Abstract
Purpose
Our current understanding of unilateral condylar hyperplasia (UCH) was put forth by Obwegeser. He hypothesized that UCH is 2 separate conditions: hemimandibular hyperplasia and hemimandibular elongation. This hypothesis was based on 3 assumptions: (1) the direction of overgrowth, in UCH, is bimodal—vertical or horizontal, with rare cases growing obliquely; (2) UCH can expand a hemimandible with and without significant condylar enlargement; (3) there is an association between the condylar expansion and the direction of overgrowth—minimal expansion resulting in horizontal growth and significant enlargement causing vertical displacement. The purpose of this study was to test these assumptions.
Patients and Methods
We analyzed the computed tomography (CT) scans of 40 patients with UCH. First, we used a Silverman Cluster Analysis to determine how the direction of overgrowth is distributed in the UCH population. Next, we evaluated the relationship between hemimandibular overgrowth and condylar enlargement to confirm that overgrowth can occur independently of condylar expansion. Finally, we assessed the relationship between the degree of condylar enlargement and the direction of overgrowth to ascertain if condylar expansion determines the direction of growth.
Results
Our first investigation demonstrates that the general impression that UCH is bimodal is wrong. The growth vectors in UCH are unimodally distributed, with the vast majority of cases growing diagonally. Our second investigation confirms the observation that UCH can expand a hemimandible with and without significant condylar enlargement. Our last investigation determined that, in UCH, there is no association between the degree of condylar expansion and the direction of the overgrowth.
Conclusions
The results of this study disprove the idea that UCH is 2 different conditions: hemimandibular hyperplasia and hemimandibular elongation. It also provides new insights about the pathophysiology of UCH.
Introduction
Our current view of unilateral condylar hyperplasia (UCH) was put forth by Obwegeser. In 1986, he and Makek proposed that the anomaly is, in fact, 2 different conditions: hemimandibular hyperplasia and hemimandibular elongation.1 In hemimandibular hyperplasia, one-half of the lower jaw increases in volume. The condyle expands, the neck widens and lengthens, and the ramus and body increase in height. When the hyperplasia is rapid, the bite opens posteriorly. Otherwise, the maxillary teeth supraerupt to maintain occlusion, tilting the occlusal plane. Notwithstanding these changes, the chin stays near the midline.1, 2
In hemimandibular elongation, 1 side of the mandible lengthens in a horizontal plane, displacing the chin towards the unaffected side. The condyle remains unchanged or enlarges mildly. The neck elongates, but not always. While the jaw is growing abnormally, the occlusal plane stays flat, the lower dental midline drifts to the opposite side of jaw growth, and the contralateral posterior teeth cross buccally.
Obwegeser speculated about the existence of 2 growth regulators located in the superficial regions of the condyles, 1 responsible for the growth in the mass of the hemimandible, the other responsible for the increase in length. The hyperactivity of the first causing hemimandibular hyperplasia. The overactivity of the other, bringing about hemimandibular elongation.2
Because Obwegeser encountered some patients with features of both disorders, he fashioned the hybrid and compound forms to explain them. He considered that these patients had the synchronous appearance of both diseases.2
On detailed examination, the above classification is based on 3 assumptions: (1) the direction of overgrowth in UCH is bimodal—vertical or horizontal, with a few cases growing diagonally; (2) the hyperplasia, per se, is of 2 types: global or linear, global hyperplasia enlarging the condyle and the rest of the hemimandible, linear hyperplasia lengthening 1 side of the jaw while keeping the condyle close to its original size; (3) The type of hyperplasia determines the direction of overgrowth. Global hyperplasia producing vertical growth, while linear hyperplasia produces horizontal.
However, these assumptions may be wrong. Nitzan found that enlarged and normal-sized condyles can dilate the jaw in any direction.3 Moreover, Nolte was unable to confirm Obwegeser’s predictions of global enlargement in hemimandibular hyperplasia and thinning of the jaw in hemimandibular elongation.4 Despite these findings, Obwegeser’s classification continues to be popular.
Therefore, a study was needed to establish the validity of Obwegeser’s classification conclusively. With this goal in mind, we formulated 3 specific aims: (1) to determine if the direction of overgrowth in UCH is bimodal, (2) to confirm that in UCH the involved hemimandible can expand independent of condylar (head) enlargement; (3) to ascertain if condylar expansion determines the direction of overgrowth.
Methods
This retrospective study analyzed the computed tomography (CT) scans of patients with UCH that had been seen at Houston Methodist Hospital, in Houston, Texas, between 2016 and 2020. Before the data were collected, we received IRB approval (PRO00025764). Patients were included in the study if they met our diagnostic criteria for UHC and had a baseline CT or cone beam CT.
Our diagnostic criteria for UCH were: (1) history of asymmetric mandibular growth that began in childhood or adolescence; (2) physical evidence of lower jaw asymmetry—gonial angle asymmetry, lateral chin deviation, lower dental midline deviation, unilateral posterior open bite, or asymmetric crossbite not a result of upper jaw deformity or functional shift; (3) CT evidence of non-neoplastic unilateral condylar enlargement, neck elongation, or increase in the length or height of a hemimandible; (4) mandibular asymmetry that could not be explained by other conditions such as fluctuating asymmetry, cranial base asymmetry, hemifacial microsomia, external deformation, condylar erosion, injury, or ankylosis. Borderline cases were considered positive only if they had a positive SPECT bone scan.
Forty patients were included in the study. From each patient, we collected de-identified age and gender data and maxillofacial CT DICOM files. We segmented the CT images of each patient and constructed 3-dimensional (3D) models of the mandibles. This task was completed in the AnatomicAligner software (Houston Methodist Research Institute, Houston, Texas).
After segmentation, all right cases were mirrored, so all the mandibles showed the asymmetry on the left side. The assessments, from here on described, were done on the 3D mandibles.
The study had 3 objectives: (1) to determine the mode of growth of the sample patients (i.e., if it is it bimodal of unimodal); (2) to confirm that hemimandibular growth is independent of condylar (head) enlargement; (3) to ascertain if condylar expansion determines the direction of growth. Each of these assessments required a different methodology.
To learn how the direction of overgrowth is distributed in the sample population, we use the Silverman Cluster Analysis.5 This test is among the most popular methods of cluster analysis for its simplicity and effectiveness. Ahmed and Walther extended the technique to the study of multi-dimensional data, by the application of a principal curve, a non-linear projection of data onto 1-dimensional linear space. Our implementation followed their method.6 Our null hypothesis was that the vectors were distributed in a single cluster (k = 1). The alternative hypothesis was that the vectors were distributed in 2 clusters (k+ 1). The significant value was set at p < 0.05.
To prepare for this analysis, we first quantified the mandibular asymmetry. The assessment used a recursive weighted Procrustes superimposition of half-forms—a technique developed in our laboratory. For each patient, we digitized a set of mandibular cephalometric landmarks that covered the volume of the jaw, being careful not to over-represent 1 area (Table 1). Then, we exported the 3-dimensional (3D) coordinates of the landmarks into a custom MATLAB (MathWorks, Natick, MA) program written for this study. For each mandible, the custom program divided the mandibular landmarks into 3 groups: right, left, and central (Fig. 1). Then, the program created 2 hemimandibles: the first 1 by grouping all the right and central landmarks; the second by grouping the left and again the central landmarks (Fig. 2).
Table 1.
List of Mandibular Landmarks
| Mandibular Landmarks | |
|---|---|
| 1 | Point B |
| 2 | Gnathion |
| 3 | Pogonion |
| 4 | Menton |
| 5 | Gonion Inferior |
| 6 | Gonion |
| 7 | Gonion Superior |
| 8 | Condylion |
| 9 | Sigmoid |
| 10 | Coronion |
| 11 | Mesiobuccal Cusp of 1st Molar |
| 12 | Canine Tip |
| 13 | Lower Incisal Midpoint |
Figure 1.
For each mandible, the custom program divided the mandibular landmarks into 3 groups: right (red), left (blue), and central (green)
Figure 2.
The program created 2 hemimandibles: the first 1 by grouping all the right and central landmarks; the second by grouping the left and again the central landmarks
Afterward, the right cloud of points was reflected about the sagittal plane (Fig. 3) and superimposed over the left. For the superimposition, we used a weighted Procrustes registration, without scaling. To prevent outlier landmarks from skewing the registration, the algorithm used a weighted process that successively gave less value to the outliers, during 50 iterations. The method had the effect of registering the half-forms over the most symmetrical parts of the jaw, unmasking the real asymmetry (Fig. 4).
Figure 3.
Right hemimandible (brown) reflected about the sagittal plane
Figure 4. Recursive Weighted Procrustes Superimposition of Half Forms.
Pink lines show the asymmetry vectors among corresponding landmarks of each hemimandible, arising from the unaffected side. The vectors show the direction and magnitude of overgrow/remodeling of the affected hemimandible.
After the superimposition, the program calculated the asymmetry vectors (partial Procrustes distances) of each landmark. These vectors disclosed the magnitude and direction of the overgrowth at each mandibular landmark, as they originated from the unaffected hemimandibles (Fig. 4).
To compare the condylar overgrowth vectors of all the patients, we registered the hemimandibles of the 40 patients using a Generalized Procrustes Analysis (Fig. 5). Then, we calculated the average mandible for the whole data set (Fig. 5). Finally, the overgrowth condylar vectors were registered to the Condylion of the average mandible (Fig. 6a). The purpose of this step was to place the tails of all condylar overgrowth vectors on a common origin of anatomical significance.
Figure 5. Superimposition of the 40 mandibles using generalized Procrustes registration.
See the cloud of points about each cephalometric landmark. The black lines outline the average mandible.
Figure 6.
a) All the condylar overgrowth vectors registered at Condylion of the average mandible. Note that each vector has a different length and direction. B) The same vectors after they have been scaled to a length of 1 (for the illustration, we enlarged the unit vectors). The normalized unit vectors show the different condylar growth directions.
Afterward, we converted all overgrow condylar vectors to unit vectors, i.e., vectors of length 1 (Fig. 6b). The scaling was necessary because vectors provided information about size and direction, and for the analysis, we only needed direction. Finally, we analyzed the dispersion of the overgrowth unit vectors using Silverman’s cluster analysis.
To confirm that, in UCH, hemimandibular overgrowth can occur with or without condylar (head) enlargement, we evaluated the relationship between hemimandibular overgrowth and condylar expansion. We regarded hemimandibular overgrowth to be the length of the overgrowth vector at Condylion.
Condylar expansion was calculated by measuring the volume differences between the affected and unaffected condyles. In the AnatomicAligner software, a single investigator (JG) used a cutting plane to separate the condylar heads from the necks. The boundary between these structures was set at the inferior insertion of the joint capsule (Fig. 7). Afterward, the investigator used the MeshLab software (ISTI-CNR, Pisa, Italy) to measure the volumes of the affected and unaffected condyles and calculated the volume differences between the involved and uninvolved condyles. The volume differences were expressed as percentages.
Figure 7.
Cutting plane used to separate the heads of the right (a) and left (b) condylar processes.
After hemimandibular overgrowth and condylar expansion had been calculated, we plotted a scattergram for these variables and calculated Pearson’s correlation coefficient.
We evaluated the association between condylar expansion and the direction of overgrowth, by plotting a scattergram of these data, and by calculating Pearson’s correlation coefficient. The condylar expansion was measured as we had done before. However, the direction of overgrowth had to be reduced from being 3D to only having 2 dimensions. To reduce 1 dimension, we first calculated the principal components (PC1, PC2, and PC3 for the group of 3D-vectors (40 patients). Next, we projected the 3D vectors of each patient onto the 2-dimensional plane defined by PC1 and PC2 (Fig. 8). Finally, on this plane, we measured the direction of pathological growth in degrees, with PC1 indicating zero degrees and PC2 indicating 90.
Figure 8. Principal components of growth.
The first principal component (PC1, red arrow) shows that most of the growth in UCH occurs along an oblique vector that points superiorly, posteriorly, and medially. The second principal component (PC2, blue arrow) shows the most variation along a vector that aims posteriorly, inferiorly, and medially. The third principal component (PC3, green arrow) shows the least common variation along a vector that points posteriorly and laterally.
Results
Of the 40 patients, 52.5% were female, ranging in age at initial presentation from 11–38 years, with a median age of 19.1 years. The age distribution is shown in Fig. 9. The left condyle was affected in 22 cases (12 females and 10 males). The right condyle was affected in 18 cases (9 females and 9 males). The mean overgrowth was 8.1 mm, 95% CI [6.8, 9.4], SD 4.2.
Figure 9.
Age distribution of the sample population—age at initial patient presentation
On visual inspection, the overgrowth vectors appear to be evenly distributed, like a bouquet of flowers. There was no apparent clustering (Fig. 10). The Silverman analysis confirmed this impression. It resulted in a P-value of 0.9. Therefore, the null hypothesis that the condylar overgrowth vectors in UCH are unimodally distributed could not be rejected. A histogram confirmed a normal distribution for the sample (Fig. 10).
Figure 10. Silverman’s Cluster Analysis.
The top left and bottom images show the overgrowth direction-vectors of the 40 mandibles, projected on the surface of a sphere. The tails of all the vectors emanate from the center of an imaginary sphere (Condylion); the heads of the vectors project on its surface as black dots. On visual inspection, the vectors seem to be evenly distributed, like a bouquet of flowers. The curvy multicolored line drawn on the surface of the sphere is the principal-curve that fits all the data points, like a trend line. The red dotted lines show how the heads of all the vectors (black dots) are projected onto the principal curve. Each projected point is color-coded from purple posteriorly to yellow anteriorly. The top right image is the histogram showing the mode of distribution of the pathologic growth vectors. The horizontal axis of the histogram is the straightened principal-curve that was drawn on the surface of the sphere. The vertical axis shows the relative frequencies of each direction. The shape of the histogram curve reveals the unimodal distribution of the overgrowth vectors.
A principal component analysis (Fig. 8) shows that most of the condylar overgrowth (64.2%) occurred along an oblique vector that points superiorly, posteriorly, and medially (PC1). The second principal component (PC2) explains 22.3% of the variation. This component is oriented posteriorly, inferiorly, and medially. The third principal component (PC3) shows the least common variation (13.5%) in the posterior and lateral direction.
We found a moderate positive correlation between the magnitude of the condylar expansion and the lengthening of the affected hemimandible (r=0.64). This association is logical; the larger the condyle, the more significant the hemimandibular overgrowth. Nonetheless, it is also true that patients can have the same amount of hemimandibular overgrowth with drastically different condylar expansions. Fig. 11 shows an example. Two patients (red dots) experienced similar hemimandibular lengthening of 10.4 and 10.7 mm, respectively. However, in the first patient, the condyle enlarged minimally (7%), while in the second patient, the condyle double in volume (104% enlargement).
Figure 11.
Correlation between condylar expansion and hemimandibular distention
We found no correlation (Pearson’s r=0.2) between condylar expansion and the direction of the overgrowth (Fig. 12).
Figure 12.
Correlation between condylar enlargement of direction of growth (r=0.23)
Discussion
Key Findings
Our first investigation demonstrates that the general impression that UCH is either vertical or horizontal, with rare cases growing obliquely, is wrong. Our data proves that the growth vectors in UCH are unimodally distributed, with the vast majority of cases growing diagonally. Horizontal and vertical presentations lay at the tails-ends of a normal distribution.
Our second investigation confirms Obwegeser’s observation that UCH can expand a hemimandible with and without significant condylar enlargement.
Our last inquiry assessed Obwegeser’s assumption that there is an association between the condylar expansion and the direction of the overgrowth. This assumption is incorrect; there is no association.
Limitations
The current study is a retrospective case series. These studies are generally considered inferior to others because the records can have biases.7 However, in this study, we did all the appraisals on CT scans, which would have been the same had the images been obtained prospectively. Notwithstanding, one can argue the patient selection would have been different would the study have been prospective. However, to minimize inclusion bias, we rediagnosed each patient. The additional evaluations excluded 4 patients because they had skull base asymmetry instead of UCH.8
Another possible limitation relates to the precision of measuring condylar volumes. Although a computer did these measurements, they depended on where we placed the planes that separated the condylar heads from the necks. In a few patients, the boundary was fuzzy. These cases were revisited a few days later to confirm the cutting planes. Also, in 2 cases, the contralateral condyles were smaller than normal because of mild degeneration.
A final limitation relates to testing the last hypothesis: there is an association between the condylar expansion and the direction of overgrowth. This determination used 2-dimensional vectors even though the real overgrowth vectors were 3-dimensional. As described in the methods, we reduced dimensionality by projecting the 3D vectors on the plane created by the first and second principal components, which together account for 86.5% of the variance. Although mathematically, this method is robust, the resultant plane is not perfectly aligned with the standard anatomical frame of reference. Notwithstanding this misalignment, the lack of association between the type of hyperplasia and overgrowth direction is evident.
Interpretation of Results
Our first investigation demonstrates that the general impression that UCH is either vertical or horizontal—with rare cases growing oblique—is wrong. How come we have had a wrong impression for so long? Obwegeser gave us the notion that UCH is 2 separate diseases and encouraged us to categorize patients into 2 groups. This belief biased our clinical observations; for every time we examined a patient, we endeavored to place them in 1 of 2 categories. However, as proven in this study, the direction of overgrowth is not categorical but a continuous variable that takes an infinite number of values. Our data refute the idea that UCH is 2 separate diseases. Also, that oblique growth is less common. The opposite is the truth.
Our second investigation confirms Obwegeser’s observation that UCH can expand a hemimandible with and without significant condylar enlargement. From this observation, Obwegeser inferred the existence of 2 growth regulators located in the condylar cartilage, one responsible for the growth in the mass of the hemimandible, the other for growth in length. Nevertheless, there is a more plausible explanation: that the chondrocyte hyperplasia may be of different degrees of organization.9–11 In a healthy growth plate, the enlarging chondrocytes march in parallel columns, following a clear direction. This arrangement produces linear growth without significant condylar expansion. Cases of UHC that exhibit linear growth without significant condylar enlargement, likely retain this organization. Cases that expand the condyle may have disorganized hyperplasia, with cells multiplying in different directions.
Our last investigation assessed Obwegeser’s assumption that there is an association between the condylar expansion and the direction of overgrowth. The data shows no association. Nitzan’s classical study reached the same conclusion.3 There is a more straightforward explanation for the different growth directions. The condylar cartilage covers an ovoid condyle and cartilage hyperplasia can originate from any condylar area and proliferate in different directions.
Generalizability
The results of this study disprove the idea that UCH is 2 different conditions: hemimandibular hyperplasia and hemimandibular elongation. They also provide new insights into the pathophysiology of UCH.
In addition to Obwegeser, Wolford et al. also developed a classification system for conditions that cause condylar hyperplasia. They classify condylar hyperplasia into 4 groups. Type 1 corresponds to Obwegeser’s hemimandibular elongation. Type 2, which is subdivided into 2 groups, conforms to Obwegeser’s hemimandibular hyperplasia (2A), or typical osteochondromas (2B). Type 3 includes benign neoplasms other than osteochondroma. Finally, type 4 accommodates malignant neoplasms. 12 In pathology, however, hyperplasia and neoplasia are distinct processes.13 Therefore, we believe that no classification system of hyperplasia ought to include neoplasias. Notwithstanding, we do recognize that hyperplasia is a fertile ground for the development of neoplasia.13, 14
As mention above, hyperplasia is a distinct cellular growth process. It can be physiologic or pathologic.13 Unilateral condylar hyperplasia is a form of pathologic hyperplasia.15 Most pathologic hyperplasia forms, like prostatic hyperplasia, are caused by excessive or inappropriate actions of hormones or growth factors acting in growing cells.13 However, the cells of individuals with overgrowth syndromes like Beckwith Wideman, Proteus, and Hemihyperplasia are genetically programmed to produce an exaggerated response to physiological growth stimuli. They can initiate and prolong the growth activity even in the absence of such stimuli.14
Overgrowth syndromes can be generalized or segmental. In generalized overgrowth, there is excessive growth of the whole body (stature and weight), a condition that is usually caused by germline mutations (i.e., eggs or sperm).14 In segmental overgrowth, there is excessive growth in a part of the body but normal growth elsewhere. This presentation is a result of a somatic mosaic mutation.14, 15 Somatic means any cell of the body other than a germ cell. Mosaic denotes that the mutation is present only in a fraction of the adult cells.
Current evidence indicates that UHC is primarily a disorder of the condylar cartilage of the mandible, most likely caused by a somatic mosaic mutation that results in overgrowth.10, 15 The particular mutation or mutations have not been uncovered. Still, we should expect heterogenous mutations because some patients stop growing at the end of adolescence while others continue to grow as adults. One can speculate that some mutations may produce overgrowth only in the presence of growth hormones; others escape hormonal regulation and become actual tumors. The conclusion that UCH is a disorder primarily of condylar cartilage is supported by 4 observations: (1) in UCH, the deformity of the condylar process is always more extensive than the deformity of other parts of the mandible; (2) when positive, scintigraphy shows increase uptake only in the mandibular condyle;16 (3) resection of the condylar cartilage arrests the abnormal growth;17–19 (4) histopathologic changes are limited to the condylar cartilage and the adjacent subchondral bone.9–11
To appreciate UCH, we should recognize that what we observe clinically is not the primary disorder, but the secondary deformity from condylar overgrowth. Moreover, we should accept the fact that UCH can have different clinical presentations. The ultimate jaw configuration is governed by the direction, extent, and velocity of the condylar overgrowth—as well as the adaptations of the surrounding tissues.
Vertical overgrowth and the secondary adaptations to this overgrowth can produce a deformity that is identical to Obwegeser’s hemimandibular hyperplasia, without having to explain it as hyperplasia of the whole hemimandible.
Likewise, a horizontal overgrowth can produce a deformity that is indistinguishable from hemimandibular elongation without having to implicate a lengthening process that involves the whole hemimandible.
Notwithstanding the above comments, it is clear that the primary disorder may affect the size and shape of the condyle. Linear (organized) proliferation of chondrocytes, and the orderly replacement of cartilage by bone, can lengthen a hemimandible without enlarging the condyle, while non-linear growth may expand it.
Acknowledgement:
This work was sponsored in part by National Institutes of Health / National Institute of Dental and Craniofacial Research grants R01 DE022676, R01 DE027251 and R01 DE021863.
Footnotes
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