CHAPTER 18
Histology of Condyles in Mandibular Growth Anomalies
18.1 General Considerations
A survey of the presented cases discloses the marked variability of most types of mandibular growth anomalies, not only with respect to clinical appearance, but also regarding age at onset, duration and age at surgical intervention. Thus, in cases of condylar hyperactivity, i.e., H.H., H.E. and hybrid forms, growth can apparently turn abnormal during the regular growth period, continue beyond the age of regular growth cessation or resume activity during adulthood. Depending on the interval between the start of the disorder and condylectomy, some of the resected condyles may have been growing actively, while in others growth may have ceased. The questions we hoped would be answered by the histological examination were therefore: 1. Was condylar growth still going on at the time of sur-
gery? 2. Did it proceed at a normal rate? 3. Was the mechanism of growth normal? 4. Is there any relationship between the structure of the
condyle and the clinical picture of the growth disorder?
As the normal microscopic appearance of mandibular condyles alters during the growth period, after growth has terminated, and finally also during adulthood (H. Luder 1996), the interpretation of histological findings in specimens affected by growth disorders has to primarily rely on age-matched controls. This should allow answers as to whether growth was still active or had ceased. Also, conclusions should be possible regarding the mechanism and timing of growth. However, as will be outlined below, estimates regarding the rate of growth are more problematic. Finally, attempts at relating histological characteristics of condyles to particular types of growth anomalies are impeded by the great variability in clinical appearance and, hence, the limited number of uniform cases.
18.2 Normal Condyles in Different Age Groups
Growth Stage. Throughout the period of active growth, the articular tissue of the condyle comprises firstly a
layer of dense fibrous connective tissue which forms the articular surface and is called the articular layer, secondly a subjacent layer of loose connective tissue termed the proliferative layer, because it contains proliferating pluripotent stem-cells, and thirdly a deep layer of hypertrophic hyaline cartilage (Figs. 37dd, 48v, 53n). While this basic appearance remains more or less constant throughout the period of growth, details change (H. Luder 1996). Cells of the articular layer, for instance, gradually assume a chondrocyte-like appearance around the time of puberty. Most major changes, however, occur during the first years after birth. Thus, condyles from newborns and infants regularly exhibit soft tissue columns containing large blood vessels, that protrude downwards from the articular layer, invaginate the proliferative layer, and extend through the hyaline cartilage to the subchondral marrow spaces (Fig. 19g). These columns which are also referred to as vascular canals and are considered remnants of the embryonic pattern of blood supply, normally disappear gradually during infancy. Also, during the first few years of postnatal life, the hypertrophic layer that is most prominent at birth, decreases dramatically in thickness. Subsequent age-dependent changes in the width of the hyaline cartilage, however, hardly exceed individual variation (Figs. 37dd, 48v, 53n, 79q).
The association between the various articular tissue layers and condylar growth is evident from experimental studies in suitable animal models that resemble humans with respect to the microscopic structure of the condyle (H. Luder 1996). The proliferative layer contributes to condylar growth by producing new cells committed to subsequent differentiation into chondrocytes, which are in apposition on top of the hypertrophic layer. Through this apposition of new cells, the hypertrophic cartilage grows in thickness and older cartilage cells are displaced deeper into the hypertrophic layer. As soon as new cartilage cells are fully differentiated, they start enlarging and synthesizing extracellular matrix. As a result, cells of the hypertrophic layer become separated from top to bottom by widening septa of the matrix and at the same time grow in size. Once chondrocytes have attained their final stage of hypertrophy at the lower border of the hypertrophic layer, most of them die, collapse, and leave empty lacunae for subsequent endo-
H. L. Obwegeser, Mandibular Growth Anomalies© Springer-Verlag Berlin Heidelberg 2001
348 CHAPTER 18 Histology of Condyles in Mandibular Growth Anomalies
N F (10·5) H.H. M (12-4) H.E. F (13-4) N F (14-8) H.E. M (15-9) N M (16·1 ) N M (19-10) H.H. M (20)
Fig. 79a-h. Histological findings in cases of condylar hyperactivity. Comparative age-dependent appearance of the articular tissue and subchondral bone in normal (N) condyles (a, d, f, g) as well as specimens from H. H. (b, h) and H.E. (c, e) cases at the growth stage (M male, F female, age in years-months). Note the cone-shaped thickening of the articular tissue in one of the H.E. cases (c) as well as the pattern of trabeculae and depth of cartilage islands (arrowheads) in the subchondral spongiosa. To appreciate the features of the spongiosa, note that the bone appears dark in the paraffin (b, c, e, h) and light in the plastic sections (a, d, f, g). Toluidine blue, original magnification x33 (bar=0.5 mm)
chondral ossification. This involves invasion by capillaries, chondroclasts which resorb cartilage matrix, and bone forming osteoblasts. Thus, endochondral ossification continuously converts into primary spongiosa what has been added to the hypertrophic layer through apposition of new cells, interstitial production of new matrix, and enlargement of the chondrocytes. In so doing, it maintains a more or less stable thickness of the hypertrophic layer.
During the conversion of the hyaline cartilage into primary spongiosa, chondroclasts do not resorb all of the extracellular matrix, but leave a cartilaginous scaffold for subsequent bone formation by osteoblasts. These primary trabeculae, which contain islands of cartilage, are remodelled only at some distance from the zone of erosion of the hypertrophic layer and replaced by trabeculae consisting only of lamellar bone. The depth of cartilage rests in the subchondral bone is apparently related to the rate of condylar growth (Fig. 79r). In specimens from newborns and infants, they can be traced as far down as the condylar neck. In individuals of more than 10 years of age, however, the distance of cartilage rests from the zone of erosion decreases dramatically, and in adults older than 30 years, they are confined to a very narrow subchondral band, if
present at all. This justifies the wide-spread practice of histologists of taking the frequency and depth of subchondral cartilage islands to decide, whether and at what rate growth had been active in specimens of condylar hyperplasia (M. Rushton 1944, 1946; T. 0berg et al. 1962; P. Egyedi 1969; J. de Burgh Norman and D. Painter 1980; L.G. de Bont eta!. 1985; P. Slootweg and H. MUller 1986; H. Obwegeser and M. Makek 1986; F. Gray et a!. 1990). However, it should be borne in mind that cartilage remnants are related primarily to cartilage erosion and could also occur when this process is slowed down or cannot keep pace with cartilage formation.
Considering the limited alterations of condylar microscopic appearance after infancy, which contrast strikingly with the variations observed in the rates of mandibular growth (A. Bjork 1963), it would appear that a balance is normally maintained between cartilage growth and endochondral ossification, that keeps the thickness of the hypertrophic layer within narrow bands. Rather than variations in rates of growth, significant changes in cartilage thickness would thus reflect disturbance of the steady-state conditions between cell proliferation, matrix production, chondrocyte enlargement and cartilage erosion.
18.2 Normal Condyles in Different Age Groups 349
N M (26-2)
Fig. 79i-n. Histological findings in cases of condylar hyperactivity. Comparative age-dependent appearance of the articular tissue
and subchondral bone in normal (N) condyles (i, I, n) as well as specimens from H.H. cases (j, m) and a case of"simple" condylar hyper
plasia (C.H.; k) at the transitional and adult stages (M male, F female, age in years-months) . Note the fraying of the articular surface in
the C. H. case (k) and the vertical cleft across the entire articular tissue in the H.H. case (m). j, k, m paraffin sections, i, I, n plastic sec
tions, toluidine blue, original magnification x33 (bar=O.S mm)
Transitional Stage. The interval between late adolescence and the late twenties constitutes a period of transition from the microscopic appearance of the condyle during growth to the appearance prevailing for the rest of adulthood. The articular layer becomes almost entirely fibrocartilaginous and thereby is converted into the superficial zone of the adult articular tissue. In the proliferative layer, cell replication comes to a standstill, the density of constituent cells decreases, and some cells assume a chondrocyte-like structure. Unlike as claimed by some investigators (F. Gray et al. 1990), the layer does not disappear, although at this stage it should be more appropriately referred to as the intermediate zone. The hypertrophic layer is converted into the deep zone of the adult articular tissue. During this conversion, chondrocytes, although increasing in size from top to bottom of the zone, remain smaller than during growth, become separated by wider septa of matrix, and acquire prominent pericellular halos (Fig. 361). In contrast to the situation during growth, the deepest calcified part of the cartilage becomes clearly visible as a distinct, darkly staining layer that is separated from the non-calcified tissue by a sharp line of demarcation, the so-called tidemark (Fig. 39k). In the subchondral zone, a continuous bone plate is gradually built. Therefore, calcified cartilage borders in decreasing proportions on marrow spaces and in increasing proportions directly on bone
(Fig. 361). In the marrow spaces, bone formation clearly predominates over cartilage resorption (H. Luder 1996). As a result, subchondral cartilage rests become scarce and located only in close proximity to the calcified cartilage (Fig. 79r).
Adult Stage. At the adult stage, the condylar articular tissue essentially constitutes fibrocartilage with varying prominence of fibrous and cartilaginous components (H. Luder 1997). In the superficial zone, chondrocytes occur scattered or in small groups, interspersed between masses of thick collagen fibres. In the intermediate zone, the proportion of chondrocytes rises further with age at the expense of fibroblasts, while the total number of cells continues to decrease. As a result, the remnants of the proliferative layer disappear as a distinct cell layer along an increasing proportion of the condylar articular surface. The fibrocartilage of the deep zone is characterized by scattered, small chondrocytes embedded in a lattice of obliquely arranged collagen fibres (Figs. 32n, 39k). Unlike the intermediate zone, the superficial and deep zones lack systematic age-related changes in appearance (H. Luder 1998). However, they can show signs of cartilage remodelling, mostly progressive remodelling characterized by the formation of chondrocyte clusters or the accumulation of cartilage matrix that is unusually rich in proteogly-
350 CHAPTER 18 Histology of Condyles in Mandibular Growth Anomalies
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Fig. 79o-r. Histological findings in cases of condylar hyperactivity. Thickness of articular tissue layers or zone (o-q) and depth of subchondral cartilage rests (r) against age in normal condyles (asterisks and solid line indicating average) as well as specimens from H.H. (squares), H.E. (dots) and C.H. (triangle) cases. Please note that cartilage rests (r) in the H.H. cases of about 12.5 and 20 years of age, similar to those of normal newborns, were observed down to the resection border, which may not have coincided with the maximum depth
cans and, therefore, displays a strong metachromatic staining reaction with toluidine blue (Fig. 32n). This type of remodelling seems to be particularly frequent in individuals around 40-45 years of age and is associated with reactivated endochondral ossification that can produce small subchondral cartilage islands similar to those found during the period of transition from growth to adulthood (H. Luder 1998}. In comparison with progressive remodelling, regressive remodelling involving dissolution of cartilage and its replacement by vascular fibrous tissue is very rarely seen in individuals below 50 years of age (H. Luder 1996). Similarly, signs of degeneration, i.e., osteoarthrosis, are scarce in this age range. If present, degenerative changes are mostly confined to fibrillation of the articular surface and hardly
ever involve splitting or clefting of the deeper articular tissue zones (H. Luder 1996}.
18.3 Condyles in Mandibular Growth Anomalies
18.3.1 Condylar Hypoactivity
The only specimen from this class of growth anomaly, that was available for histological examination, was the resected condyle of an 18-months-old girl with hemifacial microsomia. Not unexpectedly in such a case, this condyle was hypoplastic, its overall size corresponding approximately to that of a normal newborn. Interesting-
ly, however, the otherwise inconspicuous hypertrophic cartilage was also much thinner than normal, even when its thickness was related to the reduced overall size of the specimen. On the other hand, subchondral cartilage remnants were observed down to a depth of about 4.5-5 mm from the zone of erosion, which corresponds perfectly to the values found in normal agematched specimens (Fig. 79r). Also, the trabecular pattern of the condylar spongiosa did not deviate significantly from that observed in controls (Fig. 19f,g). This could be taken to indicate that endochondral ossification and remodelling of the primary spongiosa in this condyle were fairly normal, whereas the production of hypertrophic cartilage through stem cell proliferation, matrix production and chondrocyte enlargement was deficient.
18.3.2 Condylar Hyperactivity
From cases of unilateral condylar hyperactivity, seven resected condyles were obtained as paraffin blocks embedded earlier for routine pathological diagnosis. Four of these cases, one female (Fig. 32) and three males (Figs. 36, 37, 68), were classified as hemimandibular hyperplasias (H.H.) or hybrid forms with a predominance of H.H., one case of a female (Fig. 39) as "simple" unilateral condylar hyperplasia (C.H.) and two cases, one female (Fig. 48) and one male (Fig. 53), as hemimandibular elongation (H.E.). Based on the patients' ages at condylectomy, one specimen of H.H. and both specimens of H.E. had been removed during the growth period, two specimens of H.H. at the beginning and end of the transitional stage, respectively, and the last specimen of H.H. as well as the one condyle with C.H. at the adult stage. From all the existing paraffin blocks, new sections were cut, stained with toluidine blue for better comparison with control material, and analysed histometrically using a light microscope equipped with an eyepiece micrometer.
In addition, micrographs taken earlier from condyles of five patients were available for a qualitative examination. These cases were classified as H.H. at the growth stage (Fig. 31), a hybrid form with predominance of H. H. (Fig. 74), a hybrid form with predominance of H.E. (Fig. 73), H.E. (Fig. 28) and a hybrid form without predominance of either the H.H. or H.E. component (Fig. 69). A summary of the histopathology findings in all these specimens is displayed in Table 1.
18.3.3 Hemimandibular Hyperplasia
All condyles removed from cases of H.H. at the growth stage as well as one specimen from a male hybrid case with predominance of H. H. resected at the beginning of
18.3 Condyles in Mandibular Growth Anomalies 351
the transitional stage exhibited regular hypertrophic growth cartilage and active or even intensive endochondral ossification. Thus, they constituted cases of condylar hyperplasia type I as defined by P. Slootweg and H. Mi.iller (1986). Compared with normal condyles, the two specimens from males available for histometric analysis revealed some, although insignificant, thickening of the hypertrophic cartilage and abundant subchondral cartilage rests at significantly greater distance from the zone of erosion (Figs. 79q,r). The spongiosa comprised comparatively small marrow spaces interspersed in an abnormally tight, almost tumour-like network of thin, mixed cartilaginous-bony trabeculae lacking clear orientation (Figs. 79b,h). This pattern suggests that endochondral ossification and remodelling of the primary spongiosa cannot keep pace with cartilage growth, either because the latter processes are reduced or cartilage growth is increased in rate. Imbalanced or disturbed endochondral ossification and remodelling of the primary spongiosa could indeed explain the grossly distorted condylar shape that is frequently observed in cases of H.H .. How such a mechanism could account for the malformation of the mandibular ramus, angle and corpus, remains, however, mysterious. Rather than being responsible for these malformations, the abnormal endochondral ossification and remodelling of the condyle could also conceivably be the result of an as yet unknown, common cause that interferes with growth and remodelling of the entire hemimandible.
Apart from being compatible with the clinical picture, the trabecular pattern seen in the preceding first two cases also seemed to be typical of cases of H.H., thus allowing a distinction from cases of H.E .. Yet the histological appearance evident from micrographs of a condyle from a female patient classified as a "classical" case of"pure" H.H. (Fig. 31) did not fit the description given above. Rather, the condylar spongiosa gave an impression of normality, although the depth of subchondral cartilage remnants could not be ascertained. This suggests that the mechanisms leading to H.H. may vary, which would mean that a histopathological diagnosis based on condylar appearance alone would not be possible.
The only condyle removed during the transitional stage of development from a male patient suffering from H.H. revealed partly fibrocartilage, as typically seen in adult specimens, and partly a type of cartilage characterized by hypertrophic chondrocytes interspersed between arcades formed by prominent collagen fibre bundles. The latter type of cartilage resembled that described as occurring in condylar hyperplasia type II (P. Slootweg and H. Mi.iller 1986). In agreement with this classification, there were signs of active endochondral ossification, which, however, did not exceed those seen in normal specimens (Fig. 361), and a subchondral bone plate which exhibited abnormally numerous marrow
352 CHAPTER 18 Histology of Condyles in Mandibular Growth Anomalies
Table 1. Summary of histopathological findings in cases of H.H. and H.E. as well as hybrid forms and a case of "simple" condylar hyper-plasia (C.H.)
Clinical Case Sex Ageb Cartilage Endochondral Subchondral Subchondral Cartilage rests diagnosis• ossification marrow bone
spaces trabeculae
H. H. 37 Male 12-4 Regular hypertrophic Intensive Narrow Numerous, Numerous, deep thin, ill-oriented
H.H. 31 Female 16-6 Regular hypertrophic Active Inconspicuous Inconspicuous in Inconspicuous in number and size number and depth
Hybrid, 68 Male 20 Regular hypertrophic Intensive Narrow Numerous, thin, Numerous, depth H.H.~H.E. ill-oriented
H.H. 36 Male 28 Partly hypertrophic, Active Slightly Inconspicuous Present
partly fibrocartilage increased in number
H.H. 32 Female 40 Fibrocartilage with Missing Inconspicuous Inconspicuous Absent severe degenerative changes
Hybrid, 74 Female 40 Fibrocartilage with Missing Inconspicuous Inconspicuous Absent H.H.~H.E. severe degenerative
changes
C.H. 39 Female 31 Fibrocartilage with Minor Inconspicuous Inconspicuous Few initial degenerative changes
H.E. 48 Female 13-4 Regular hypertrophic Active large Few, slender, Inconspicuous in well oriented number and depth
Hybrid 73 Male 13-10 Regular hypertrophic Intensive Large Few, slender Inconspicuous in H.E.~H.H. well oriented number and depth
H.E. 53 Male 15-9 Regular hypertrophic Active Large Few, slender, Inconspicuous in well oriented number and depth
H.E. 28 Female 17-6 Transitional from Minor Large Almost compact Few hypertrophic to bone plate and fibrocartilage slender trabeculae
Hybrid 69 Male 16-10 Regular hypertrophic Intensive Inconspicuous Inconspicuous Numerous, deep
• In hybrid forms, predominance of either the H.H. or H.E. component is indicated by "greater than" -signs (>)
h Age (years-months) at condylectomy
spaces in direct contact with cartilage. This indicates regular, well-coordinated condylar growth continuing beyond the age when it normally terminates.
All condyles removed at the adult stage, i.e., two specimens from H.H. cases and the one from the only case of "simple" condylar hyperplasia, notably all females, revealed degenerative disintegration of the articular tissues, i.e., signs of osteoarthrosis, but none of significant on-going growth. This characterization corresponds to that given by P. Slootweg and H.Miiller (1986) regarding condylar hyperplasia type III. In the condyle from the youngest individual, degenerative changes were superficial and mild, whereas in those obtained at about 40 years of age they were severe, affected all zones down to the osteochondral junction, and were accompanied by marked regressive remodelling. These alterations clearly exceeded those found in age-matched control specimens and, therefore, cannot be considered "normal" aging-associated changes. However, it cannot be decided, whether they presented the cause or effect of the abnormal condylar enlargement and distortion.
18.3.4 Hemimandibular Elongation
All condyles obtained from cases of H.E. or from hybrid forms with a predominance of the H.E. component were removed at the growth stage. All but one revealed the normal layered appearance of the articular tissue typical of this stage. The one exceptional specimen, shown already in a previous publication (H. Obwegeser and M. Makek 1986), exhibited a central cone-shaped thickening of the articular layer, that displaced the proliferative and hypertrophic layers downwards. This peculiar structure that, although lacking any blood vessels, resembled somewhat the vascular canals found in condyles from infants, could not be observed in any other specimen. Thus, unlike the assumption of H. Obwegeser and M. Makek ( 1986), it cannot be considered typical of H.E.cases.
In all condyles of this type of growth anomaly, including that with the local thickening of the articular layer, the hypertrophic cartilage exhibited a perfectly normal structure and thickness (Fig. 79q), and there
was obviously active endochondral ossification. According to the classification ofP. Slootweg and H. Muller (1986), they all constituted condylar hyperplasia type I, similar to the specimens from H.H. cases removed at the same age range. However, there were some striking differences. In contrast to specimens removed because of H.H., those from H.E. cases disclosed subchondral cartilage rests down to normal distances from the zone of erosion (Fig. 79r), and the condylar spongiosa was characterized by slender, well-oriented, sometimes almost parallel bone trabeculae arranged between comparatively large marrow spaces (Fig. 79c, e). This suggests enhanced but well-coordinated cartilage growth, endochondral ossification and remodelling of the primary spongiosa, i.e., a growth pattern fitting well to the clinical and radiographic appearance of H.E ..
18.3.5 Hybrid Forms
The only condyle from a case classified as hybrid form without predominance of either the H.H. or H.E. component (Fig. 68) was removed at the growth stage and had to be examined based on old micrographs alone. These micrographs indicated uniform thickening of the articular tissue, but did not allow identification of the proliferative layer. Regarding structure, the hypertrophic cartilage and the trabecular pattern of the subchondral spongiosa appeared inconspicuous. The conclusion that can be derived from these limited findings is that the histological appearance of the condyle, lacking any sign of either H.H. or H.E., fairly well reflected the clinical picture.
18.4 Summary
Irrespective of the clinical classification of the condylar hyperactivity cases, the histological appearance of excised condyles presented in this work is in good agreement with the descriptions given in the literature on condylar hyperplasia (M. Rushton 1944, 1946; L. Schultz et al. 1960; T. 0berg et al. 1962; R. Walker 1967; P. Egyedi 1969; J. de Burgh Norman and D. Painter 1980; L. de Bont et al. 1985; P. Slootweg and H. Muller 1986; H. Obwegeser and M. Makek 1986; R. Gray et al. 1990). These observations suggest that the microscopic structure of the cartilage covering the condylar bone only depends on the age at condylectomy, supporting the notion of R. Gray et al. (1990) that the types of condylar hyperplasia distinguished by P. Slootweg and H. Muller ( 1986) mainly reflected the different stages of physical development at onset of the growth disorder. In contrast to the report of R. Gray et al. (1990), however, the findings obtained
18.3 Condyles in Mandibular Growth Anomalies 353
from the present investigation do not suggest that significant changes in the thickness of the articular tissue are associated with any of these growth anomalies. Rather, alterations at the cartilage level proved to be very subtle and did not exceed the range of normal variation. It would appear, therefore, that nature fairly successfully maintains a steady-state between the various growth components, even if overall growth of the condyle is highly disturbed. As a consequence, a distinction of the different clinical forms of growth anomalies based on the microscopic appearance of condylar cartilage does not seem possible.
The histological features that provided the most reliable, although not absolutely flawless, discrimination of H.H. and H.E. cases of the present material were the trabecular pattern of the condylar spongiosa and the depth of the cartilage remnants embedded in the subchondral bone trabeculae. While cartilage rests have consistently been considered by previous investigators (M. Rushton 1944; T. 0berg et al. 1962; P. Egyedi 1969; J. de Burgh Norman and D. Painter 1980; L. de Bont et al. 1985; P. Slootweg and H. Muller 1986; H. Obwegeser and M. Makek 1986; R. Gray et al. 1990), usually to decide whether or not condylar growth was active, the arrangement of trabeculae, to the best of my knowledge, has not been taken into account so far. The validity of this diagnostic feature, therefore, needs confirmation from further studies.
If proven to be useful, the appearance of the spongiosa would enable a distinction between normal, H.H.and H.E.-condyles, as long as growth has not yet come to a standstill. Once growth ceases, however, subchondral bone trabeculae apparently remodel, thus assuming an inconspicuous arrangement, which no longer offers clues for a diagnosis. Moreover, even in cases operated on during active enlargement of the condyle, the characteristics of the spongiosa do not allow a decision to be made whether condylar growth was hyperactive or normal at the time of the surgical intervention.
Although virtually all previous reports on cases of condylar hyperplasia have speculated about its aetiology, this issue is still far from being clear. Considering the low numbers of uniform cases and the limited conclusions that can be derived from the minor alterations in the microscopic appearance of the condyles, histopathology is unlikely to offer useful explanations regarding aetiology and pathogenesis of mandibular growth anomalies. From the distinct histological manifestations of growth disturbances setting in during and after the normal growth period, it would appear that respective causes vary as well. Also, distinct aetiologies may account for H. H. and H.E., as the components of condylar growth in these two types of anomalies seem to be affected to strikingly different extents.