American Journal of ORTHODONTICS

Founded in 1915 Volume 88 Number 3 September, 1985

Copyright 0 1985 by The C. V. Mosby Company

ORIGINAL ARTICLES

The control of condylar growth: An

experimental evaluation of the role of the
lateral pterygoid muscle
Lance L. Whetten, D.D.S., M.S., atid Lysle E. Johnston, Jr., D.D.S., Ph.D.
Lar Vegas, Nev., and St. Louis, MO.

The present study used 21 male albino rats to test the hypothesis that lateral pterygoid traction regulates the
growth of the mandibular condyle. The condyles, the rami, and the top of each glenoid fossa were marked with
metallic implants, and, following bilateral sectton of the condylar neck, one lateral pterygoid muscle was extirpated.
On the basis of the literal details of Petrovfc’s cybernetic model, ft was assumed that the conttnued forward growth
of the mkiface and the backward translation of the glenoid. fossa would combine to produce a progressive
disturbance in the buccal occlusion that would, in turn, generate a reflex contraction of the remaining lateral
pterygoid muscle. Initially, however, growth of the isolated condyles would have little impact on the spatial position
of the rest of the mandible. As a result, the condyles on the side with the intact lateral pterygokl should grow
for a time at a maximal, open-circuit rate, whereas the experimental condyle, deprived of all muscle traction,
should show only a minimal “commanded” rate of growth. The serial change in the position of the condylar and
ramal implants was assessed cephalometrlcally for 6 weeks, and between-sides differences were analyzed by
randomized block analysis of variance. The presence or absence of the lateral pterygokl’muscle had no significant
effect on the anteroposterior position of the condylar implants and only a slight, transitory effect on their vertical
position. The translation of the ramal implants, however, was greatly affected by the condylotomy. On both
control and experimental sides, the mandible collapsed upward and backward until contact between the growing
condyle and ramus had been achieved, whereupon a downward and forward pattern of translatory growth was
m-established. Although it could not be shown that lateral pterygoid traction per se is a stgnifi~nt factor in
the growth of isolated condyles, it was concluded that the condyle is vitally important to the translatory growth of
the mandible as a whole. On the basis of these data and the current literature, a simple hypothesis was
advanced for the control of condylar growth by the ongoing pattern of functional loading and for the role of this
growth in the normal downward and forward displacement of the rest of the mandible.

Key words: Mandibular growth, bilateral condylotomy, pterygoidectomy, feedback control, implants

It has been said that the ability to exert con-

n-01 is the final test of the degree to which a system is
understood. To a first approximation, the current in-
Based on a thesis submitted by the senior author to the Graduate School, St.
Louis University.
terest in functional appliances would seem to be a case
in point. Many have discarded the belief that condylar
growth is immutable and, instead, have begun to en-
tertain-and act on-the possibility that mandibular
growth is therapeutically modifiable. Indeed, the ability
to “grow mandibles” is the central dogma of what has
181
182 Whetten and Johnston
Max.
Ave.
- Min.
IF-____--- _- 31 ---- -- 0
STH
Fig. 1. Mandibular growth as a function of somatotrophic hor-
mone and reflex lateral pterygoid traction driven by periodontal
ligament afferents. 7, Maximal lateral pterygoid activky. 2, Min-
imal lateral pterygoid activity. 3, Lateral pterygoid muscle ab-
sent; the growth of condylar cartilage proceeds at a minimal
“commanded” level dictated by the level of growth homtone
and somatomedin. (After Petrovic et al: In McNamara JA Jr,
editor: Determinants of mandibular form and growth, Mono-
graph No. 4, Craniofacial Growth Series, Ann Arbor, 1975, Cen-
ter for Human Growth and Development, University of Miiigan,
Fig. 7, p. 145.)
become an orthodontic “growth industry.” Unfortu-
nately, it is difficult to infer a rigorous theoretical and
experiential basis for the action and clinical application
of functional appliances.
Perhaps the simplest and most popular “explana-
tion” for the increased condylar growth said to accom-
pany the use of functional appliances may be inferred
from Moss’s “functional matrix’ ’ hypothesis. ‘-’ Spe-
cifically, Moss5 has stated:
The mandible, then, is passivelylowered in spaceduring
orofacial capsularexpansion. One result of this is a tendency
to distract the head of the condyle away from its superior,
functional articulating surfaces. As a response to this dis-
traction, the condylar cartilage proliferates. This effect is not
at all mystical, but is well known in orthopedicsasthe Heuter-
Volkmannlaw. . . . Further, in both experimental and clinical
studies, when the appropriate methods are used, it has been
shown by many workers that when the compressiveloadings
(brought about by normal joint functioning) are ieduced, as
by appropriate repositioning of the lower jaw, adaptive con-
dylar growth occurs . .
Within the conceptual framework of the functional
matrix hypothesis, however, this argument is mystical.
If condyles lack an intrinsic ability to grow, what then
is the nature of the control signal generated by a re-
duction in “compressive loadings”? What tells the con-
dyle to grow?
At present, there is really but one proposed expla-
nation: lateral pterygoid traction on the head of the
condyle. Because “postural hyperpropulsion”-but
Am. J. Orthod.
September 1985
OCCLUSION
SNOUT ERROR
Flg. 2. Cybernetic representation of Petrovic’s hypothesis.
Snout growth produces an occlusal disturbance that is sensed
by the phasic and tonic receptors of the periodontal ligament.
The resukii afference ptoduces a reflex contraction of the
lateral pterygoid muscle. The contraction is said to have two
effects: (1) an immediate mandibular shift 10 correct the occlu-
sion and (2) a long-term increase in condylar growth to make
the correction permanent. If the correction is equal and opposite
to the perturbation, the occlusal error will go to 0. In the present
experiment, condylotomy would cut the connection between
condylar growth and mandibular translation on both the exper-
imental and control sides (E and C). Pterygoidectomy on the
experimental side would eliminate the short- and long-term con-
dylar and mandibular loops (E). As a result, for any given level
of growth hormone, the experimental condyle would be ex-
pected to grow at its lowest possible rate. On the control side,
the condylo&my would (at least for a time) prevent condylar
growth from having an effect on mandibular position. In the
absence of an arror correction, continued transtatory growth of
the glenoid fossa and snout would increase the o&lusal dis-
turbance, and eventually the control condyle Wu# be expected
to grow at its maximal, open-circuit rate. As a result, each animal
should demonstrate a between-sides difference approximately
equal to the range of condylar growth regulation that can be
effected by the lateral pterygoid muscle.
not extraoral traction-seemed to produce increased
proliferation in the prechondroblastic layer of condylar
cartilage, Petrovic and co-workers6-’ have concluded
that lateral pterygoid pull constitutes “the final common
link,” the signal to which the cells of condylar cartilage
actually respond. Indeed, Petrovic has suggested re-
peatedly that modulation of condylar growth by lateral
pterygoid activity constitutes an important element in
a feedback mechanism that serves to maintain a stable
occlusion in the face of varying rates of maxillary
growth (Fig. 1).
Although Petrovic’s cybernetic model implies that
the condyle is an active “growth center,“” and fails to
consider the role of dentoalveolar compensation in max-
illomandibular “fine tuning,” it is sufficiently spe-
cific-and influential-to warrant independent corrob-
oration.
In light of the observation that isolated condylar
segments have an intrinsic ability to gro~,“-‘~ bilateral
condylotomy in conjunction with unilateral removal of
v01l4m? 88
Number 3
Fig. 3. Surgical preparation. A, Condyle and ramus exposed and implant holes prepared. B, Amalgam
implants placed. C, Division of condylar neck. A fifth implant was placed in the root of the zygomatic
arch above the glenoid fossa.
the lateral pterygoid muscle should provide a gross test
of the extent to which direct muscle traction can alter
the rate of condylar growth. Given the properties of
control systems and the details of Petrovic’s cybernetic
formulation, the present experimental model should
produce a between-sides difference in condylar growth
that approximates the range of adjustment that can be
achieved by modulating the pull of the lateral pterygoid
muscle (Fig. 2).
MATERIALS AND METHODS
Twenty-one male Sprague-Dawley albino rats were
employed in this study. At the time of surgery, all were
at least 6 weeks old and weighed an average of 180 gm
(125 to 220). The rats were first injected intramuscu-
larly with 4 to 5 mg/kg of ketamine hydrochloride,
followed in 2 to 5 minutes by 20 mg/kg of sodium
pentobarbital, intraperitoneally, and subcutaneous atro-
pine sulfate, 0.5 mg/kg. The surgical procedure was
performed on one side at a time (the first 7 on successive
days; the remainder in one sitting). For the sake of
brevity, however, bilateral procedures will be charac-
terized in a single description.
Implants and condylotomy
Both condyles were exposed, and five metallic im-
plants were placed on each side: two in the head of the
condyle, two in the ramus, and one in the temporal
Control of condylar growth 183
bone above the glenoid fossa (Fig. 3, A and II). To
permit the two sides to be differentiated radiographi-
tally, one set of implants was made of pure amalgam
and the other was made of a 50-50 mixture of amalgam
and acrylic. Following implant placement, both con-
dylar necks were divided with a No. 6 round bur in a
low-speed handpiece (Fig. 3, C).
Lateral pterygoldectomy
On a side chosen at random (twelve times on the
right; nine on the left), the condylar fragment was ro-
tated outward to expose the lateral pterygoid muscle,
which was then removed bit by bit with fine rat-tooth
forceps and tenotomy scissors. On the control side, the
condyle was rotated, but the muscle was left intact.
Finally, the cut margin of each condylar fragment was
coated with a layer of cranioplastic acrylic to retard the
ultimate union of the condyle and ramus. Following the
surgical procedures, the animals were fed ground com-
mercial rat chow and water (containing tetracycline, 14
mg/liter). As judged by an average weight gain of 90
gm during the course of the experiment, the animals
tolerated the extensive surgical procedures reasonably
well.
Cephalometric analysis
The growth of the control and experimental con-
dyles was assessed from lateral cephalograms taken at
184 Whetten and Johnston Am. .I. Orrhod.
Sqxember 1985

Fig. 4. Cephalometric analysis. The Cartesian coordinates of implants 1 to 4 were measured relative
to the palatal plane and an ordinate erected through the glenoid fossa implant (ff).

Tsbk I. Descriptive statistics: Means and SD by time and side for the weekly change in the X and Y
coordinates of the two condylar (1 and 2) and two ramal (3 and 4) implants (in mm x 10)
Condylar implants Ramal implants

I 2 3 4

X Y X Y X Y X Y

Week Side* x SD 2 SD x SD 2 SD x SD x SD ? SD x SD

1 C 2.4 5.3 -1.0 2.9 1.7 5.9 -0.1 2.8 -4.7 4.9 2.8 4.8 -5.3 5.0 0.3 3.9
E 0.1 3.0 0.1 3.4 0.2 2.3 0.4 3.5 -4.6 2.8 2.3 4.3 -4.1 2.8 0.7 3.7
2 C 1.3 3.7 -2.2 2.0 1.1 3.6 - 1.7 2.5 -0.8 4.8 0.2 4.3 -0.7 5.0 - 1.5 4.0
E 1.3 3.4 -0.4 3.1 1.2 3.4 -0.9 2.2 -2.2 3.3 3.0 5.9 -2.5 3.5 0.3 5.1
3 C 0.3 2.9 -2.2 3.1 1.4 3.0 -2.5 3.1 0.7 2.2 -2.4 3.4 1.3 3.0 -2.9 3.1
E 2.4 2.1 -1.0 3.4 1.9 3.2 -0.2 3.1 1.8 4.2 - 1.1 5.1 2.5 4.0 - 1.2 5.3
4 C 0.3 3.2 -1.1 1.9 0.3 2.9 - 1.0 2.0 1.0 3.2 - 1.7 2.5 2.1 3.4 -1.7 3.4
E 0.4 4.2 -1.6 3.0 1.1 4.6 - 1.5 2.7 0.3 4.5 - 1.9 2.6 0.2 5.9 - 1.8 3.7
5 C 0.9 2.5 - 1.7 2.4 0.5 2.4 - 1.6 2.0 1.2 3.1 - 1.4 2.3 0.9 3.1 -0.5 2.9
E 1.2 2.9 -0.5 2.2 1.3 3.3 -0.6 2.1 2.1 3.8 - 1.5 2.5 2.2 4.2 -0.9 3.7
6 C 1.4 2.2 -0.4 2.2 2.1 2.3 - 1.0 1.3 2.7 2.8 -0.8 1.7 3.2 3.3 - 1.0 2.1
E 1.5 3.8 -1.1 2.2 0.7 1.8 -0.9 2.1 -0.5 2.8 0.0 2.1 0.1 2.6 0.0 2.9

TOTAL C 6.5 8.8 -8.6 5.7 7.1 9.4 -8.0 5.2 0.1 8.2 -3.4 6.1 1.5 7.2 -7.3 1.4
E 6.9 8.3 -4.5 7.4 6.3 6.2 -3.8 5.2 -3.1 7.6 0.8 9.1 - 1.7 7.5 -2.8 8.2

*C = Control (lateral pterygoid intact). E = Experimental (lateral pterygoid removed)

a source-film distance of 50 cm. To minimize the im- palatal plane as the X axis and a perpendicular through
plant-film distance, separate left- and right-facing ceph- the temporal implant as the Y axis (Fig. 4). Each film
alograms were used to measure the movement of each was enlarged 10X by projection, traced, and the X
set of implants. No attempt was made to manipulate and Y coordinates of the condyhu and ramal implants
the mandible or hold it in occlusion. The animals were were measured to the nearest 0.05 mm with dial vernier
radiographed immediately after surgery (film 0) and calipers.
weekly thereafter for a period of 6 weeks (films 1 During the 6 weeks of the experiment, 16 of the
to 6). 210 implants failed-7 condylar and 9 ramal. When an
Condylar and ramal implant movement was ana- implant proved unstable (as judged by a change in in-
lyzed relative to a Cartesian coordinate system with the ter-implant distance, obvious rotation, or outright loss),
Volume 88 Control of condylar growth 185
Number 3

R R
l l

Control Experimental

2mm
1

3 4 3 4

1 0
20’ 2t l .2 2 1
3. : :
P--S-
30 "'r' l 3: .O
4'.
‘. %* 4 0 ." 4.
5 6’ 42. 6 65 5w6

Flg. 5. Translation of condylar (7 and 2) and ramal (3 and 4) implants. Each point represents the
mean; the interrupted lines represent the change in the position of the midpoint of each implant pair.
Note the initial lag in condylar growth on the experimental side (pterygoidectomy) and the looped
pattern of ramal implant tratklation.

increments from previous weeks were discarded and
data from the contralateral implant were used only in
the calculation of descriptive statistics.
Statistlcal design
Because of unavoidable variation in the initial po-
sition of the 10 implants, weekly increments constituted
the data. In addition to means and standard deviations,
a separate analysis of variance (ANOVA) was calculated
for the X and Y coordinates of each condylar and ramal
implant. The experiment was cast in the form of a mixed
2 by 6 randomized block factorial design: each animal
constituted a block to which the two levels of condylar
treatment (lateral pterygoid present or absent) were ap-
plied and evaluated over six time periods. Time (T) and
pterygoidectomy (P) constituted fixed effects, whereas
blocks (B) were chosen at random. Accordingly, after
division by the appropriate degrees of freedom, the
three interaction terms that comprise the residual sum
of squares, P X: B, T X B, and PT X B, were used
in the denominators of the F ratios for P, T, and P x T,
respectively. I6
RESULTS
Means and standard deviations for the X and Y
coordinates of the condylar (I and 2) and ramal (3 and
4) implants are presented in Table I, and the average
weekly displacement is depicted graphically in Fig. 5.
Both the control and experimental condylar fragments
grew and displayed similar downward and forward vec-
tors. In contrast, growth increments for the ramal im-
plants-both control and experimental-displayed a
circular trajectory: upward and backward for the tirst 2
weeks or so and then downward and forward for the
rest of the experiment.
The analyses of variance for condylar and ramal
translatory growth are summarized in Table II. For only
two of the eight implant coordinates was there a sta-
tistically significant (P < 0.05) between-sides differ-
ence: the posterior condylar and ramal implants (2 and
3) showed approximately 0.4 mm of increased vertical
displacement on the intact side. In addition, the F ratios
for time were significant for three of the four ramal
coordinates.
DISCUSSION
Condylar growth
That isolated condyles grow and do so in an orderly
fashion is not a unique finding: it has now been dem-
onstrated in rats,‘2*‘3 guinea pigs,“9’4 and cats.” Data
from the present experiment, however, fail to lend ob-
vious support to the hypothesis that lateral pterygoid
186 Whetten and Johnston
Table II. Analysis of variance: F-ratios for pterygoidectomy, time, and interaction
Condylar implants
I 2
Source of
variation X Y X Y
Pterygoidectomy 0.03 4.15 0.12
Time 0.31 0.99 0.25
Interaction 2.02 2.04 0.99
Sample size 18 18 17
*P < 0.05.
**p < 0.01.
traction plays a significant role in the general process
of condylar growth modulation.
The only significant (P < 0.05) effect of lateral
pterygoidectomy on condylar growth was a slight (0.4
mm) reduction in the vertical displacement of the pos-
terior condylar implant (2). Although the anterior im-
plant (I) showed a similar translatory deficit, the be-
tween-sides difference fell just short of conventional
statistical significance (P < 0.06). From the standpoint
of Type II errors, however, it would seem prudent to
assume that both differences are real and to consider
their potential significance to Petrovic’s cybernetic
model of mandibular growth.
A reduction in vertical growth is to a first approx-
imation consistent with the contention that there is a
correlation between muscle pull and condylar growth.
If the lateral pterygoid is removed, muscle traction ob-
viously would be eliminated. Unfortunately, so too
would the condyle’s blood s~pply.‘~ A temporary re-
duction in condylar growth would seem inevitable and,
as recently suggested by Kantomaa and Riinning,‘*
would thus constitute a purely methodologic explana-
tion for the effect of lateral pterygoidectomy on con-
dylar growth.
Examination of the present data (Fig. 5, Table I)
shows that the majority of the difference between con-
trol and experimental sides occurred during the first 2
to 3 weeks; thereafter (perhaps coincident with revas-
cularization of the. experimental condyles), the incre-
ments were essentially indistinguishable. Accordingly,
the gross effects seen here and the histologic changes
reported elsewhere can perhaps more easily be ascribed
to diminished condylar circulation than to a loss of
“ . . . transmission of information of either a biome-
chanical nature, such as tension, or of a chemical or
Am. .I Orthod
September 1985
Ramd implants
3 4
X Y X Y
4.74* 2.14 4.51* 3.26 2.66
1.99 13.55** 7.01** 9.32** 1.30
1.02 2.36 1.46 2.36 0.54
17 19 19 14 14
even electrical nature. ’ ’ ’ 9 In plain words, given the cir-
culatory embarrassment that must inevitably accom-
pany lateral pterygoidectomy, it should come as no
surprise that cells fail to respond normally to blood-
borne chemicals (say, somatotrophic hormone or so-
matomedin) or to ‘ ‘functional h yperpropulsion .’ ’
Moreover, Petrovic’s reports of a lack of condylar
response to anterior mandibular displacement effected
by extraoral elastic traction7.” apparently fail to con-
sider the impact of a daily regimen of 8 to 12 hours of
immobilization (and anesthesia?) on the physical con-
dition of the experimental animals. Thus, the basic dis-
tinction between the effects of “active” and “passive”
hyperpropulsion that originally led to the lateral pter-
ygoid hypothesis may be largely artifactual.
It is perhaps significant to note that of late Petrovic’s
group has turned its attention to the possibility that
lateral pterygoid function affects condylar growth in-
directly via the vasculature of the “menisco-temporal
condylar fraenum. “7-9~‘9This newer conjecture in effect
provides independent support for the contention that the
effects generally ascribed to lateral pterygoideetomy
may have more to do with the condylar blood supply
than to some unspecified property of muscular traction.
At this point, it is important to remember that the
presumed long-term significance of pull from the lateral
pterygoid is that it adjusts the anteroposterior growth
of the mandible to that of the maxilla (see Fig. 10, p.
28 1, Petrovic and Stutzmann7). In the present study,
however, the presence or absence of this muscle had
no significant effect on the horizontal displacement of
the condylar implants. Obviously, it could be argued
that the present bilateral condylotomy model alters
“function” (whatever that much-abused word may
mean) to such a degree that the data are irrelevant to
Volume 88
Number 3
the hypothesis under investigation. Several comments
are in order.
First, as has already been noted, condylar isolation
was relatively evanescent; at the end of the experiment,
the condylotomy channel was completely obliterated
and remodeled. Second, the probability of pterygoid
dysfunction or hypofunction cannot be inferred from
the details of Petrovic’s cybernetic model. Specifically,
given a progressive deterioration of the buccal occlusion
caused by the ongoing translatory growth of midface
and glenoid fossa combined with a marked initial up-
ward and backward mandibular collapse, the lateral
pterygoid mechanism should become hyperactive, es-
pecially during the early weeks when condylar and man-
dibular growth are largely independent (Fig. 2). Indeed,
control condyles showed an early horizontal displace-
ment that is consistent with this interpretation (Fig. 5).
Finally, Petrovic’s hypothesis holds that even a com-
pletely hypoactive lateral pterygoid muscle should pro-
duce more condylar growth than would be seen follow-
ing pterygoidectomy (Fig. 1; contrast 2 and 3). Thus,
if lateral pterygoid traction per se works the way much
of the literature says it does, the present experiment
should have had the power to resolve at least some of
the effect.
Despite the present negative results, it should be
noted that Petrovic has reported histologic changes that
are consistent with the assumption that there is some-
thing special about lateral pterygoid traction. Although
it has already been suggested that the properties imputed
to lateral pterygoid traction may well be artifactual, it
cannot be denied that some could perhaps be due to a
control signal generated by muscle pull (as opposed to
the effect of this pull on mandibular position). Given
this possibility, it is appropriate to examine the signif-
icance of the various measures that have been used to
characterize the regulation of condylar growth.
The radiographic methods employed here provide
a direct linear estimate of condylar (and mandibular)
growth relative to glenoid fossa, not an indirect and
equivocal measure of some intermediate step (mitotic
index, thickness of condylar cartilage, etc.). For ex-
ample, reports that a given functional appliance can
produce a posterosuperior thickening of condylar car-
tilage (and, by implication, an acceleration of mandib-
ular growth) could just as well be interpreted as sig-
nifying a retardation of endochondral ossification lead-
ing ultimately to a reduction in the rate of mandibular
growth. Cellular events also require a selective suspen-
sion of disbelief. As noted by Meikle*‘:
. . . The addition of several layers of cells to the condylar
head described by some investigators, although impressive
Control of condylar growth 187
under the microscope, would appear unlikely to alter the
length of the mandible significantly as claimed, reminding
one that “ah that glitters is not gold.”
Finally, although often invoked to “explain” the
mode of action of various functional appliances, Pe-
trovic’s hypothesis actually runs counter to contem-
porary clinical thought. For example, if increased lateral
pterygoid traction were needed to augment the growth
of the condyle, it would be very difficult to infer a
theoretical justification for the use of the Herbst appli-
ance or, for that matter, any “growth-regulating” de-
vice that does not involve “functional hyperpropul-
sion.” The lateral pterygoid hypothesis, however, is
based on the assumption that some types of mandibular
protraction should yield extra growth and some should
not. Clinical practice does not support this dichotomy,
and recently even Petrovic’s group’* has reported an
augmentation of mandibular growth by Class II elastics,
a modality of treatment that is generally thought not to
depend on the lateral pterygoid.
The distinction between the results of active versus
passive hyperpropulsion are no less blurred than the
classification itself. Although reports from the labora-
tories of both McNamara*’ and Petrovic*’ have empha-
sized the potential significance of a transitory increase
in lateral pterygoid activity following the insertion of
bite-jumping splints (thereby suggesting the need to
reactivate functional appliances to maintain a high level
of muscle traction on the head of the condyle), Mc-
Namara and Car1son24have recently noted:
The activity of the lateral pterygoid muscle per se may
not be necessaryto produce an adaptive responsein the tem-
poromandibular joint region. These ongoing experiments[*5]
indicate that the critical factor may be the alteration in the
biomechanical or biophysical environment of the joint pro-
duced by either muscular or nonmuscular (for example, in-
termaxillary traction) forces which initiates the adaptive re-
sponsein the temporomandibular region.
Indeed, Auf der Mau? has shown electromyo-
graphically that mandibular protrusion in a series of
activator patients “ . . . did not depend on the activity
of the lateral pterygoid muscle.” Thus, with respect to
Petrovic’s hyperpropulsion experiments, Auf der Maur
concluded:
If, however, the hyperpropulsor acts like the activator to
maintain the forward position of the mandible mechanically,
it would appearthat Petrovic’shypothesisconcerning the role
of the lateral pterygoid muscle should be reconsidered to
exclude the possibility that increasedmandibular growth rates
in activator groups are due to the passiveforward position of
the mandible maintained by the appliance.
188 Whetten and Johnston
In this context, it may be noted that Kantomaa and
Riinning18 have reported that 16 days of unilateral elec-
trical stimulation of the lateral pterygoid muscle pro-
duced a significant increase (0.4 mm) in mandibular
length. Their conclusions, however, were decidedly cir-
cumspect:
Although the present results appear to corroborate the
postulate that the lateral pterygoid muscle is a controlling
factor of mandibular growth, the findings from this and earlier
experiments could also be interpreted in a manner attributing
less significance to the lateral pterygoid muscle, since mere
anterior displacement of the condyle, by whatever means,
could possibly lead to the changesobserved.
To test the effect of changes in condylar position
relative to the glenoid fossa, Killiany and Johnston27-29
performed unilateral condylotomies in growing rats and
then reunited the condyle with the ramus to achieve
varying (and measurable) amounts of candylar distrac-
tion, compression, or rotation. On the basis of implant
measurements, they found not only that the amount
of condylar growth was a statistically significant (r =
- 0.6) function of prior surgical displacement but also
that the direction of condylar growth remained essen-
tially constant with respect to the head, regardless of
the direction and amount of surgical rotation. Woodside
and Altuna have recently reported a similar response
to condylar distraction produced by bite blocks, and
others have observed an increase in mandibular growth
following experimental posterior displacement of the
glenoid fossa.3’*32
Although a change in mandibular position is the one
obvious constant in those modalities of treatment that
are said to increase condylar growth, there remains the
problem of inferring a control mechanism. Because at-
tempts to invoke some sort of condylar version of the
“pressure/tension hypothesis” have at best only an in-
tuitive appeal, one is drawn to the Heuter-Volkmann
hypothesis as espoused by Moss? a decrease in com-
pressive loading increases condylar growth, whereas an
increase in loading produces decreased growth. Unfor-
tunately, this analysis begs the question of the nature
of the signal generated by altered compression.
Most contemporary hypotheses hold that the con-
dyle must in some way be told to grow. Accordingly,
it is implied that, in the absence of a positive control
signal, the condyle will at best fall back to some min-
imal “commanded” level of growth or even stop grow-
ing completely. The present study, however, fails to
support the contention that condylar growth is corre-
lated with lateral pterygoid traction, and, as has been
noted, the contention that condylar cartilage has no
intrinsic growth potential makes it difficult to see why
Am. .I. Orthod.
September 1985
a decrease in “compressive loadings” should lead to
“adaptive condylar growth.“’ In the absence of evi-
dence to the contrary, perhaps it may be useful to en-
tertain the possibility that the condyle must be told nor
to grow.
Recently, Copray and associates33have reported that
cultured rat condylar cartilage can exert a maximal
growth pressure of only 2.6 gm/mm*, as compared to
9.5 gm/mm’ for epiphyseal cartilage. A similar esti-
mate-l .5 gmlmm*--can be obtained from Yozwiak’s
data for spring-loaded, isolated guinea pig condyles in
vivo. ‘4,34Thus, if it is assumed that the condyle has an
intrinsic ability to grow, but not to generate the force
usually imputed to a growth center, then it can be in-
ferred that the condyle would have sufficient autonomy
to grow whenever it is not subjected to functional
compression. Accordingly, condylar growth would be
a function of the pattern of condylar loading.
It has been shown that the condyle is loaded during
mastication,35 and it has long been known that man-
dibular excursions produce measurable changes in the
usually subatmospheric synovial fluid pressure.36Given
that the ongoing pattern of mandibular “function” has
a physical impact on the joint, the present conjecture
suggests that the condyle constitutes a functional rec-
tifier, a “ratchet” whose ability to resist episodic
compression and then grow when unloaded would serve
to preserve the downward and forward portion of the
mandible’s envelope of motion. The present scheme,
however, does not deny a genetic component to man-
dibular growth: the condyle’s intrinsic rate of growth
while unloaded, as well as its ability to respond to
circulating levels of growth hormones, may well be
under genetic control and thus serve to explain familial
similarities in mandibular size.
Moreover, it would no longer be necessary to as-
sume that the various appliances currently used to aug-
ment condylar growth do so through some unspecified
effect of a change in the activity of the musculature.37.38
Anything that distracts the condyle would increase its
opportunity to grow. What, then, is the relationship
between condylar growth and that of the mandible as
a whole?
Mandibular growth
By the end of the present experimental period, the
condyles were fused to the ramus. Thus, because im-
plant translation was measured weekly, it was possible
to reconstruct the two-dimensional pattern of mandib-
ular growth, first in the absence of condyles and then
* following the re-establishment of bony continuity be-
tween segments.
vohme 88
Number 3
In marked contrast to the contention that “condy-
lectomized mandibles translate normally,“3g separation
of the mandible proper from its condyles produced a
marked (P < O.Ol), time-related upward and backward
collapse during the first 2 weeks, followed by a down-
ward and forward translation during the rest of the ex-
periment. If the amount of ramus collapse in weeks 1
and 2 is added to the vertical growth of the condyle
during this same period, it is apparent that the two
segments would have come together enough (0.6 to 1.O
mm) to obliterate the condylotomy channel (the di-
ameter of a No. 6 bur minus the thickness of the cap
of acrylic on the condylar stump), thereby initiating
bony union. Thus, normal mandibular translatory
growth appears to be linked in some way to the presence
of condyles. Indeed, a link between condylar and man-
dibular growth is supported by the present finding that
the posterior ramal implant (3) on the experimental side
showed a significant (P < 0.05) vertical deficit that was
identical to the: reduction (0.42 mm) seen in the trans-
lation of the corresponding condylar implant (2).
To a first approximation, whatever the motive force
initially responsible for downward and forward man-
dibular translation (the envelope of mandibular motion,
growth-regulating appliances, Class II elastics, but
probably not “push” from the condyle or expansion of
spaces), for a given amount of this translation to be
made permanent, it must be accompanied by an equal
amount of condylar growth. Thus, given any definition
of mandibular growth and size that includes the condyle
and at the same time excludes functional shifts (contrast
with Kantomaa3*), condylar growth would consti-
tute the rate-limiting factor in mandibular translatory
growth.
Interestingly, although the present data deny a
unique role for lateral pterygoid traction, our analysis
suggests that anything that unloads the condyle will
contribute to the ultimate growth of the mandible-if
the hormonal titer will support a response. Lateral pter-
ygoid traction is obviously one means by which the
pattern of loading could be changed; however, as sug-
gested by Kantomaa and R(inning,‘* other muscles (for
example, parts of the masseter, medial pterygoid, and
temporalis) might well be able to produce the same
degree of unloading and thus in a nonspecific way be
equally important, even interchangeable. Accordingly,
the common (and crucial) element in most contempo-
rary functional appliances (including the Herbst appli-
ance40‘42)may be not their ability to alter the pattern of
muscle activity but, rather, their capacity to produce a
significant, long-term change in condylar position and,
with it, the ongoing pattern of compressive loading.
Control of condylar growth 189
SUMMARY AND CONCLUSIONS
Petrovic’s cybernetic hypothesis for the control of
condylar (and mandibular) translatory growth was
tested experimentally in 21 male albino rats that had
undergone bilateral condylotomy and unilateral ptery-
goidectomy. Analysis of weekly cephalograms revealed
that the presence or absence of the lateral pterygoid
muscle had little effect on the growth of isolated con-
dyles or on the position of the mandible as a whole. In
contrast, mandibular growth was profoundly affected
by the condylotomies. The rami collapsed upward and
backward until they approached the condyles and began
the process of bony fusion (2 to 3 weeks), at which
time a normal downward and forward pattern of trans-
latory growth was re-established. Although it could not
be shown that lateral pterygoid traction per se is a sig-
nificant factor in the modulation of condylar growth, it
was concluded that the condyle is vitally important to
the translatory growth of the rest of the mandible. On
the basis of available data, a simple provisional hy-
pothesis was advanced for the regulation of condylar
growth and for its significance to the growth of the
mandible as a whole.
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Reprint requests to:
Dr. Lysle E. Johnston, Jr.
Department of Orthodontics
St. Louis University Medical Center
3556 Caroline
St. Louis, MO 63104