Page 142 - Color Atlas Of Pathophysiology (S Silbernagl Et Al, Thieme 2000)

Pathophysiology of Bone
Bone consists of connective tissue or bone ma- However, most often the cause remains un-
trix (sulfate-containing proteoglycans, glyco- known (primary osteoporosis).
proteins and hydroxyproline-containing col- Effects of osteoporosis include skeletal pain
lagen fibers) and the bone minerals (alkaline even at rest, intervertebral disc prolapse, lower
2–
2+
2+
+
salts of Ca , phosphate, Na , CO 3 , Mg , K , + arm or femoral neck fractures. Hypercalcemia
–
and F ). may be present in extreme cases. Depending
Construction and mineralization. Formation on its cause, the osteoporosis may be localized
of the bone matrix is promoted, among others, (e.g., under a rigid cast) or generalized (e.g.,
Kidney, Salt and Water Balance It is probably initiated through splitting of py- growth plate is disturbed (→ A5). Before longi-
due to excess glucocorticoids).
by insulin and inhibited by glucocorticoids.
In osteomalacia and rickets the mineraliza-
Bone mineralization is inhibited by pyro-
tion of the bone matrix (osteoid) or of the
phosphate (two esterified phosphoric acids).
rophosphate by alkaline phosphatase. The plas-
tudinal growth is concluded and before epiph-
ma concentration of this enzyme, produced by
yseal fusion has occurred, the abnormality
osteoblasts, is a measure of osteoblast activity.
mostly leads to rickets (widening of the growth
plates and distorted growth). After longitudi-
The mineralization is fostered by increase of
2+
nal growth has ceased the decreased minerali-
and phosphate plasma concentration—an
Ca
occurs
the course of normal bone remodeling), leads
in
(1,25-[OH] 2 -D 3 )
steps
several
(→ A1): under the influence of ultraviolet light
to osteomalacia. Both rickets and osteomalacia
vitamin D 3 is formed in the skin from 7-dehy-
can be caused by a reduced formation of calci-
5 effect of calcitriol. The formation of calcitriol zation of the newly formed osteoid (formed in
drocholesterol. Vitamin D 3 is converted in the triol, for example, in lack of ultraviolet light
liver to 25-OH 2 -D 3 under the influence of es- and of vitamin D, by estrogen deficiency (post-
trogens, and in the kidney to 1,25-(OH) 2 -D 3 un- menopausal), or by renal failure (→ p.110ff.).
der the influence of PTH. The building up of Even without calcitriol deficiency, hypophos-
bone and mineralization are additionally stim- phatemia (phosphate diabetes, Fanconi’s syn-
ulated by mechanical use of the bone. drome; → p. 96, 110ff.) or chronic renal tubular
The breaking down of the bone matrix leads acidosis can result in osteomalacia. Osteoma-
to the increased renal excretion of hydroxypro- lacia can occur in dialyzed patients who suffer
line (→ A2), while demineralization leads to from aluminum intoxication. Lastly, a rickets-
increased renal excretion of Ca 2+ and phos- like or osteomalacia-like clinical syndrome oc-
phate (urolithiasis; → A3). curs in the rare, genetic deficiency of alkaline
The breakdown of bone is, among other fac- phosphatase (hypophosphatasia).
tors, due to lacking mechanical stress (immo- The effects of rickets are retarded growth,
bilization). Localized breakdown of bone can bow-legs or knock-knees, vertebral column
be caused by osteoclast activating factor deformities, prominence of the costochondral
(OAF), which in tumors results in demineral- junctions (rachitic rosary) as well as thin and
ization of bone. soft cranial, particularly occipital, bones (cra-
The most important abnormalities of bone niotabes). Osteomalacia leads to bone pain
are osteopenia (or osteoporosis) and osteoma- (pain on movement), translucent bands of de-
lacia (or rickets in children). Osteopenia is de- mineralization in bone (pseudofractures or
fined as reduction of bone mass below the Looser’s zones), and muscular weakness (Ca 2+
norm for age, race, and sex, caused by prolong- deficiency).
ed imbalance between buildup and break-
down of bone. Osteoporosis is defined as the
clinical state resulting from reduced bone
mass (→ A4). Causes include excess glucocor-
ticoids, lack of estrogen (postmenopausal), in-
132 sulin deficiency (diabetes mellitus), and inac-
tivity (rigid cast, tetraplegia, microgravity).
Silbernagl/Lang, Color Atlas of Pathophysiology © 2000 Thieme
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