclination during the craniofacial growth period. Angle Orthod 2002;72:258-64.
4Hinton RJ. Form and function in the temporom and ibular joint. Craniofacial biology; Craniofacial growth series, Carlson DS, Ribbens KA, and University of Michigan, editors. Center for Human Growth and Development. 1981, Ann Arbor, Mich.: Center for Human Growth and Development, University of Michigan, 269 p.
5Thilander B, Rygh P, Reitan K. Tissue reactions in orthodontics, in Orthodontics: Current Principles C & Techniques, Graber TM, Vanarsdall RJ, Vig K, editors. 2005, Elsevier: St. Louis, Missoiuri. p. 145-219.
6Standerwick RG, Roberts WE. The aponeurotic tension model of craniofacial growth in man. Open Dent J 2009;3:100-13.
7Dibbets JM, Dijkman GE. The postnatal development of the temporal part of the human temporomandibular joint. A quantitative study on skulls. Ann Anat 1997;179:569-72.
8Okeson JP. Management of temporomandibular disorders and occlusion. 5th ed. 2003, St. Louis, Mo.: Mosby. xi, 671 p.
9Nickel JC, McLachlan KR, Smith DM. Eminence development of the postnatal human temporomandibular joint. J Dent Res 1988;67:896-902.
10Nelson SJ, Ash MM. Wheeler’s dental anatomy, physiology, and occlusion. 9th ed. 2010, St. Louis, Mo.: Saunders/Elsevier. xvi, 346 p.
11Moyers R et al. Standards of human occlusal development. 1976, Ann Arbor, Michigan 48104: Center for Human Growth and Development, The University of Michigan.
12Papargyriou G, Kjellberg H, Kiliaridis S. Changes in masticatory mandibular movements in growing individuals: a six-year follow-up. Acta Odontol Scand 2000;58:129-34.
13Hurme VO. Ranges in normalcy for eruption of permanent teeth. J Dent Child 1949 11.
14Lundeen HC, Gibbs CH. Advances in occlusion. 1981, Boston: J. Wright −PSG. xi, 232 p.
15Proffit WR, Fields HW. Contemporary orthodontics. 3rd ed. 2000 St. Louis: Mosby. x, 742 p.
16Wickwire NA et al. Chewing patterns in normal children. Angle Orthod 1981;51:48-60.
17Hinton RJ. Changes in articular eminence morphology with dental function. Am J Phys Anthropol 1981;54:439-55.
18Mack PJ. A functional explanation for the morphology of the temporomandibular joint of man. J Dent 1984;12:225-30.
19Huang BY et al. Ipsilateral interferences and working-side condylar movements. Arch Oral Biol 2006;51:206-14.
20Koyoumdjisky E. The correlation of the inclined planes of the articular surface of the glenoid fossa with the cuspal and palatal slopes of the teeth. J Dent Res 1956;35:890-901.
21Dawson P. Functional Occlusion: From TMJ to Smile Design. 2007, St. Louis, Missouri: Elsevier.
22Katsavrias EG, Dibbets JM. The growth of articular eminence height during craniofacial growth period. Cranio 2001;19:13-20.
23Hoyte DA. The cranial base in normal and abnormal skull growth. Neurosurg Clin N Am 1991;2:515-37.
24Granados JI. The influence of the loss of teeth and attrition on the articular eminence. J Prosthet Dent 1979;42:78-85.
25Moffett B. The morphogenesis of the temporomandibular joint. Am J Orthod 1966;52:401-15.
26Owen CP, Wilding RJ, Adams LP. Dimensions of the temporal glenoid fossa and tooth wear in prehistoric human skeletons. Arch Oral Biol 1992;37:63-7.
27Taddei C, Frank RM, Cahen PM. Effects of complete denture wearing on temporomandibular joints: a histomorphometric study. J Prosthet Dent 1991;65:692-8.
28Sulun T et al. Morphology of the mandibular fossa and inclination of the articular eminence in patients with internal derangement and in symptom-free volunteers. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 2001;92:98-107.
29Seward FS. Tooth attrition and the temporomandibular joint. Angle Orthod 1976;46:162-70.
30Kurita H et al. Is the morphology of the articular eminence of the temporomandibular joint a predisposing factor for disc displacement? Dentomaxillofac Radiol 2000;29:159-62.
31Kerstens HC et al. Inclination of the temporomandibular joint eminence and anterior disc displacement. Int J Oral Maxillofac Surg 1989;18:228-32.
32Sato S et al. Morphology of the mandibular fossa and the articular eminence in temporomandibular joints with anterior disk displacement. Int J Oral Maxillofac Surg 1996;25:236-8.
33Cardoso AB, Vasconcelos BC, Oliveira DM. Comparative study of eminectomy and use of bone miniplate in the articular eminence for the treatment of recurrent temporomandibular joint dislocation. Rev Bras Otorrinolaringol (Engl Ed) 2005;71:32-7.
34Isberg A, Westesson PL. Steepness of articular eminence and movement of the condyle and disk in asymptomatic temporomandibular joints. Oral Surg Oral Med Oral Pathol Oral Radiol Endod, 1998;86:152-7.
35Atkinson WB, Bates RE Jr. The effects of the angle of the articular eminence on anterior disk displacement. J Prosthet Dent 1983;49:554-5.
36Perrini F et al. Generalized joint laxity and temporomandibular disorders. J Orofac Pain 1997;11:215-21.
37Deodato F et al. Predisposition for temporomandibular joint disorders: loose ligaments. Cranio 2006;24:179-83.
38Woo SL et al. Injury and repair of ligaments and tendons. Annu Rev Biomed Eng 2000;2:83-118.
39Nitzan DW. The process of lubrication impairment and its involvement in temporomandibular joint disc displacement: a theoretical concept. J Oral Maxillofac Surg 2001;59:36-45.
40Seedorf H et al. Impact of posterior occlusal support on the condylar position. J Oral Rehabil 2004;31:759-63.
41Paesani D et al. Prevalence of temporomandibular joint disk displacement in infants and young children. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 1999;87:15-9.
42Hans MG et al. A comparison of clinical examination, history, and magnetic resonance imaging for identifying orthodontic patients with temporomandibular joint disorders. Am J Orthod Dentofacial Orthop 1992;101:54-9.
43Isberg A, Hagglund M, Paesani D. The effect of age and gender on the onset of symptomatic temporomandibular joint disk displacement. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 1998;85:252-7.
44Katzberg RW et al. Anatomic disorders of the temporomandibular joint disc in asymptomatic subjects. J Oral Maxillofac Surg 1996;54:147-53; discussion 153-5.
45Nebbe B, Major PW. Prevalence of TMJ disc displacement in a pre-orthodontic adolescent sample. Angle Orthod 2000;70:454–63.
46Ribeiro RF et al. The prevalence of disc displacement in symptomatic and asymptomatic volunteers aged 6 to 25 years. J Orofac Pain 1997;11:37-47.
47Takatsuka S et al. Disc and condyle translation in patients with temporomandibular disorder. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 2005;99:614-21.
48Gauer RL, Semidey MJ. Diagnosis and treatment of temporomandibular disorders. Am Fam Physician 2015;91:378-86.
49Al-Qawasmi RA et al. Genetic predisposition to external apical root resorption. Am J Orthod Dentofacial Orthop 2003;123:242-52.
50Iwasaki LR et al. Human interleukin-1 beta and interleukin-1 receptor antagonist secretion and velocity of tooth movement. Arch Oral Biol 2001;46:185-9.
51Iwasaki LR et al. Speed of tooth movement is related to stress and IL-1 gene polymorphisms. Am J Orthod Dentofacial Orthop 2006;130:698e1-9.
52Iwasaki LR et al. IL-1 gene polymorphisms, secretion in gingival crevicular fluid, and speed of human orthodontic tooth movement. Orthod Craniofac Res 2009;12:129-40.
53Sondhi A. Anterior interferences: their impact on anterior inclination and orthodontic finishing procedures. Seminars in Orthodontics 2003;9:204-15.
54Thurow RC. Edgewise Orthodontics (Millenium Edition). 2001: GAC International Inc.
55Marinelli A et al. Tooth wear in the mixed dentition: a comparative study between children born in the1950s and the 1990s. Angle Orthod 2005;75:340-3.
56Fishman LS. Dental and skeletal relationships to attritional occlusion. Angle Orthod 1976;46:51-63.
57Lim WH et al. IL-1beta inhibits TGFbeta in the temporomandibular joint. J Dent Res 2009;88:557-62.
58Roberts W, Huja S, Roberts J. Bone modeling: biomechanics, molecular mechanisms, and clinical perspectives. Seminars in Orthodontics 2004;10:123-61.
59Roberts W, Garetto L, Katona T. Principles of orthodontic biomechanics: metabolic and mechanical control mechanisms, in Bone Biodynamics in Orthodontic and Orthopedic Treatment, Carlson DS, Goldstein SA, editors. 1991, University of Michigan: Ann Arbor. p. 189-255.
60Gogly B et al. Morphometric analysis of collagen and elastic fibers in normal skin and gingiva in relation to age. Clin Oral Investig 1997;1:147-52.
61Behrents RG. The biological basis for understanding craniofacial growth during adulthood. Prog Clin Biol Res 1985;187:307-19.
62Behrents RG, University of Michigan. Center for Human Growth and Development. Growth in the aging craniofacial skeleton. Craniofacial growth series ; monograph no. 17. 1985, Ann Arbor, Mich.: Center for Human Growth and Development, University of Michigan. vii 145 p.
63Sassouni V. A classification of skeletal facial types. Am J Orthod 1969;55:109-23.
64Bjork A, Skieller V. Facial development and tooth eruption. An implant study at the age of puberty. Am J Orthod 1972;62:339-83.
65Bjork A, Skieller V. Normal and abnormal growth of the mandible. A synthesis of longitudinal cephalometric implant studies over a period of 25 years. Eur J Orthod 1983;5:1-46.
66Bjork A, Skieller V. Growth of the maxilla in three dimensions as revealed radiographically by the implant method. Br J Orthod 1977;4:53-64.
67Bjork A, Skieller V. Postnatal growth and development of the maxillary complex, in Factors affecting the growth of the midface : proceedings of a sponsored symposium honoring Professor Robert E. Moyers, held February 6 and 7, 1976, in Ann Arbor, Michigan, Moyers RE, McNamara JA, Editors. 1976, Craniofacial Publications, CHGD: Ann Arbor. p. 61-99.
68Dale JG, Dale HC. Interceptive Guidance of Occlusion with Emphasis on Diagnosis. 4 ed. Orthodontics: Current Principles C & Techniques, ed. Graber T, Vanarsdall RJ, Vig K. 2005, Elsevier Mosby: St. Louis, Mo. 405-489.
69You ZH et al. Dentoalveolar changes related to mandibular forward growth in untreated Class II persons. Am J Orthod Dentofacial Orthop 2001;120:598-607; quiz 676.
70Marshall SD et al. Chin development as a result of differential jaw growth. Am J Orthod Dentofacial Orthop 2011;139:456-64.
71Rose JM et al. Mandibular skeletal and dental asymmetry in Class II subdivision malocclusions. Am J Orthod Dentofacial Orthop 1994;105:489-95.
72Bishara SE. Class II malocclusions: diagnostic and clinical considerations with and without treatment. Seminars in Orthodontics 2006;12:11-24.
73Moss ML, Young RW. A functional approach to craniology. Am J Phys Anthropol 1960;18:281-92.
74Moss ML, Salentijn L. The capsular matrix. Am J Orthod 1969;56:474-90.
75Moss ML. Ontogenetic aspects of cranio-facial growth, 1st ed. Cranio-facial growth in man; proceedings of a conference on genetics, bone biology, and analysis of growth data, held May 1-3, 1967, Ann Arbor, Michigan, Moyers RE, Krogman WM, eds. 1971, Oxford, New York,: Pergamon Press. ix, 360 p.
76Moss ML. The functional matrix concept and its relationship to temporomandibular joint dysfunction and treatment. Dent Clin North Am 1983;27:445-55.
77Vig PS, Hewitt AB. Asymmetry of the human facial skeleton. Angle Orthod 1975;45:125-9.
78Gokalp H, Turkkahraman H, Bzeizi N. Correlation between eminence steepness and condyle disc movements in temporomandibular joints with internal derangements on magnetic resonance imaging. Eur J Orthod 2001;23:579-84.
79Kinniburgh RD et al. Osseous morphology and spatial relationships of the temporomandibular joint: comparisons of normal and anterior disc positions. Angle Orthod 2000;70:70-80.
80Throckmorton GS, Ellis E 3rd, Hayasaki H. Jaw kinematics during mastication after unilateral fractures of the mandibular condylar process. Am J Orthod Dentofacial Orthop 2003;124:695-707.
81Hoppenreijs TJ et al. Long-term evaluation of patients with progressive condylar resorption following orthognathic surgery. Int J Oral Maxillofac Surg 1999;28:411-8.
82Sekikawa M, Kanazawa E, Ozaki T. Cusp height relationships between the upper and lower molars in Japanese subjects. J Dent Res 1988;67:1515-7.
83Pirttiniemi P, Kantomaa T., Ronning O. Relation of the glenoid fossa to craniofacial morphology, studied on dry human skulls. Acta Odontol Scand 1990;48:359-64.
84Kantomaa T. Effect of increased posterior displacement of the glenoid fossa on mandibular growth: a methodological study on the rabbit. Eur J Orthod 1984;6:15-24.