ORIGINAL RESEARCH ARTICLE
Collagen Metabolism Markers as a
Reflection of Bone and Soft Tissue
Turnover During the Menstrual Cycle
and Oral Contraceptive Use
U. Wreje,* J. Brynhildsen,† H. Åberg,* B. Bystro ¨ m,‡ M. Hammar,† and B. von Schoultz‡
Two different groups of women, 23 healthy young adults
and 13 women with chronic posterior pelvic pain, were
studied before and during use of oral contraceptives (OC).
Collagen metabolism markers— here, the amino-terminal
propeptide of type I procollagen, the carboxy-terminal
telopeptide of type I collagen, and the amino-terminal of
procollagen type III—as well as hormones and other endo-
crine factors indicating the balance between androgen
expression/anabolism and catabolism of the subjects (tes-
tosterone, sex-hormone binding globulin, and insulin-like
growth factor I were measured. Type I procollagen, the
carboxy-terminal telopeptide of type I collagen, and the
amino-terminal of procollagen type III were all signifi-
cantly decreased during OC use. These findings implicate
OC use-induced changes in collagen type I and III turn-
over. A shift in the anabolic/catabolic balance was also
recorded indicating a less anabolic situation during OC
use. CONTRACEPTION 2000;61:265–270 © 2000 Elsevier Sci-
ence Inc. All rights reserved.
KEY WORDS: bone metabolism, blood, collagen metabolism,
oral contraceptives, menstrual cycle, women
Introduction
C
ombined oral contraceptives (OC) have been
widely used by millions of women all over the
world for nearly 4 decades. In spite of this
length of time and widespread use, the effects of OC
use have not yet been thoroughly studied in all
physiological systems. Several investigators have
studied the effect of OCs on bone mineral density, but
the results are contradictory. OC use has been shown
to have both long-term beneficial effects
1–4
and no
effect
5–7
on bone mineral density in both the pre- and
postmenopausal period. At least some of these differ-
ent results might derive from the use of different OCs
during the different studies. In analogy with the
positive effect of estrogen replacement therapy on
bone mass in the post-menopausal period,
8
it has
been suggested that OC use confers protection against
osteoporosis during the later parts of reproductive
life.
9
The use of OCs has been recommended in
certain groups of women, such as oligomenorrhoic
female athletes at high risk for later development of
osteoporosis.
9
In a cross-sectional study, Garnero et al.
10
investi-
gated bone turnover among OC users and non-users.
After studying different collagen metabolites in urine
and serum and also bone density, they concluded that
bone turnover was decreased during OC use. Bone
density was not affected. In a British prospective
study, earlier OC users had a higher risk for fractures
than earlier non-users.
11
Muscular and skeletal problems are reported to
occur more often in OC users than in non-users.
12,13
If bone density is not adversely affected,
1–7
the expla-
nation of these findings should lie elsewhere, perhaps
in soft tissues such as ligaments and tendons.
The main constituent of connective tissue is colla-
gen, which appears in different forms. Type I collagen
accounts for more than 90 per cent of bone protein
contents, but type I is also found in loose connective
tissue together with other collagen types.
14,15
Colla-
gen type III is found in most dense and loose connec-
tive tissue in the body, especially bone marrow, the
liver, and the soft tissues.
16
Serum concentrations of
the amino-terminal propeptide of type I procollagen
(PINP) reflect bone collagen synthesis and correlate
well with bone formation rate.
17
The carboxytermi-
The study was financially supported by Stockholm County Council, Swedish
Medical Research Council, and for the Linkoping part, Swedish Sports Feder-
ation and Lions Health Research Foundation.
*Department of Clinical Sciences, Division of Family Medicine, Stockholm,
Karolinska Institute, Novum, S-14157 Huddinge, Sweden; †Department of
Health and Environment, Division of Obstetrics and Gynaecology, Faculty of
Health Sciences, Linkoping, Sweden; ‡Department of Women’s Health, Division
of Obstetrics and Gynaecology, Karolinska Institute, Stockholm, Sweden
Name and address for correspondence: Ullacarin Wreje, Department of
Clinical Sciences, Section of Family Medicine, Stockholm, Karolinska Institute,
Novum SP-14157 Huddinge, Sweden, +468-58585325; Fax +468-58585305
Submitted for publication October 19, 1999
Revised February 25, 2000
Accepted for publication February 25, 2000
© 2000 Elsevier Science Inc. All rights reserved. ISSN 0010-7824/00/$20.00
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