Beruflich Dokumente
Kultur Dokumente
BY PROF.
DEFORMANS DEFORMANS
F. J.
LANG, INNSBRUCK,
CONTRASTED JUVENILIS
AUSTRIA
WITH
*
Professor
of Pathology Institute
of the
Pathological-A
natonucal
of Innsbruck and
the disease. non-infectious, proliferative
The
arthritis changes
comparative
deformans present must. in the
of
based types
adult
upon this chronic
juvenile
types
and
of
osteo-
be two
anatomical
histological
Osteo-arthritis
deformans
that importance
deformans. the decisive arise
to presence
a deformity of marginal
marginal for t.he
of the as well
diagnosis
joint. as the
of
structures have
are this
1). of
and
development
exostoses
exostoses
always
anatomical
These
histological
characteristic disease ossification
(Fig. which,
2).
of vascularization
and
beginning calcified
This and follow ticity cartilage prise diagnostic the
in the cartilage.
vascularizat ossification the of first loss the and features
subchondral
ion
marrow
spaces,
invade
the
overlying
non-
of elasjoint comdefinite of
arthritis (Pommer)
These exostoses
ossified (\rolkmann),
ost.eal or
drial
and
(Kimnura,
proliferat.ions Richardson),
osteophytes
periosteal
they are (as
lippings Ziegler);
Pommer bone
FIG.1
maintains)
formations,
arising
*
that,
from the the College
Lecture).
lesions.
Arthritis
(Maccrated
deformans
specimen.)
of a hip
joint,
showing
characteristic
Read
Newbold
before
of Physicians 563
of Philadelphia,
November
4, 1931
) Mary
Scott
564
F.
J.
LANG
FIG.
Head section.
of the
femur
in art hritis
deformans
subchondra.l possess
marrow a laminated
t.issue, structure,
grow
out
into
the
joint
cartilage.
They
are
usually
covered
with
new
to
the
spongiosa
(Fig.
2),
and
,.\,%,,i.
FIG.
3 basal cartilage
and
of
ossification
of the
the
joint
cartilage.
(Hip
joint
of
of the man.)
OSTEO-ARTHRITIS
DEFORMANS
565
The
presents ations,
joint.
various chief
cartilage
alteramong
which
in ciated of stance alterations damage of These the the
are
consistency with (Fig. the
alterations
assoa splitting ground 3). disturb elasticity in cartilage. subThese and
ft
alterations
the
tural the
physical
normal first. sites of into those
and
strucof
most for
about the
comthese
the fovea
and
at
the
FIG
lying
of the
deep
hip
within
joint
to thus
the
vascularizat.ion
and
the
ossification of the
are mark
of the The
found site of
cartilage portions
to the lie deep original does
is the
within
underthe
mining
spongiosa
of the
separated and
deeper
by in this
portions
undermining position
cartilage.
often the
of cartilage
boundary not in take the any more
between
As part. by in newly
cartilage
previously the formation
and
bone
of the
(Figs.
the marginal
3 and
peniosteum
4).
in general exostoses. However,
mentioned,
advanced The
cases
of arthritis
deformans,
peniosteal
bone
proliferat
ions
covered
can l)e seen at the insertion of the tendons. may also be the site of proliferative changes.
in the cartilage surface layer zone compact. mechanical (Pommer). for its circumstances. cartilage is and dependent. anatomical and of the rarely of the The cartilage, take joint damage vascularization place. cartilage subchondral in Hence, development spite it The is very bone of cause broad, is thus the loss the and for
calcification is very
protected elasticity
is obvious upon
combination
F.
J.
LANG
worn
rise
covering bone
by and
wear. impaired
why
trauma side
is considered,
increased
is found
with
new the
bone
In
this
union
phenomena is found of the joints in arthritis more advanced cases bone resorptive of the and
along the junction tissue proliferations. splitting and cracking processes that make is so
between cartilage and This callus formation of the bone and of the the in striking picture the macerated
These and
reactive condensation
clear obvious
Microscopic cysts are likewise found in the exposed subchondral marrow spaces (Fig. 5). These cysts are either the result of encapsulation of hemorrhages or of areas of detritus. Thus is disproved the theory of Kimura and Ziegler that the cause of arthritis deformans lies in regressive changes in the subchondral bone (Pommer). In far advanced arthritis deformans, the so called cartilage in the marrow spaces of the surface. According to Pommer can originate tures, and, transported
where progressive atrophy, they
nodules are observed ; these are situated spongy bone beneath the polished joint and Lang (1924), the cartilage nodules as callus of joint capillaries local origin
occurs
along
the
With
of the
arthritis and
of the
it at can the
various
be same
deformans,
caused
by
inactivity,
other
polished distinction
changes
areas Considering
are
are between
taking
observed. the above the
place.
described atrophic
Thus,
not
findings
only
sclerotic
and their
but
also
atrophic
the the
explanations, or between
and
the
hypertrophic
and
the
types the
of
arthritis
deformans of arthritis
is not deformans
to Pommer
varieties
present no distinctive differences; they are but gradations of a process that is uniform as regards its origin. Naturally, in the explanation of these differences, individual variations must be considered. These variations have their origin in the anatomical structure, in the functional requirements, and in the effacement of the part by use (Lang, 1924). A distinction
deformans is also
between
unnecessary.
the
chondral
For, in the
and final
osseous analysis,
forms
of
arthritis damage
it is the
OSTEO-ARTHRITIS
DEFORMAXS
567
FIG.
Polished (Arthritis
articular deformans
with
cyst
of
joint
formation a fifty-three-year-old
.,
. --.4
FIG.
6 juvenilis. Note
56S
F.
J.
LANG
FIG.
Arthritis tion
deformans exostoses
juvenilis and
(Leggs mushrooming
disease)
of marginal
to for
as
the
cartilage
with
its
resultant
loss
of
elasticity
that
is
responsible
the In
to the
origin spite
nature
of the of the
disease numerous
origin,
(Lang,
arthritis
1931). and
deformans
anatomical
pathological
has more
investigations
recently been
of its
called,
Sis of
.
from The
as degenerative
points as
of vinw, arthrosis
to indicate
an
arthrois
to
be
any
avoi(led, a (legenerative
eSS.
changes proc-
indicates to the be
inflammatory designation
considered
is not inflamtype, process histological t.he
is preferable
however,
important
structure nevert.heless, of to keep
for
is the an
every
site affect inflammatory
inflammatory
of the the the
is absolutely
in mind
between processes
inflammatory
superfluous and
and
is of value
degenerative
since
processes.
inflammatory and 1931).
This
de-
frequently
side and,
.
by
side
Under justifiable
deformans
proliferative, only
t.herefore,
OSTEO-ARTHRITIS
DEFORMANS
the
causes
of
arthritis
that a direct relationship systemic diseases. But are that not the main are sometimes inflammation
to the
circulatory
in the advanced cases of arthritis deformans. Likewise, that under natural and non-experimental conditions the is due confirmation subchondral to
primary arthritis deformans Furthermore, there is no atrophic changes of the development The the cartilage,
marrow
necrotic changes of the cartilage. of the view that regressive and bone are of importance in the for arthritis the Following deformans presupposes subchondral
jarrings,
only
in joint its
pres-
functional
from
This protects
effects
theory
through
the
elasticity,
localized
of impacts,
sures
arising
from
normal
function.
damage
joint of
cartilage, with subsequent loss of its elasticity, the mechanical effects normal joint function become more or less localized and are transmitted unmodified to the joint structure resulting in a reactive vascularization and ossification The damage of the cartilage. to the joint strains, in tabes
-
cartilage
arises
: first,
from
unequally
diseases
diseases of the joint capsule, bone ; and, fourth, through (Lang, The joint 1931). recognition as the of the
the synovial membrane, endogenous metabolic and functional covering and mechanical of the
importance bone
cartilage
protective
subchondral
demands that the mechanical and functional damages to the joint cartilage be adjudged the most important. factor, not only for t.he pathogenesis, but also as the etiological factor of arthritis deformans. An especial confirmation for t.he functional theory of arthritis deformans is the fact that this disease is frequently found in certain for this statement is given in the literature.
occupations. Sufficient proof
R. Beneke
changes. in which traumatic
substantiated:
has pointed
sequelae
of old traumatic
I was able to confirm his idea I found evidences of the end changes (Lang, 1922, 1924).
that arthritis deformans
by my studies of juvenile joints, results of more or less extensive By these studies, this theory is
is already initiated in the early
the disease has to be considered over from childhood and adolescence. in early life are considered, it becomes oft-repeated of the adult functional traumata (Lang, 1931).
after
of chronic, deformans
570
F. J. LAN(;
FIG.
Fissure year-old
formation girl.
in the
cartilage
of the
I was
Ilfl(l SeCond
able
to investigate
disease bones,
the
of the and
juvenile
hip other joint,
form
so
of arthritis
K#{246}hlers disease called aseptic
deformans
of the necroses first
in
Perthes-Legg-Calv#{233}s metatarsal
(Lang, features
joint marginal In presents
1931).
deforinans vascularization (Figs. type typical changes, striking cartilage, epiphyseal the the with of
In
these
were and 7). arthritis
diseases
ossification
the
characteristic
changes of the occurs the
diagnostic
of the and zone of in the arthritis splintering adults. cartilage, epiphyseal
present,-namely:
6 and of those
ileformans in arthritis of ossification cases fissure (Fig. of 8). new juncture; The of bone, These cartilage
As a sequel portion
involved
deforand bone stimulate so charfissuraand
epiphyseal
mans
cartilage callus acteristic tions are in
formations,
fragmentation
the
juvenile
along parallel
splintering
are
part
found
of direction
an(l
angles
the size,
to the
position,
lines
of strains
and struewhether
(Fig.
ture tion
8. The
of of
behavior
the the epiphyseal vibrations
epiphyseal
bone determine impacts
and
whether jarrings
and or
distribu-
OSTEO-ARTHRITIS
DEFORMANS
571
.-sc
-
CI)
=
C
ct
bL bL
C,2
-C
CC
572 splintering
occur
F. J. LANG
and fragmentation with displacement of the fragments will 1931). More or less extensive hemorrhage with subsequent hemosiderin deposits and blood-cyst formation complete the picture of previous trauma. From my studies it is evident that functional traumata are delermin(Lang,
of
ing factors
effects
for the origin of juvenile this trauma are responsible deformans. following two cases of
first
patient
was
a normal
twenty-two-year-old
male
who
fell
from
a ladder,
thigh. After
subtrowith the
Two years
x-ray
later
examination
a pronounced
and a half limitation
at this
time
showing
complete
healing
of
the
fracture.
three
and
only
by postulating formations
equilibrium, were processes lined by
which, of pain and a mushroom-shaped femoral head damages to the joint cartilage andin the subchondral hone with a consedamages to continued areas which were, functional The final of osteitis of course,
visible because
After
of reconstruction.
characteristic
containing
hemorrhages
and
debris,
and
second patient was a fifteen-year-old boy who developed Perthes disease a gunshot wound of the soft parts about his right hip. Neither hone nor joint structures were involved. X-rays were taken immediately and at periods of nine and eleven months after the injury (Just). The first roentgenological examination failed to show any damage to bone or joint. In the examination made nine months after injury there existed well advanced changes in the femoral head characteristic of Legg-Perthes disease. These changes were more marked in the last x-ray. Here, as a result of a
relatively mild localized indirect trauma (as compared with the first case cited), there
developed
a characteristic
deformation
of the femoral
head.
from: direct.
of latent second,
Leggs
exceptional. When the disease is bilateral it is usually found that there existed a developmental malformation of both femoral epiphyses. It is well recognized that a developmental malformation of an epiphysis predisposes that structure to damage by relatively mild functional and actual The
formans
9). of trauma
lessened because
for
the
no
origin
history
of
juvenile
can
arthritis
dein severe
of injuries
be elicited.
giving
more (Fig.
changes
OSTEO-ARTHRITIS
DEFORMANS
573 or must by and until objective consider of this collapse some time that is of K#{252}mmell.
is a history of trauma without present immediately after the may lead be found of at the a later vertebrae not become date. atrophy but
example
to almost it does
complete
of a vertebra
of trauma,
be no doubt activity
damage to a joint, due lead to arthritis deformans conclusion, arthritis of the with functional
a causative
it is evident that there are no fundamental deformans of the adult and juvenile arthritis disease the and
agent
types protection
subsequent that
of its elasticity.
in adults,
excessive direct
and, especially, to the osteochondral The decisive factor for the progressive
deformans is the of constant
acting character
as a source
action of the functional requirements which, irritation, forms the basis for the progressive
of the disease.
REFERENCES
BEITZKE
H. : tber
215,
die Sogen.
1911-12.
Arthritis
Deformans
Atrophica.
Beitr. Arzte, Juvenilis
Ztschr.
z. Wiss.
f. KIm. Med.
vom Wiener
Med.,
LXXIV,
BENEKE,
R. : Zur Lehre von der Spondylitis Deformans. d. LXIX. Vers. Deutscher Naturforscher und Braunschweig, Staatsministerium, p. 109, 1897.
E.: Zur Aetiologie XLIV, der 889, und 225, Osteochondritis 1931. Untersuchungen Arthritis 591, Befunde 1900. bei Juveniler Coxae Wchnschr.,
Festschr.
Herzogl. Klin. Folgen, u. z.
JUST;
KIMURA,
Coxa
Allg. LANG,
#{252}berKnochenatrophie
Deren Anat.
Deformans.
Zieglers Arthritis
Path.,
f. Path.
XXVII,
F. J.:
Mikroskopische
Virchows Deformans.
Arch.
Virchows
Anat.
CCXXXIX, Anat.,
76, 1922.
Zur Kenntnis
Arch.
der Veranderungen
CCLII,
der HUftpfanne
578, 1924.
bei
Arthritis
f. Path.
Die
1931.
NIcHoLS, (New
Osteo-Arthritis
RICHARDSON,
Deformans.
F. L.: Arthritis 1909.
Befunde bei Krankheiten Pt. 2. Erlangen, Arthritis Klasse,
Wiener
Kim.
Wchnschr., J. Med.
Denkschr. 65, 1914.
XLIV, Research,
der Handhuch bei Arthritis 502,
861, XXI
Kaiser!. der De-
Deformans.
Deformans. LXXXIX, der 1865. der Bewegungsorgane.
149,
POMMER,
Akad.
Mikroskopische Verletzungen
Naturw.
VOLKMANN,
Allg.
ZIEGLER,
u.
E.:
Veranderungen
Knochen Anat.,
formans
und
#{252}ber Knochencysten.
Virchows
Arch.
f. Path.
LXX,
1877.