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J Dent Res 85(12):1118-1123, 2006
© 2006 International and American Associations for Dental Research

RESEARCH REPORT
Biological

Bilateral TMJ Disk Displacement Induces Mandibular Retrognathia

F. Bryndahl1, L. Eriksson2, P.E. Legrell1, and A. Isberg1,*

1 Department of Odontology, Oral and Maxillofacial Radiology, Umeå University, SE-901 87 Umeå, Sweden; and
2 Department of Oral and Maxillofacial Surgery, Faculty of Odontology, Malmö University and Malmö University Hospital, Malmö, Sweden

* corresponding author, Annika.Isberg{at}odont.umu.se


   ABSTRACT
TOP
 ABSTRACT
INTRODUCTION
 MATERIALS & METHODS
 RESULTS
 DISCUSSION
 REFERENCES
 
Unilateral non-reducing TMJ disk displacement has been shown to retard mandibular growth on the ipsilateral side, with facial asymmetry a sequela. We hypothesized that bilateral affliction would impair mandibular growth bilaterally, generating mandibular retrognathia. Non-reducing TMJ disk displacement was surgically created in 10 growing New Zealand White rabbits. Ten additional rabbits served as a sham-operated control group. Facial growth was followed in serial cephalograms, with tantalum implants, during a period corresponding to childhood and adolescence in man. The results verified that bilateral non-reducing TMJ disk displacement retarded mandibular growth bilaterally, the extent corresponding to mandibular retrognathia in man. Maxillary growth was also retarded, but to a lesser degree. Growth impairment fluctuated over time, the most striking retardation occurring during periods of general growth acceleration. This should be taken into consideration when orthodontic treatment, aimed at stimulating mandibular growth, is initiated in adolescent individuals with non-reducing TMJ disk displacement.

KEY WORDS: adolescence • mandibular growth • maxillary growth • temporomandibular joint


   INTRODUCTION
TOP
 ABSTRACT
 INTRODUCTION
MATERIALS & METHODS
 RESULTS
 DISCUSSION
 REFERENCES
 
Functional strain on bone tissue constitutes a controlling stimulus for adaptive bone remodeling (Tang and Rabie, 2005). The temporomandibular joints (TMJ) represent important growth sites within the facial skeleton, and a change in condylar biophysical environment has been reported to lead to a significant change in mandibular growth (Chayanupatkul et al., 2003). Clinical studies of craniofacial asymmetry reported an association with co-existing unilateral non-reducing TMJ disk displacement, but without revealing the cause-effect sequence (Yamada et al., 1999; Nakagawa et al., 2002; Gidarakou et al., 2003). In a previous series of prospective studies, we clarified that unilateral non-reducing displacement of the TMJ disk retarded mandibular growth on the ipsilateral side (Legrell and Isberg, 1998, 1999; Legrell et al., 1999), with facial asymmetry a sequela (Isberg and Legrell, 2000).

The fact that unilateral non-reducing TMJ disk displacement impairs ipsilateral mandibular growth makes it plausible that bilateral joint involvement would induce mandibular retrognathia. This assumption is supported by clinical studies of mandibular retrognathia, suggesting an association with co-existing bilateral non-reducing TMJ disk displacement in adults as well as in children and adolescents (Schellhas et al., 1993; Nebbe et al., 1998; Yamada et al., 1999; Gidarakou et al., 2004). It is noteworthy that non-reducing TMJ disk displacement occurs in children and adolescents, with a prevalence of about 4% in the absence of symptoms and 60% in adolescents with TMJ symptoms (Ribeiro et al., 1997). Bilateral affliction is reported in 50% of both these groups (Sanchez-Woodworth et al., 1988; Ribeiro et al., 1997). More than 10% of the girls in a general pre-orthodontic population had non-reducing disk displacement (Nebbe and Major, 2000) and the onset of symptomatic TMJ disk displacement peaks during puberty (Isberg et al., 1998).

Hence, clarification of whether bilateral non-reducing TMJ disk displacement in adolescents induces mandibular retrognathia is essential for the practicing clinician to provide a basis for choice of treatment modality, for prognosis, and for prediction of treatment outcome in growing individuals.

The aim of the present study was: (i) to test experimentally the hypothesis that bilateral non-reducing TMJ disk displacement impairs craniofacial growth to an extent corresponding to mandibular retrognathia in man, and (ii) to elucidate the impact on the mandibular and maxillary growth patterns over time.


   MATERIALS & METHODS
TOP
 ABSTRACT
 INTRODUCTION
 MATERIALS & METHODS
RESULTS
 DISCUSSION
 REFERENCES
 
The study was reviewed and approved by the Ethics Committee on Animal Experiments, Umeå University, Sweden (Registration Nr. A 128-00).

Animals
Twenty New Zealand White rabbits (Oryctolagus cuniculus) were randomized into two groups: (i) an experimental group (n = 10), in which bilateral non-reducing TMJ disk displacement was surgically created; and (ii) a sham-operated control group (n = 10), in which the same surgical procedure was performed, but with no manipulation of the TMJ disk.

The inclusion of a third non-operated control group was not considered ethically justified, because the sham operation, as performed in this study, had previously been proven not to influence facial growth (Legrell and Isberg, 1998, 1999).

The animals were 10 wks old at the beginning of the study, and were allowed to grow for a mean of 96 days (range, 93–98 days), the rabbits’ growth period (Bang and Enlow, 1967; Masoud et al., 1986) approximating childhood and adolescence in man (Losken et al., 1992).

Weight Gain
To detect signs of malnutrition that could presumably affect growth, we registered the animals’ body weight at inception and throughout the study period.

Anesthesia
Before surgery and at radiographic examination after 1 and 2 mos, respectively, each animal was given local and general anesthesia and analgesia (Bryndahl et al., 2004). Before the final radiographic examination, the animal was killed by an intravenous injection of approximately 1.2 mL pentobarbital-natrium (Pentotal® 60 mg/mL, Abbott Scandinavia AB, Solna, Sweden) per kilogram of body weight.

Surgery
    TMJ Surgery
Bilateral TMJ disk displacement was created in each experimental animal (Ali et al., 1993; Legrell and Isberg, 1998). The TMJ was approached through a skin incision, followed by blunt dissection until the joint capsule was disclosed. The capsule was incised and the disk exposed. The medial, anterior, and lateral disk attachments were detached with scissors, and the disk was pulled anteriorly, with the intact posterior disk attachment placed above the condyle. A ligature that looped through a hole drilled in the anterior zygomatic arch anchored the displaced disk anteriorly. Maintenance of the incorrect disk position was checked, the surgical area was flushed with saline solution, and the wound was closed in layers.

The sham operation followed the same procedure until the disk was exposed. The wound was flushed and closed without any disk manipulation.

    Implant Surgery
At study inception, tantalum spheres (Ø = 0.5 mm) were inserted on the left side and tantalum pins (Ø = 0.37 mm) on the right side of both jaws, to allow for identification of sides in subsequent radiographic images. Two titanium alloy screws were inserted into the calvarium, serving the dual purpose of (i) reproducibly guiding the animal’s head into a specially designed cephalostat, and (ii) providing reference structures at superimposition of serial cephalograms (Bryndahl et al., 2004) (Fig. 1Go).


Figure 1
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  		Figure 1. Lateral cephalogram of rabbit skull showing titanium screws in the calvarium (arrowheads), and tantalum implants in the maxilla and the mandible (arrows). A horizontal reference plane (bold white line) was constructed in the inceptive cephalogram as a straight line running through the maximum occipital point (MOP) and the most superior point of the hard palate anterior to the molars (HP). The position of each tantalum implant in the inceptive cephalogram was defined as the implant’s origin (T1), and both the magnitude and direction of mandibular and maxillary growth were followed in subsequent superimpositions throughout the three-month study period (T1–T4).

 
Radiographic Examinations and Analyses
Lateral cephalograms of each animal were exposed on 4 occasions—i.e., at study inception (T1), and after 1 (T2), 2 (T3), and 3 (T4) mos. Each cephalogram was digitized, and superimpositions and measurements were conducted on a personal computer. For each animal, the T2, T3, and T4 cephalograms were superimposed on the T1 cephalogram, with the titanium alloy screws in the calvarium as reference structures. The precision in matching the titanium alloy screws was 15 µm (Bryndahl et al., 2004). We constructed a horizontal reference plane in the T1 cephalogram by inserting a line through the maximum occipital point (MOP), running as a tangent to the hard palate anterior to the upper molars (HP) (Fig. 1Go). This individual reference plane was carried forward in the subsequent superimpositions. The position of each tantalum implant in the jaws was digitally plotted in each cephalogram, with x- and y-coordinates given to the nearest tenth of a millimeter. The position of each tantalum implant in the T1 cephalogram was defined as the implant’s origin, and the magnitude and direction of growth in relation to the constructed horizontal reference plane were followed over time (Fig. 1Go). The cephalometric method has been reported to have a precision of 0.4 mm in longitudinal studies (Bryndahl et al., 2004). The magnitude of growth was calculated as a mean of the values from the left and right sides of each jaw. Measurements from 3 mandibular tantalum implants were discarded because of interference with the lower incisors. Therefore, unilateral mandibular values were achieved in 1 control and 2 experimental animals. All measured values were corrected for radiographic magnification in the cephalograms prior to statistical analysis.

We used Mann-Whitney’s non-parametric test to compare groups regarding differences in weight gain and mandibular and maxillary growth throughout the study period. P-values less than 0.05 were regarded as statistically significant.


   RESULTS
TOP
 ABSTRACT
 INTRODUCTION
 MATERIALS & METHODS
 RESULTS
DISCUSSION
 REFERENCES
 
Clinical Data: Weight Gain Throughout the Study Period
In the experimental group, the mean body weight increased from 2.0 kg to 4.1 kg during the study period. Corresponding figures for the control group were 2.1 kg to 4.4 kg. The significant difference of 0.2 kg in mean weight gain between groups occurred during the first post-operative month (p = 0.011). There was no significant difference in mean weight gain between groups during the second (p = 0.529) and third (p = 0.218) months (Fig. 2aGo). No animal was lost during the study period.


Figure 2
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  		Figure 2a. Animal weight throughout the study period. Experimental group (n = 10): Mean weight increased from 2.0 kg (1.8–2.2) to 4.1 kg (3.8–4.7), and mean weight gain was 2.1 kg (1.6–2.6). Control group (n = 10): Mean weight increased from 2.1 kg (1.9–2.3) to 4.4 kg (4.0–4.9), and mean weight gain was 2.3 kg (2.0–2.7). The difference of 0.2 kg in mean weight gain between groups occurred in the first postoperative month (T1–T2), during which the sham-operated controls showed a significantly larger weight gain (p = 0.011). There was no significant difference in weight gain between groups during the second (T2–T3) and the third (T3–T4) months of the study period.

 
Horizontal Growth
    Mandible
Over the study period, mandibular horizontal growth was impaired, consistently bilaterally (Fig. 2bGo). The reduction was 19% as a mean in the experimental group, compared with the control group (p = 0.011) (Fig. 3Go) (TableGo). During the first month, the mean reduction was 24% (p = 0.001), and during the third month, 42% (p = 0.003), with no significant difference between groups during the intermediate month.


Figure 2
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  		Figure 2b. Mandibular and maxillary horizontal growth throughout the study period (T1–T4) for the control group (Contr, n = 10) and for the experimental group (Exp, n = 10). All measured values are stacked for left (sin) and right (dx) sides, respectively. Mean growth for left mandible: 8.7 mm (7.4–10.2) in the control group and 6.9 mm (5.2–9.0) in the experimental group. Mean growth for right mandible: 8.6 mm (7.4–9.6) in the control group and 7.1 mm (5.4–9.4) in the experimental group. Mean growth for left maxilla: 14.6 mm (13.6–15.9) in the control group and 13.5 mm (11.1–14.8) in the experimental group. Mean growth for right maxilla: 14.4 mm (13.2–15.9) in the control group and 13.5 mm (11.5–15.6) in the experimental group. Growth impairment was consistently bilateral. Blocks with matching color in paired columns represent left and right sides in the same animal. In 3 animals (1 control, 2 experimental), a discarded mandibular measurement from one side was replaced by the value from the contralateral side.

 

Figure 3
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  		Figure 3. Throughout the study period (T1–T4), the experimental animals displayed a 19% reduction in mean mandibular horizontal growth (p = 0.011), and a 7% reduction in mean maxillary horizontal growth (p = 0.023), in comparison with the sham-operated control group. During the first month (T1–T2), the experimental animals showed a 24% reduction in mean mandibular horizontal growth (p = 0.001), and a 9% reduction of mean maxillary horizontal growth (p = 0.004). During the third month (T3–T4), the experimental animals showed a 42% reduction of mean mandibular horizontal growth (p = 0.003), and a 25% reduction of mean maxillary horizontal growth (p = 0.001). There was no significant difference in horizontal growth during the second month (T2–T3), nor were there any significant differences in mandibular or maxillary vertical growth during any month. Number of animals in each group (n) = 10. For details, see the TableGo.

 

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  		Table. Means, Medians, and Ranges of Mandibular and Maxillary Horizontal and Vertical Growth in the Two Groups, Presented for Each Month (T1–T2, T2–T3, and T3–T4) and Throughout the Experimental Period (T1–T4)
 
    Maxilla
Maxillary horizontal growth was also impaired, consistently bilaterally (Fig. 2bGo). The reduction was 7% as a mean in the experimental group, compared with the control group (p = 0.023) (Fig. 3Go) (TableGo). During the first month, the mean reduction was 9% (p = 0.004), and during the third month, 25% (p = 0.001), with no significant difference between groups during the intermediate month.

Vertical Growth
There was no statistically significant difference in vertical mandibular or maxillary growth between the two groups, at either the termination of the study or during any specific period. The mean amount of vertical growth among the experimental animals, however, was larger compared with that in the control animals, with a more ’downward backward’ rotational growth pattern during the third month (Fig. 3Go) (TableGo).


   DISCUSSION
TOP
 ABSTRACT
 INTRODUCTION
 MATERIALS & METHODS
 RESULTS
 DISCUSSION
REFERENCES
 
The results confirmed our hypothesis that bilateral non-reducing displacement of the TMJ disk, with onset during the craniofacial growth period, can induce significant impairment of mandibular and maxillary horizontal growth. No association has been found between body weight and the amount of skeletal growth in rabbits (Putz et al., 2000). Therefore, it is unlikely that the transient difference in weight gain of 0.2 kg between groups, at the beginning of this study, influenced the results.

In medicine, extrapolation of data and conclusions from experimental animal studies to man is commonly indispensable in the quest for deeper knowledge about pathological conditions and pharmacological agents. It is also common in studies of facial skeletal growth. The rabbit model has been well-established in experimental studies of the TMJ (Mills et al., 1994; Shen and Darendeliler, 2005). The present study on rabbits showed that bilateral non-reducing TMJ disk displacement retarded horizontal mandibular growth by 19%. The experimental period corresponded to the age range of 6 to 18 yrs in man (Losken et al., 1992). According to the Bolton Standards of Dentofacial Developmental Growth, the length of the human mandible increases by approximately 25 mm (Ar-Gn) between the ages of 6 and 18 yrs (Broadbent et al., 1975). When the amount of growth retardation, observed in the rabbit, is extrapolated to the human mandible, it corresponds to a shortening of approximately 5 mm at the end of the growth period. The human maxilla increases by approximately 9 mm in length (PNS-ANS) during the same period (Broadbent et al., 1975). The reduction by 7% in maxillary horizontal growth, as observed in this study, thereby corresponds to a 0.6-mm shortening of the maxilla in man, suggesting a subclinical adverse effect, by non-reducing TMJ disk displacement, on maxillary horizontal growth.

The implication of the results is that bilateral non-reducing TMJ disk displacement in man, with an onset during the craniofacial growth period, would result in retrognathia, mainly assigned to the mandible. They also imply that the documented clinical association between mandibular retrognathia and bilateral non-reducing TMJ disk displacement (Schellhas et al., 1993; Nebbe et al., 1998; Yamada et al., 1999; Gidarakou et al., 2004) is a nexus, where the TMJ affliction is the cause, and the aberrant skeletal morphology the sequela.

The curves, illustrating facial growth during the third experimental month, displayed an overall pattern that was directed downward more in the experimental animals than in the controls. This seemingly evident adverse growth pattern lacked statistical significance, due to a large intra-individual variation in the vertical aspect of facial growth among the experimental animals. This variation included negative vertical mandibular growth in stray animals, i.e., an ’upward backward’ rotational growth pattern, during periods of the study. The resulting large spread of the vertical values embraced the span of control animals.

Unlike epiphyseal cartilage, mandibular condylar cartilage has the capability of adaptive remodeling in response to external stimuli during and after natural growth (Shen and Darendeliler, 2005). Condylar growth is regulated by various local growth factors, and pulling and compressing forces trigger or impair their endogenous expression, leading to increased or decreased condylar growth (Rabie and Hägg, 2002; Chayanupatkul et al., 2003; Shen and Darendeliler, 2005). A decrease of functional load at intramaxillary fixation has been shown to induce a significant reduction of condylar cartilage (Isacsson et al., 1993), as observed with low masticatory function (Kiliaridis et al., 1999), but with no longitudinal impairment of mandibular growth (Isacsson et al., 1993). Conversely, increased non-physiological load at condylar hypomobility impaired mandibular growth significantly. The impairment occurred whether restriction of condylar translation was due to an extra-articular obstacle adjacent to the anterior TMJ capsule (Isberg et al., 1990), or by the intra-articular impediment of a displaced disk without reduction, as observed in this study. In both situations, the obstacle can be assumed to exert non-physiological compression force to the anterior aspect of the condyle on attempted condylar translation. Such compression forces decrease condylar growth (Shen and Darendeliler, 2005).

The degree of growth reduction was found to fluctuate distinctly over time. This variability, induced by TMJ disk displacement, is of clinical significance. A locally induced growth reduction, as observed in this study, appeared to counteract the general growth acceleration by cutting the peaks of growth, induced by general hormonal regulation. In rabbits, the blood level of skeletal-regulating growth hormones has been reported to peak between 10 and 14 wks of age, with a general acceleration of facial growth rate. A smaller peak has been reported to appear between 20 and 22 wks (Masoud et al., 1986). The general acceleration of growth rate corresponds to the first and third months of this study, i.e., when growth retardation was observed.

In the untreated human adolescent, such locally induced growth impairment can be expected to diminish the spurt of mandibular growth during puberty significantly. When an adolescent with bilateral non-reducing TMJ disk displacement and mandibular retrognathia requires growth-stimulating treatment, it should be taken into account that growth retardation, induced by the displaced disks, will counteract the growth stimulation intended to result from mandibular advancement with the aid of a jaw-protrusion device. The present results offer an explanation for why adolescent orthodontic patients can become refractory to growth-stimulating treatment, or even display a relapse of earlier orthodontic corrections. Clinicians have previously been advised to consider that TMJ disk displacement may be overlooked, because symptoms might not occur until growth has ceased (Nebbe et al., 1999; Gidarakou et al., 2003). The present results show that full appraisal of TMJ disk position in the orthodontic adolescent population should not be neglected. A paradigm shift regarding indications for radiographic evaluation of TMJ soft tissues prior to growth-stimulating treatment should be considered.

In conclusion, bilateral non-reducing TMJ disk displacement in growing rabbits can cause significant reduction of mandibular and maxillary horizontal growth. Extrapolated to man, the growth reduction is estimated to result in mandibular retrognathia. The status of the TMJ disk must be taken into account as a factor with adverse effects on facial development and on the outcome of orthodontic growth-stimulating treatment.


   ACKNOWLEDGMENTS
 
We express our gratitude to Professor Hans Nyquist, Department of Statistics, Stockholm University, Sweden, for statistical advice and analysis. This project was supported by grants from The Swedish Research Council (project nr 6877), the County Council of Västerbotten, and the Swedish Dental Society, Sweden.

Received May 18, 2005; Last revision September 26, 2006; Accepted September 26, 2006


   REFERENCES
TOP
 ABSTRACT
 INTRODUCTION
 MATERIALS & METHODS
 RESULTS
 DISCUSSION
 REFERENCES
 
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