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At least 595 records · Page 33Linked to original sources
PubMed2006

Fluorotoxic metabolic bone disease: an osteo-renal syndrome caused by excess fluoride ingestion in the tropics.

BACKGROUND: There is scant data available on the pathogenetic mechanisms of varied clinical presentation of bone disease in patients with excess fluoride ingestion in the Indian subcontinent. The present study is comprehensive and state of the art, incorporating all essential elements of bone mineral metabolism in patients with excess fluoride ingestion. METHODS: We studied 24 patients (age 31 +/- 16 years) with fluorotoxic metabolic bone disease (FMBD) for their clinical, radiological and biochemical parameters like serum calcium, phosphorous, alkaline phosphatase (SAP), 25-hydroxyvitamin D, 1,25 dihydroxyvitamin D, and parathyroid hormone levels, nephrologic parameters that assess renal handling of calcium and phosphorous and skeletal dynamics as revealed by bone histomorphometry. FINDINGS: Major clinical manifestations were bone pain (79%), Tetany (12.5%) and dental mottling (38%). Radiological findings included osteosclerosis (96%), pseudofracture and ligamentous calcification (50%). These patients manifested hypocalcemia and raised SAP with normal serum phosphorus. There was a positive correlation between serum creatinine and phosphorous excretion index (PEI) and a negative correlation between declining endogenous creatinine clearance (Cr.Cl) and increasing renal loss of calcium and phosphorus as indicated by increased calcium to creatinine ratio and PEI. Bone histomorphometry revealed impairment of primary mineralization with hypomineralized lacunae, interstitial mineralization defects and very thick and extended osteoid seams. Autopsy findings in a patient who died of azotemia showed tubular atrophy with secondary glomerular changes. INTERPRETATION: Fluoride intoxication plays an important role in the pathogenesis of the unique osteo-renal syndrome.

Adolescent↗
PubMed2006

Osteopetrosis complicated by osteomyelitis of the mandible: a case report including characterization of the osteopetrotic bone.

A case of a 53-year-old Japanese man with osteopetrosis complicated by osteomyelitis of the mandible is presented. The patient experienced frequent exacerbations and remissions of osteomyelitis of the mandible, despite undergoing several surgical debridements and sequesterectomies with appropriate antimicrobial therapy, for 3 years. Finally, the patient underwent mandibular segmental resection followed by reconstruction with a titanium reconstruction plate. Fifty-one months after surgery there is no evidence of recurrent osteomyelitis of the mandible, suggesting that a more radical surgical approach is preferable for patients with severe complications resulting from osteopetrosis. Also presented here are the histopathological and biochemical features of the osteopetrotic bone. The osteopetrotic cortical bone was morbidly sclerotic with compact and irregular laminations. Degradation of osteocytes in the osteopetrotic bone was due to hypoxia and lack of nutrition resulting from osteosclerosis. There were no significant differences between osteopetrotic and normal bone according to X-ray diffraction, Fourier transform infrared spectroscopy, collagen content or mineral content. Micro-Vickers hardness measurements showed that osteopetrotic bone was significantly harder than normal bone, and the standard deviation of hardness was greater in osteopetrotic bone. Such a loss of integrity in osteopetrotic bone is considered to be a primary reason for the greater risk of a variety of complications such as pathological fracture and refractory osteomyelitis.

Bone Plates↗
PubMed2006

Rheumatologic manifestations of chronic hepatitis C infection.

The many rheumatologic manifestations associated with chronic hepatitis C virus (HCV) infection include arthralgia, myalgia, arthritis, vasculitis, and sicca syndrome. Arthralgia is the most common extrahepatic manifestation and may indicate mixed cryoglobulinemia or an adverse reaction to interferon therapy. HCV arthritis unrelated to cryoglobulinemia is far less common but constitutes an independent entity. The picture may mimic rheumatoid arthritis (RA), particularly as rheumatoid factor is present in 50-80% of cases. Tests are usually negative for antibodies to cyclic citrullinated peptides (anti-CCP), which may help to differentiate the two conditions. The management of HCV arthritis is empirical and poorly standardized. Although low-dose glucocorticoid therapy, hydroxychloroquine, and methotrexate have been used successfully in several patients, little is known about their hepatic safety profile. Arthritis associated with cryoglobulinemia usually responds to antiviral treatment. Sicca syndrome is common in patients with chronic HCV infection and shares similarities with primary Sjögren syndrome, suggesting that HCV infection may deserve to be included among the causes of secondary Sjögren syndrome. HCV-associated vasculitis is usually related to cryoglobulinemia, although a few cases of polyarteritis nodosa-like disease affecting the medium-sized vessels have been reported. Other conditions reported in patients with chronic HCV infection include fibromyalgia, systemic lupus erythematosus (SLE), antiphospholipid syndrome, and osteosclerosis.

Autoimmune Diseases↗
PubMed2026

Cerebrovascular involvement in Erdheim-Chester disease: a case report and systematic literature review.

BACKGROUND: Intracranial perivascular/vascular infiltrations and stenoses related to Erdheim-Chester disease (ECD), often associated with ischemic events, are rarely documented. This study aims to characterize intracranial perivascular/vascular infiltrations and stenoses. METHODS: We first report a new case of strokes revealing ECD with intracranial arterial involvement. We then searched all English- and French-language publications from database inception to November 2025 across 12 different search interfaces, including grey literature sources. Vascular involvement was defined by the presence of intracranial perivascular/vascular infiltrations and stenosis on imaging and/or histopathological evidence of small-vessel involvement. Cases with intracranial nodules or masses abutting vessels but without clear longitudinal perivascular infiltration were excluded. RESULTS: We present a case of recurrent strokes with intracranial vertebral and basilar artery wall stenosis, and aortitis. Initially diagnosed as giant cell arteritis, the patient was treated with corticosteroids, cyclophosphamide followed by methotrexate, but relapsed. The identification of tibial osteosclerosis led to the diagnosis of ECD, with a favorable response to anakinra. Twelve relevant articles were retrieved, in addition to our own case. Most patients exhibited focal cerebrovascular signs (11/13) and associated parenchymal involvement (11/13). Intracranial perivascular/vascular infiltrations and stenoses involved the carotid arteries (7/13), the vertebrobasilar arteries (1/13), or both territories (4/13). Aorta was involved in 8/12 cases. Among the nine patients with available follow-up data, five had poor overall or neurovascular outcomes. CONCLUSIONS: Intracranial perivascular/vascular infiltrations and stenoses, which leads to recurrent focal ischemic events, represents a likely underdiagnosed CNS pattern in ECD, referred to as "cerebrovascular ECD", which worsens overall prognosis. Vascular imaging should be included in brain MRI protocols for patients with ECD, given the overlap with parenchymal involvement.

Humans↗
PubMed1999

Deficiency of SHP-1 protein-tyrosine phosphatase activity results in heightened osteoclast function and decreased bone density.

Mice homozygous for the motheaten (Hcphme) or viable motheaten (Hcphme-v) mutations are deficient in functional SHP-1 protein-tyrosine phosphatase and show severe defects in hematopoiesis. Comparison of femurs from mev/mev mice revealed significant decreases in bone mineral density (0.33 +/- 0.03 mg/mm3 for mev/mevversus 0.41 +/- 0.01 mg/mm3 for controls) and mineral content (1.97 +/- 0.36 mg for mev/mevversus 10.64 +/- 0.67 for controls) compared with littermate controls. Viable motheaten mice also showed reduced amounts of trabecular bone and decreased cortical thickness. These bone abnormalities were associated with a 14% increase in numbers of multinucleated osteoclasts and an increase in osteoclast resorption activity. In co-cultures of normal osteoblasts with mutant or control bone marrow cells, numbers of osteoclasts developing from mutant mice were increased compared with littermate control mice. Although mev/mev osteoclasts develop in the absence of colony-stimulating factor (CSF)-1, nevertheless cultured osteoclasts show increased size in the presence of CSF-1. CSF-1-deficient osteopetrosis (op/op) mutant mice develop severe osteosclerosis. However, doubly homozygous mev/mevop/op mice show an expansion of bone marrow cavities and reduced trabecular bone mass compared with op/op mice. Western blot analysis showed that several proteins that were markedly hyperphosphorylated on tyrosine residues were detected in the motheaten osteoclasts, including a novel 126-kd phosphotyrosine protein. The marked hyperphosphorylation of a 126-kd protein in motheaten osteoclasts suggests that this protein depends on SHP-1 for dephosphorylation. These findings demonstrate that the decreased SHP-1 catalytic activity in me/me and mev/mev mice results in an increased population of activated osteoclasts and consequent reduction in bone density.

Animals↗
PubMed1999

Hyperthermic isolated regional perfusion for the treatment of osteosarcoma in the lower extremity.

BACKGROUND: In order to reduce the systemic toxity of cisplatin and to increase the effect on the local tumor, facilitating limb-preserving procedures, we have been using hyperthermic isolated regional perfusion (HIRP) for the treatment of osteosarcoma in addition to preoperative chemotherapy. MATERIALS AND METHODS: Twenty patients with an osteosarcoma in a lower extremity were treated with both preoperative chemotherapy and HIRP. RESULTS: The chemotherapeutic effects of preoperative chemotherapy with HIRP was grade III in 6, and grade IV (no viable cell areas observed) in 7. The surgical margins could be reduced in these 13 cases of good responders showing over 90% necrosis (grade III or grade IV), which mainly involved postnecrotic fibrosis and osteosclerosis. CONCLUSION: HIRP can help to control the tumor locally. A more conservative operation was then possible in cases of good responders to preoperative chemotherapy with HIRP.

Adolescent↗
PubMed2002

Osteoprotegerin secretion from prostate cancer is stimulated by cytokines, in vitro.

Osteoprotegerin (OPG), a member of the tumor necrosis receptor family, is produced by various tissues and inhibits osteoclast differentiation and activity. Since the metastasis of prostate cancer to bone often induces osteosclerosis, the possibility that these tumor cells secrete OPG is of interest. We have investigated whether the prostate cancer cell lines LNCaP, PC-3, and DU-145 produce and secrete OPG in vitro and if the production might be regulated by cytokines involved in remodeling of bone. OPG transcripts were detected by RT-PCR in all cell lines. OPG in culture media was analyzed by ELISA. In all three lineages, treatment with tumor necrosis factor-alpha and interleukin-1 beta dose dependently (5-5000 pM) stimulated the OPG secretion. Treatment with tumor necrosis factor-beta in increasing concentrations (1-1000 pM) stimulated OPG secretion in PC-3 but had no effect on the DU-145 and LNCaP cells. Dexamethasone (100 pM) had a small, but not significant, inhibitory effect on OPG secretion from DU-145 and LNCaP. In human non-malignant prostate cells, used as controls, there was no effect of IL-1 or TNFs on the secretion rate of OPG.

Cytokines↗
PubMed1988

The petrous temporal bone and deafness in X-linked hypophosphataemic osteomalacia.

Radiological anatomy of the petrous bones and skull base has been studied in a group of 11 patients with X-linked hypophosphataemic osteomalacia and hearing loss, and comparison made with a control group of normal subjects. Patients with X-linked hypophosphataemic osteomalacia were found to have generalised osteosclerosis and thickening of the petrous bone, with some narrowing of the internal auditory meatus, particularly in its mid-portion. No evidence of platybasia nor of basilar impression was found in the hypophosphataemmic group. The aetiology of the hearing loss which occurs in patients with X-linked hypophosphataemic osteomalacia is discussed in relation to the radiological abnormalities described.

Chromosomes↗
PubMed1989

Periosteal new bone formation in chronic renal failure.

A retrospective analysis of the skeletal surveys of 47 patients with periosteal new bone formation (PNB) associated with chronic renal failure was performed in order to determine the radiological features of this abnormality. Sequential skeletal surveys identified the time of development of PNB in 11 patients. The aetiology of PNB was investigated by reviewing biochemical and pathological data for these patients during this period. Symmetrical involvement of weight bearing bones was a typical feature of PNB. PNB was often identified at multiple sites. No association of PNB with radiological, biochemical or pathological evidence of aluminium induced osteomalacia was found. Both hyperparathyroidism and osteosclerosis were common in patients with PNB but since hyperparathyroidism is a frequent occurrence in patients with chronic renal failure its relationship to PNB is not necessarily causal.

Adolescent↗
PubMed2004

[Cerebral Erdheim-Chester disease].

We report the case of a 26-old-year man hospitalized for first partial complex epileptic seizure. Brain MRI showed an asymptomatic pseudo-tumor lesion in the brainstem. Diabetes insipidus, hypophyseal gonadotropic deficiency and osteosclerosis of long bones strongly suggested Erdheim-Chester disease, a rare histiocytosis, confirmed after tibial biopsy. Six months later, the patient remained stable. A persistent, and even increased, enhancement with Gd-DTPA on brain MR images was noted as previously described. The review of the literature collected 64 cases, and only 7 cases of cerebral "tumor".

Adult↗
PubMed1999

Imaging features of posterior fossa neoplasms in children and adults.

Masses in the posterior fossa may be divided into extra-axial and intra-axial lesions. Because of its multiplanar capabilities, improved soft-tissue resolution and contrast, and the absence of scanning artifacts related to the osseous skull base, which are frequently present on CT, MRI is the imaging modality of choice in evaluating lesions arising in the posterior fossa. It is the best means of critically localizing lesions and determining the extent of disease. Analysis of the signal characteristics of a lesion on multiple different imaging sequences (T1-weighted, T2-weighted, and enhanced images) may provide information about the tissue constituents within a mass/neoplasm, such as the presence of cellularity, necrosis, and hemorrhage. MRI is also useful in guiding localization for brain tumor biopsies and assists in planning radiation therapy. However, CT also plays an important role. CT is frequently the first imaging study performed in patients with posterior fossa masses who often present with nausea, vomitting, ataxia, and other signs of increased intracranial pressure. It is a quick, available, and relatively inexpensive study to assess neurological emergencies including hydrocephalus, hemorrhage, and herniation syndromes. In addition, it frequently provides complimentary information, such as the presence of calcification or bony remodeling (osteosclerosis or osteolysis), which MRI is less sensitive in detecting.

Adult↗
PubMed1985

Bone marrow findings in systemic mastocytosis.

The neoplastic proliferation of tissue mast cells constitutes a group of rare diseases that have localized and systemic variants. The cytologic (n = 7) and histologic (n = 38) findings in bone marrow from a total of 45 patients with systemic mastocytosis were evaluated. Three distinct histologic patterns of marrow involvement were distinguished. In 21 cases a patchy or focal infiltration pattern was encountered. Mast cell aggregates were located predominantly in peritrabecular and perivascular areas. The adjacent trabeculae were thickened. A dense network of reticulin fibers and foci of lymphocytes accompanied the mast cell infiltrates. Increased numbers of eosinophils frequently demarcated the mast cell infiltrates from the surrounding tissue. In the noninfiltrated marrow areas hematopoiesis and the distribution of fat cells appeared to be normal. This histologic pattern, designated type 1, was observed exclusively in patients showing primary involvement of the skin, indistinguishable from urticaria pigmentosa. In 14 additional cases peritrabecular and perivascular sheets of mast cells, with concomitant fibrosis and osteosclerosis, were also present. Unlike the findings in type 1, however, the noninfiltrated marrow areas showed marked reductions in fat cell content and markedly increased granulocytopoiesis or increased numbers of blast cells (infiltration pattern type 2). On the basis of the hematologic and clinical findings, chronic myeloid leukemia was diagnosed in six of these cases, myelomonocytic leukemia in three cases, and acute myeloid leukemia in two cases. The bone marrow of three patients was diffusely infiltrated by atypical mast cells, leading to marked hypoplasia of fat cells and blood cell precursors. These histologic features were identified as infiltration pattern type 3. The diagnosis of mast cell leukemia was confirmed in all three cases by the presence of numerous mast cells in the blood. The prognosis for patients with the type 1 marrow infiltration pattern and primary skin involvement was favorable (actuarial survival rate five years after diagnosis, 0.75). This variant was called benign systemic mastocytosis. Primary skin involvement did not occur in the patients with type 2 or 3 infiltration patterns. The prognosis for these patients was poor (actuarial survival five years after diagnosis, 0.17 for type 2 and 0.00 for type 3). These two forms were accordingly designated malignant systemic mastocytosis.

Adult↗
PubMed2001

Health effects of fluoride pollution caused by coal burning.

Recently a huge amount of fluoride in coal has been released into indoor environments by the combustion of coal and fluoride pollution seems to be increasing in some rural areas in China. Combustion of coal and coal bricks is the primary source of gaseous and aerosol fluoride and these forms of fluoride can easily enter exposed food products and the human respiratory tract. Major human fluoride exposure was caused by consumption of fluoride contaminated food, such as corn, chilies and potatoes. For each diagnostic syndrome of dental fluorosis, a log-normal distribution was observed on the logarithm of urinary fluoride concentration in students in China. Urinary fluoride content was found to be a primary health indicator of the prevalence of dental fluorosis in the community. In the fluorosis areas, osteosclerosis in skeletal fluorosis patients was observed with a high prevalence. A biochemical marker of bone resorption, urinary deoxypyridinoline content was much higher in residents in China than in residents in Japan. It was suggested that bone resorption was stimulated to a greater extent in residents in China and fluoride may stimulate both bone resorption and bone formation. Renal function especially glomerular filtration rate was very sensitive to fluoride exposure. Inorganic phosphate concentrations in urine were significantly lower in the residents in fluorosis areas in China than in non-fluorosis area in China and Japan. Since airborne fluoride from the combustion of coal pollutes extensively both the living environment and food, it is necessary to reduce fluoride pollution caused by coal burning.

Adult↗
PubMed2003

TSH is a negative regulator of skeletal remodeling.

The established function of thyroid stimulating hormone (TSH) is to promote thyroid follicle development and hormone secretion. The osteoporosis associated with hyperthyroidism is traditionally viewed as a secondary consequence of altered thyroid function. We provide evidence for direct effects of TSH on both components of skeletal remodeling, osteoblastic bone formation, and osteoclastic bone resorption, mediated via the TSH receptor (TSHR) found on osteoblast and osteoclast precursors. Even a 50% reduction in TSHR expression produces profound osteoporosis (bone loss) together with focal osteosclerosis (localized bone formation). TSH inhibits osteoclast formation and survival by attenuating JNK/c-jun and NFkappaB signaling triggered in response to RANK-L and TNFalpha. TSH also inhibits osteoblast differentiation and type 1 collagen expression in a Runx-2- and osterix-independent manner by downregulating Wnt (LRP-5) and VEGF (Flk) signaling. These studies define a role for TSH as a single molecular switch in the independent control of both bone formation and resorption.

Animals↗
PubMed1996

Complex odontoma as a periapical and interradicular radiopacity in a primary molar.

Only rarely is a mature complex odontoma seen in a periapical location and in association with a primary tooth. Complex odontomas usually present as a radiopacity with a radiolucent rim. The differential diagnosis must include mature fibro-osseous lesions (e.g. cementoblastoma). Complex odontomas can be differentiated from fibro-osseous lesions because they usually present a nonhomogeneous radiopacity and almost always will present as solitary lesions. For complex odontomas located in the periapical region, the differential diagnosis must include idiopathic periapical osteosclerosis. In this case, the presence of the radiolucent rim and the presence of denser, sharper radiopacities produced by enamel distinguish the odontoma.

Adult↗
PubMed1982

Successful allogeneic bone-marrow transplantation for patients in the accelerated phase of chronic granulocytic leukaemia.

Nine patients underwent allogeneic bone-marrow transplantation as treatment for chronic granulocytic leukaemia (CGL) during the accelerated phase, a point in the course of the disease when it has progressed beyond the stable chronic phase but before the onset of blast crisis. After bone-marrow transplantation, haematological and cytogenetic studies showed ablation of all evidence of leukaemia, successful engraftment, and persistence of normal haemopoiesis in all patients. In one patient severe myelofibrosis and osteosclerosis disappeared after bone-marrow transplantation. Two patients have died of complications related to graft-versus-host disease (GvHD) but with no evidence of CGL. In one patient haematological and cytogenetic evidence of recurrent disease developed after bone-marrow transplantation, and she survives in chronic phase. Six patients are free of disability, do not require transfusions, possess normal marrow chromosomes, and have persistent clinical and haematological evidence of complete remission from CGL. Intervention with allogeneic bone-marrow transplantation during the accelerated phase of CGL can eradicate the disease and can provide normal haemopoiesis with acceptably low early morbidity and mortality. The long-term efficacy of bone-marrow transplantation as treatment for CGL, and the most effective timing of the transplantation with regard to the course of disease have yet to be determined.

Adult↗
PubMed2006

[Imaging of the diabetic foot].

Destruction in diabetic feet is secondary to neuropathy (peripheral and autonomic nervous system) in association with microangiopathy. The loss of sensation to pain and the static trouble lead to increase the pressure in some areas and predispose to pedal skin ulceration, the precursor of osteomyelitis. Plain radiography should be the first step in the evaluation for diagnosis and follow-up. The initial patterns are nonspecific but very rapid evolution associating osteolysis, osteosclerosis and fragmentation lead to the Charcot foot. When osteomyelitis is suspected, scintigraphy with labelled white blood cells and MRI are necessary to differentiate infection from neuropathy.

Diabetic Foot↗
PubMed2002

[An incomplete form of pachydermoperiostosis. Diagnosis of finger clubbing].

INTRODUCTION: The finger clubbing is most of the time associated with cardiovascular and pulmonary diseases. Pachydermoperiostosis also known as osteodermopathic syndrome, an hereditary disorder, is a rare cause of finger clubbing which might be difficult to diagnose in an incomplete form. EXEGESIS: We report a 36 years old black man presenting over many years polyarthralgias, broadening of fingers and clubbing of the fingers and toes extremities. This was mentioned on other family members. The physical examination was otherwise unremarkable. There were no skin thickening, no psoriasis-like and cardio-pulmonary disease features. These following exams were normal; Hemogram, fibrinogen, C reactive protein, rheumatoïd factor, serum calcium and phosphorus, thyroid hormones, growth hormone, chest X-ray, gastroduodenoscopy, electrocardiogram. The skeletal X-ray documented a widespread bone formation, a sacro-iliac osteosclerosis and interosseous ossifications betwen tibias and fibulas. CONCLUSION: Pachydermoperiostosis diagnosis was set up on 3 out of the 4 Borochowitz criteria. The absence of pachyderma defines this incomplete form. The osteoarticular manifestations lead mainly to differential diagnosis with the secondary hypertrophic osteoarthropathy and chronic inflammatory rheumatisms. The underlying pathogenic mechanism of this disease remains still unclear.

Adult↗