Page 851 - Textbook of Pathology, 6th Edition

4. Hyperparathyroidism—Leading to osteitis fibrosa 6. Hyperparathyroidism. 835
cystica (page 816). 7. Deficiency of vitamin D.
5. Pituitary dysfunctions—Hyperpituitarism causing 8. Local factors—which may stimulate osteoclastic resorption
gigantism and acromegaly and hypopituitarism resulting in or slow osteoblastic bone formation.
dwarfism (page 793). Secondary osteoporosis is attributed to a number of
6. Thyroid dysfunctions—Hyperthyroidism causing factors and conditions (e.g. immobilisation, chronic anaemia,
osteoporosis and hypothyroidism leading to cretinism (page acromegaly, hepatic disease, hyperparathyroidism,
802). hypogonadism, thyrotoxicosis and starvation), or as an effect
7. Renal osteodystrophy—Occurring in chronic renal of medication (e.g. hypercortisonism, administration of
failure and resulting in features of osteitis fibrosa cystica, anticonvulsant drugs and large dose of heparin).
osteomalacia and areas of osteosclerosis. MORPHOLOGIC FEATURES. Except disuse or immobi-
8. Skeletal fluorosis—Occurring due to excess of sodium lisation osteoporosis which is localised to the affected limb,
fluoride content in the soil and water in an area. other forms of osteoporosis have systemic skeletal
Many of the conditions listed above have been discussed distribution. Most commonly encountered osteoporotic
in respective chapters already; others are considered below. fractures are: vertebral crush fracture, femoral neck
fracture and wrist fracture. There is enlargement of the
Osteoporosis medullary cavity and thinning of the cortex.
Histologically, osteoporosis may be active or inactive
Osteoporosis or osteopenia is a common clinical syndrome type.
involving multiple bones in which there is quantitative
reduction of bone tissue mass but the bone tissue mass is Active osteoporosis is characterised by increased bone
otherwise normal. This reduction in bone mass results in resorption and formation i.e. accelerated turnover. There is
fragile skeleton which is associated with increased risk of increase in the number of osteoclasts with increased
fractures and consequent pain and deformity. The condition resorptive surface as well as increased quantity of osteoid
is particularly common in elderly people and more frequent with increased osteoblastic surfaces. The width of osteoid
in postmenopausal women. The condition may remain seams is normal. CHAPTER 28
asymptomatic or may cause only backache. However, more Inactive osteoporosis has the features of minimal bone
extensive involvement is associated with fractures, formation and reduced resorptive activity i.e. reduced
particularly of distal radius, femoral neck and vertebral turnover. Histological changes of inactive osteoporosis
bodies. Osteoporosis may be difficult to distinguish radio- include decreased number of osteoclasts with decreased
logically from other osteopenias such as osteomalacia, resorptive surfaces, and normal or reduced amount of
osteogenesis imperfecta, osteitis fibrosa of hyperpara- osteoid with decreased osteoblastic surface. The width of
thyroidism, renal osteodystrophy and multiple myeloma. osteoid seams is usually reduced or may be normal.
Radiologic evidence becomes apparent only after more than
30% of bone mass has been lost. Levels of serum calcium, Osteitis Fibrosa Cystica
inorganic phosphorus and alkaline phosphatase are usually
within normal limits. Hyperparathyroidism of primary or secondary type results The Musculoskeletal System
in oversecretion of parathyroid hormone which causes
PATHOGENESIS. Osteoporosis is conventionally classified increased osteoclastic resorption of the bone. General aspects
into 2 major groups: primary and secondary. of hyperparathyroidism are discussed on page 816. Here,
Primary osteoporosis results primarily from osteopenia skeletal manifestations of hyperparathyroidism are
without an underlying disease or medication. Primary considered. Severe and prolonged hyperparathyroidism
osteoporosis is further subdivided into 2 types: idiopathic type results in osteitis fibrosa cystica. The lesion is generally
found in the young and juveniles and is less frequent, and induced as a manifestation of primary hyperparathyroidism,
involutional type seen in postmenopausal women and aging and less frequently, as a result of secondary hyperpara-
individuals and is more common. The exact mechanism of thyroidism such as in chronic renal failure (renal
primary osteoporosis is not known but there is a suggestion osteodystrophy).
that it is the result of an excessive osteoclastic resorption and The clinical manifestations of bone disease in hyper-
slow bone formation. A number of risk factors have been parathyroidism are its susceptibility to fracture, skeletal
attributed to cause this imbalance between bone resorption deformities, joint pains and dysfunctions as a result of deran-
and bone formation. These include the following: ged weight bearing. The bony changes may disappear after
1. Genetic factors—more marked in whites and Asians than cure of primary hyperparathyroidism such as removal of
blacks. functioning adenoma. The chief biochemical abnormality of
2. Sex—more frequent in females than in males. excessive parathyroid hormone is hypercalcaemia,
3. Reduced physical activity—as in old age. hypophosphataemia and hypercalciuria.
4. Deficiency of sex hormones—oestrogen deficiency in women MORPHOLOGIC FEATURES. The bone lesions of
as in postmenopausal osteoporosis and androgen deficiency primary hyperparathyroidism affect the long bones more
in men.
severely and may range from minor degree of generalised
5. Combined deficiency of calcitonin and oestrogen.