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At least 55 records · Page 3Linked to original sources
PubMed1992

Bone metastases and tumor-induced hypercalcemia.

Tumor-induced hypercalcemia and tumor-induced osteolysis are essentially due to a marked increase in osteoclast-mediated bone resorption, although the kidneys play an important contributory role in the genesis of tumor-induced hypercalcemia. Parathyroid hormone-like protein plays an essential role in tumor-induced hypercalcemia, and maybe in tumor-induced osteolysis, but other factors could also be responsible for the osteoclast activation secondary to the neoplastic infiltration of the skeleton. Treatment of tumor-induced hypercalcemia essentially consists of volume repletion and administration of potent anti-osteolytic drugs. The bisphosphonate pamidronate is particularly useful for that matter and a dose of 1.0 to 1.5 mg/kg can normalize serum calcium in about 90% of hypercalcemic cancer patients. The apparently low response rate of bone metastases to systemic antineoplastic therapy seems to essentially reflect the relative insensitivity of our current methods for assessing response in tumor-induced osteolysis. Newly developed biochemical markers of bone turnover could be particularly useful for that matter. Bisphosphonates are the most potent of the available inhibitors of osteoclast activity. Prolonged administration of oral pamidronate could reduce by almost one half the complications of tumor-induced osteolysis, and repeated bisphosphonate infusions could induce a dramatic relief of bone pain in one third and a sclerosis of lytic lesions in one fourth of the cases. These data must, however, be confirmed in randomized, blinded trials and many questions remain unanswered concerning the optimal therapeutic schemes. Medical therapy of tumor-induced osteolysis by noncytotoxic means has nevertheless become a reality.

Antineoplastic Agents↗
PubMed1997

[Bone metastases: pathogenesis and treatment with diphosphonates].

Tumor-induced osteolysis is essentially mediated by the osteoclasts whose number and activity appear to be stimulated under the influence of tumor secretory products. In cases of hypercalcemia, there is also a variable inhibition of the bone formation rate leading to a characteristic "uncoupling" in bone turnover. An analog of parathyroid hormone--"parathyroid hormone-related protein (PTHrP)"--plays an essential role in the pathogenesis of neoplastic hypercalcemia. PTHrP concentrations are not regulated by calcium levels which is in marked contrast for PTH. We have also shown that osteoblasts could be essential target cells in the process of tumor-induced osteolysis leading to an increase in osteoclast function and number. From a therapeutic point of view, we have contributed to the optimalization of the therapeutic schemes for tumor-induced hypercalcemia and tumor-induced osteolysis for which the dose of 90 mg of pamidronate appears to be optimal.

Antineoplastic Agents↗
PubMed1996

Syringohydromyelia in Hajdu-Cheney syndrome.

We report the case of a 10-year-old boy with typical manifestation of Hajdu-Cheney syndrome. MRI demonstrated syringohydromyelia involving almost the entire spinal cord, although neurological symptoms had not yet developed. Syringohydromyelia is considered to be a sequel to progressive basilar invagination and is one of the essential features of this rare osteolytic bone dysplasia.

Brain Diseases↗
PubMed1999

[Physiopathology of tumor-induced osteolysis].

Osteolysis, the most common expression of bone tumor, can cause pain, pathological fracture, epidural spinal cord compression and hypercalcemia. Multinucleated osteoclast-like cells, the main agents in bone resorption, are numerous in benign giant cell tumor of bone and can be recruited and activated by various carcinoma cell lines in vitro in animal models. Polykarion macrophages are also able to resorb bone matrix in a favourable tumoral environment. Direct bone resorption by tumor cells has recently been described in vitro and in vivo in animals. The presence of diffusible substances such as hormones, cytokines and growth factors creates a favourable microenvironment for stimulation of osteoclast-like cells and polykarion macrophages functional ability to resorb bone matrix. These mediators act within a complex but still unelucidated network involving high cell production (tumor cells, normal and reactional stroma as well as hematopoietic cells) and many targets (tumor production (tumor cells, normal and reactional stroma as well as hematopoietic cells) and many targets (tumor cells, monocyte/macrophage lineage cells, and osteoclast-like cells). The presence in the same environment of all these stimulating factors for tumor cell growth and resorbing ability could explain the vicious circle of tumoral and osteolytic progression. A better understanding of the complex mechanism of tumor induced osteolysis is essential for improving the conventional surgical approach to this pathology.

Animals↗
PubMed1991

[Essential bone cysts of the jaw. Apropos of an unusual care].

After reviewing the literature, the authors present an unusual case of essential bone lacunae. These lesions involve part of the upper maxillary and the entire horizontal branch of the mandible. The diagnosis was confirmed by surgical exploration and histological studies. During the following 8 years, surgical curetting was performed three times, without producing a bony cicatrisation of the cavities.

Adult↗
PubMed1992

Metastatic bone disease: clinical and therapeutic aspects.

Breast and prostate carcinomas are the tumors most commonly associated with skeletal metastases, and the skeleton is the most common site of metastatic disease and of first distant relapse in breast cancer. Bone metastases are the source of considerable morbidity, including pain and functional disability, fractures, hypercalcemia, and epidural compression. The classical radionuclide bone scan remains the most effective tool for the screening of metastatic bone disease, but X-rays are more specific and remain the essential tool for the diagnosis and characterization of bone metastases. Computed tomography is much more useful to diagnose early metastatic involvement of bone, particularly of the spine. Patients with exclusive skeletal metastatic involvement are still frequently excluded from classical therapeutic trials because of the difficulties in the assessment of response. Recalcification of osteolytic lesions is indeed required when defining an objective response, but this criterion is insensitive and not quantitative. Moreover, the development of new osteoblastic lesions is often of difficult interpretation. A concomitant bone scan will help, but the absence of quantification of the changes and the "flare" phenomenon limit the usefulness of the technique. Pain and quality of life constitute simple, but frequently neglected, parameters of response to therapy. The clinical utility of tumor markers and of biochemical markers of bone turnover should also be more fully investigated. Neoplastic osteolysis is essentially mediated by the osteoclasts, which seem to be activated, maybe indirectly through the osteoblasts, by some tumor products. Various substances of tumoral origin have been proposed as mediators for this osteoclast activation, such as transforming growth factors, prostaglandins, and, more recently, products of the immune cells or parathyroid hormone-related peptide.(ABSTRACT TRUNCATED AT 250 WORDS)

Bone Neoplasms↗
PubMed2003

Gorham Stout syndrome (disappearing bone disease): two additional case reports and a review of the literature.

Gorham-Stout syndrome, or disappearing bone disease, is characterized by the proliferation of thin-walled vascular channels associated with regional osteolysis. There have been fewer than 150 cases reported in the literature. In this clinical report, we describe 2 additional cases of Gorham-Stout syndrome affecting the maxillofacial skeleton. We provide a review of the clinical diagnosis of this syndrome and describe treatment options.

Biopsy↗
PubMed1998

Further evidence that the Hajdu-Cheney syndrome and the "serpentine fibula-polycystic kidney syndrome" are a single entity.

The Hajdu-Cheney syndrome (HCS) is a rare autosomal dominant disorder. It comprises a coarse face, short neck, hirsutism, joint laxity, and normal intelligence. Bone dysplasias, include acro-osteolysis, bathrocephaly, and vertebral anomalies. In 1988, Exner [1988: Eur J Pediatr 147:544-546] coined the term "serpentine fibula-polycystic kidney syndrome" (SFPKS) when he reported on a girl with short stature, unusual facial appearance, polycystic kidneys, and elongated curved fibulae. He postulated that it was a new entity different from the Melnick-Needles syndrome. Since his report, five similar cases have been published. Similarities between both HCS and SFPKS were noticed first by us and then by other authors. In this report we show that many clinical and radiological characteristics are shared by the HCS and the SFPKS and hypothesize that they represent a single entity with a variable degree of expression.

Abnormalities, Multiple↗