가토에서 골연골종 발생기전에 관한 실험적 연구

Abstract

[영문]

[한글]

골연골종은 성장중인 장관골에 호발하며 가장 흔한 양성골종양의 하나로 알려져 있다.

이 종양의 발생 기전에 대해 연골분리설, 혹은 골막의 연골화설 등이 있으며 최근에는 성

장판 주위의 골막환 및 골막의 손상에 의해 발생된다는 학설이 지지를 받고 있다.

저자는 골연골종 발생기전을 구명하기 위하여 가토의 경골근위부 혹은 경골간부에 0.7

×O.7cm의 골막절제를 가한 실험적 연구를 통하여 다음과 같은 곁론을 얻었다.

1. 유약가토 경골근위 골간단부 골막절제군 20예중 13예에서 연골모를 갖춘 골연골종이

발생함을 관찰하였다. 13예외 골연골종은 2주에서 8주 사이에 발생하였으며 4주에서 8주

사이에 발생한 예가 다수로 12예였다.

골연골종의 성장방향은 경골종축에 대하여 50도에서 70도의 각도로 경골원위부를 향하

여 성장하고 있었다.

2. 성숙가토 경골근위 골간단부 골막절제군과 유약가토와 성숙가토의 경골간부 골막절

제군에서는 골연골종이 발생되지 않았다.

3. 골막에 손상을 가하지 않은 대조군에서는 골연골종을 관찰할 수 없었다.

이상의 결과로 미루어 보아 골연골종의 발생기전은 성장기 장관골의 골간단부에 골막손

상이 있는 경우 골막손상에 의한 골막의 횡적 성장 조절능력의 지속적인 감퇴와 이차적으

로 Ranvier씨 groove내에 존재하고 있는 연골전구세포의 비정상적인 증식의 결과로 사료

된다.

Experimental Study on Induction of Ost-eochondromas in Rabbits

Sung Kwan Hwang

Department of Medical Science The Graduate School, Yonsei University

(Directed by Professor Byeong Mun Park, M.D.)

Osteochondroma is the moat common type of benign bone tumor. It is composed of

spongy bone covered bur a cartilaginous cap. These bony growths are classified in

most texts as neoplasms of cartilaginous origin, but their etiology remains

unknown.

Virchow(1891) long ago suggested that a portion of the growth plate cartilage,

for reasons unknown, becomes separated from the patent tissue, leading to tee

formation of an osteochondroma. Muller(1913) once thought that the cambium layer of

the periosteum formed small cartilage nodules, which gave rise to the

osteochondroma. Milgram(1983) has more recently postulated that osteochondromas are

derived from aberrant cartilaginous epiphyseal growth plate tissue, which

proliferates autonomously and separates from the normal growth plate near its edge

and he could find no evidence that osteochondromas are the result of cartilagenous

metaplasia.

However, the "Periosteal-ring-defect" theory of Keith(1920) has been widely

accepted by many researchers for many years. According to thin the disease was due

to defective modeling of the bone, with an absence of a periosteal ring around the

growth plate. Ogden(1976) somewhat more recently baa demonstrated in a pathologic

specimen of multiple osteochondromatoais that the periosteal ring wart absent

around the affected portions of the epiphyseal plate and mentioned the importance

of periosteal defect. Jaffe(1943) earlier, had found that net only the periosteal

defect but the conversion of periosteum were responsible for the formation of

osteochondromas. Geschickter and Copeland(1949) had stated that focal accumulations

of embryonic connective tissue are situated at the points of tendinous attachments.

With the physical stress at these sites, conversion to osteochondroma formation was

possible. However, it is hard to find statistical significance between tendinous

attachments and osteochondromas.

Sousa and Dupertuis(1936) had pointed out that the origin of osteochondromas is

based on failure of remodeling, But this theory has failed to explain the

cartilaginous cap. Van Winkle and Mazur(1983) have, comparatively recently,

reported an iatrogenic osteochondroma in a 10-month-old child treated surgically

for osteomyelitls of the distal femur and concluded that a defect in the growth

plate or the adjacent groove of Ranvier, whether it is congenital or caused by

mechanical disruption, is probably responsible for initiating the growth of

osteochondromas. Ranvier(1873) very early described a circumferential notch at the

periphery of the growth plate, which he called the ossification notch. This area

has become known as the groove of Ranvier. Shapiro et al. (1977) have studied the

groove of Ranvier in rabbits and described three groups of cells within the groove.

A fibrous outer lurer, continuous with the periosteum of the metaphysis and

diaphysis, forms a roof over the groove plate. A group of densely packed cells

occupy the innermost portion of the groove and function as osteoblast progenitors.

A third group, between the densely packed cells and the fibrous layer, the function

of which is to increase the transverse diameter of the epiphysis anti probably the

growth plates by proliferation of cartilage progenitors.

Since the days of Virchow(1891) many articles have been published, and several

theories regarding their pathogenesis have been presented but very little

experimental work has been done in an effort to lest them.

The purpose of this experimental study was to investigate the mechanism of growth

of osteochondromas and to verify the periosteal role of the periosteum in

controlling the circumferential growth of the metaphyseal region of the growing

long bone.

Eighty healthy rabbits were used for the experiment, forty of them were young and

the remaining forty were adult animals. The animals with an equal number of young

and adult rabbits in each, were divided equally into four experimental groups which

were classified as group 1, proximal tibial metaphysis of immature rabbits; group

2, mid-tibial diaphysis of immature rabbits; group 3, proximal tibial metaphysis of

mature rabbits; and group 4, mid-tibial diaphysis of mature rabbits.

Seven-tenths by 0.7 cm of periosteal flaps were excised from the right tibias in

each group and the periosteums were left intact over the left tibias of the control

group. The animals which showed evidence of tumor growth in roentgenograms were

sacrificed at 8 weeks after surgery. Each tibia was then removed and inspected

grossly for evidence of growth. When there was any evidence of a growing mass on

cross observation, the bone was decalcified, sectioned, and stained for microscopic

examination.

The results of the experiment are as follows:

1. In 13 of the 20 animals of group 1 covered by a cartilage cap, occurred at the

site of periosteal resection between 2 and 8 reeks. In Roentgenograms they showed

bony growth toward the distal tibia at angles between 50 and 70 degrees of the long

atria of the tibia.

2. There was no evidence of tumor growth in any of the animals of group 2, 3, or

4.

3. There was no evidence of tumor growth in the control group.

In conclusion, it seems that the occurrence of osteochondroma at the metaphyseal

region of growing long bony, where the periosteal defects were made, is due

primarily to a decrease in the power of periosteum to control the circumferential

growth of metaphysis and, secondarily to an abnormal porliferation of cartilage

progenitors located in Ranvier'a groove.