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The literature contains little reference to the phenomenon of osteosclerosis in leprosy. The aim of the authors' investigations was to determine: a) the incidence of osteosclerosis as part of the radiographic picture in the distal extremities of the limbs; b) the pathological substratum; c) the possible clinical significance. The research was carried out on 233 leprosy patients at the Colonia Hanseniana di Gioia del Colle (Bari). The authors examined 260 radiographs of the hands and 1310 radiographs of the feet. A number of biopsy samples of bone were taken from four patients and examined by means of microradiography using ultraviolet fluorescent light and also by historadiography. The basic radiographic features indicative of osteosclerosis were: a) reactive osteosclerosis; b) sclerosing periostosis; c) massive osteosclerosis. The authors observed a preponderance of osteosclerosis in the bones of the first digital ray, both in the phalanges and metatarsals or metacarpals. The sesamoid bones were affected more commonly in those of the first digit than those of the fifth. The radiographic findings were confirmed microscopically. It is difficult to assess the possible clinical significance because of the transient nature of the osteosclerosis in the evolution of the lepromatous lesions with time.
Six out of 30 patients with chronic renal failure showed osteosclerosis in the lateral radiograph of the lumbar spine. When two groups with a similar degree of renal impairment were compared, the patients with osteosclerosis were younger and had a significantly higher level of circulating PTH (p less than 0.05) and total hydroxyproline excretion (p less than 0.02), than patients without overt osteosclerosis. The metacarpal cortical thickness was significantly reduced in patients with vertebral osteosclerosis. The results suggest that in patients with chronic uremia endogenous hypersecretion of PTH is one of the most significant factors responsible for the development of osteosclerosis. The mineral released from other skeletal sites could be utilized in the mineralization of the newly formed trabecular bone without any external calcium gain.
Myelofibrosis and osteosclerosis are prominent features arising in mice overexpressing thrombopoietin (TPO). The pivotal role of transforming growth factor beta 1 (TGF-beta 1) in the pathogenesis of myelofibrosis has been documented, but the mechanisms mediating osteosclerosis remain unclear. Here, we used mice deficient in osteoprotegerin (OPG), a secreted inhibitor of bone resorption, to determine whether osteosclerosis occurs through a deregulation of osteoclastogenesis. Marrow cells from opg-deficient mice (opg(-/-)) or wild-type (WT) littermates were infected with a retrovirus encoding TPO and engrafted into an opg(-/-) or WT background for long-term reconstitution. The 4 combinations of graft/host (WT/WT, opg(-/-)/opg(-/-), opg(-/-)/WT, and WT/opg(-/-)) were studied. Elevation of TPO and TGF-beta 1 levels in plasma was similar in the 4 experimental groups and all the mice developed a similar myeloproliferative syndrome associated with severe myelofibrosis. Osteosclerosis developed in WT hosts engrafted with WT or opg(-/-) hematopoietic cells and was associated with increased OPG levels in plasma and decreased osteoclastogenesis. In contrast, opg(-/-) hosts exhibited an osteoporotic phenotype and a growth of bone trabeculae was rarely seen. These findings suggest that osteosclerosis in mice with TPO overexpression occurs predominantly via an up-regulation of OPG in host stromal cells leading to disruption of osteoclastogenesis.
OBJECTIVE: Osteosclerosis of the terminal phalanges of the hand has been reported in the collagen diseases including rheumatoid arthritis (RA). The current study was made to clarify the significance of terminal phalangeal osteosclerosis in RA. METHODS: Hand x-ray films of 108 patients (male 13, female 95) with RA for more than 10 years were assessed by Halim's grading. Grade 2, (Distance between both cortices is < 1 mm but there is still an intermediate space discernible), and grade 3, (Complete fusion of both cortices, but the base of the terminal phalanx is open), were classified as the positive group. Grades 0 and 1 were classified as the negative group. Both groups were compared and sigma GS/D values was measured at terminal phalanges, middle phalanges and metacarpuses of right middle fingers using digital image processing method. sigma GS/D index was calculated as being equal to the ratio of sigma GS/D value of the terminal or middle phalanx to sigma GS/D value of the metacarpus. RESULTS: Thirty cases (28%) were positive (male 1, female 29). Osteosclerosis of terminal phalanges usually appeared in more than two digits bilaterally. It was located as follows; thumb-1 case, index-13 cases, middle-24 cases, ring-51 cases, little-58 cases. Obliteration of the medullary space of middle phalanges was seen in 5 cases. No difference was observed between the positive and negative groups about sex, age, the mean value of C-reactive protein, the incidence of Steinblocker's class classification and the rate of seropositive patients. Osteosclerosis of terminal phalanges was observed at first consultation in 93% of positive cases. Osteosclerosis is expected to appear in the early phase of RA and to last for more than 10 years. sigma GS/D index of the positive group (1.03 +/- 0.24, mean +/- SD) was greater than that of the negative group (0.63 +/- 0.25) (p < 0.05).
OBJECTIVE: The aim of this study is to investigate the mechanism of osteosclerosis in IMF in relation to OPG derangement. METHODS: Plasma OPG level was assayed by OPG ELISA in 19 patients with IMF, 15 patients with other myeloproliferative disorders (MPDs), and 12 normal volunteers as controls and correlated with the degree of osteosclerosis. Furthermore, the level of OPG mRNA, in the cultured bone marrow stromal (BMS) cells of patients with IMF and anemia patients used as controls, in the presence or absence of TGF-beta1, was studied by real-time RT-PCR. RESULTS: The present study showed that blood OPG level was significantly elevated in patients with IMF as compared to patients with other MPDs (p < 0.01) or normal volunteer controls (p < 0.05), and there was no significant difference in the level between patients with MPDs and controls. In addition, there was a positive correlation (r=0.67, p=0.04) between plasma OPG levels and the degree of osteosclerosis. There was no difference in the OPG mRNA in patients with IMF as compared with controls even on TGF-beta1 stimulation. CONCLUSION: These results suggest that osteosclerosis in IMF may be related to overproduction of OPG and enhanced level of OPG is not due to the effect of TGF-beta1 on the BMS cells. It could be due to the effect of TGF-beta1 or other growth factors on cells other than BMS cells such as the osteoblasts.
Thrombopoietin (TPO) regulates megakaryocytopoiesis and platelet production in vivo and in vitro. Exogenous overexpression of TPO in vivo by viral-mediated gene transfer induced bone marrow (BM) fibrosis and osteosclerosis. On the other hand, transgenic mice (Tg) overexpressing TPO using a liver-specific apolipoprotein E (Apo-E) promoter did not exhibit myelofibrosis or osteosclerosis. These discrepancies in phenotype are not fully understood. Then we have investigated the consequences of long-term in vivo overexpression of TPO in a mouse model. Murine TPO Tg mice driven by the IgH promoter were generated. The number of platelets and neutrophils in peripheral blood, and the number of megakaryocytes and granulocytic immature cells in the BM was elevated, together with the number of progenitor cells for megakaryocyte and myeloid cells. TPO Tg mice demonstrated anemia but the number of progenitor cells for the erythrocyte was increased. TPO Tg mice developed myelofibrosis and osteosclerosis as they aged with extramedullary hematopoiesis in the spleen. As plasma transforming growth factors (TGF)-beta1 and osteoprotegerin (OPG) levels were higher in TPO Tg mice than in wild-type mice, the development of myelofibrosis and osteosclerosis depends on local TPO levels in BM and might be due to elevated TGF-beta1 and OPG.
Standardized panoramic radiographs were used to determine and compare the prevalences of focal osteosclerosis (including condensing osteitis) and apical periodontal pathoses in a sequential presenting sample of 600 European and 600 Cape Coloured dental outpatients. Most cases of focal osteosclerosis were found in edentulous zones or associated with carious or inadequately restored teeth; however, some were subjacent to apparently sound teeth. Focal osteosclerosis of definite dental origin was just as common in participants aged 25 years and older as in younger individuals. While focal osteosclerosis occurred predominantly in the mandible, apical periodontal pathoses were distributed more evenly between both jaws.
OBJECTIVE: The purpose of this study was to determine the frequency and anatomic location of idiopathic osteosclerosis in the jawbones and to present computed tomographic findings of this lesion in Japanese patients. STUDY DESIGN: Panoramic radiographs of 1047 patients were examined for the presence of idiopathic osteosclerosis in the jawbones. Computed tomography was performed in 11 patients of this series. RESULTS: A total of 64 patients (6.1%) showed this radiopacity. The highest occurrence was in the mandibular first molar region. There was no statistically significant difference in the prevalence of idiopathic osteosclerosis between males and females. On computed tomography images, these radiopaque areas were divisible into two types: enostosis (five cases) and central sclerosis (six cases). CONCLUSION: This is the first report of computed tomographic findings on idiopathic osteosclerosis in the jawbones, although the results on panoramic radiographs are similar to other investigators.
AIM: To compare the prevalence of idiopathic osteosclerosis in the jaws in Hong Kong and Britain. METHODS: The panoramic radiographs of consecutive patients who attended the primary care departments of the dental hospitals in Hong Kong in 1981 and 1990 and London in 1990 and of Edinburgh in 1993 were reviewed. The size of the Hong Kong lesions was measured. The literature was subjected to systematic review. RESULTS: The prevalence of idiopathic osteosclerosis in Hong Kong in 1981 and 1990, London and Edinburgh was 6.7, 5.5, 2.7 and 4.1% respectively. The prevalence of idiopathic osteosclerosis was greater in the Oriental (Chinese and Japanese) than in Western surveys. The lesions in the 1990 Hong Kong survey in the third decade were significantly smaller than those in the 1981 survey. The decrease in size in Hong Kong 1990 was also accompanied by a reduction in overall prevalence. The predilection for the mandible, especially in the premolar area, was observed in the Chinese and London series; this feature was also common to all other reports. CONCLUSION: The Chinese have a greater prevalence of idiopathic osteosclerosis than Western populations.
Advanced chronic idiopathic myelofibrosis (IMF) with osteosclerosis and increase and thickening of bone trabeculae is typically contrasted by the absence or sparse presence of osteoclasts. Because osteoclast formation can be inhibited by osteoprotegerin (OPG) we investigated OPG expression in IMF with severe fibrosis and osteosclerosis, which expressed significantly higher (up to 71-fold) OPG mRNA levels when compared with prefibrotic cellular IMF and control cases. The receptor activator of nuclear factor kappaB ligand (RANKL), a positive regulator of osteoclast differentiation and putative antagonist of OPG was overexpressed by up to 34-fold exclusively in advanced IMF. Case-specific calculation of the RANKL/OPG ratio in advanced IMF showed a wide range without significant differences when compared with the prefibrotic IMF and non-neoplastic haematopoiesis. Immunohistochemical detection of OPG protein revealed strong labelling of endothelial cells within proliferating vessels in fibrotic IMF and heterogeneously labelled megakaryocytes, and fibroblasts. Osteosclerosis and impaired osteoclast function in IMF appears to be associated with upregulated endothelial OPG expression but concomitant reduction of the antagonist RANKL could not be demonstrated. We conclude that osteosclerosis in IMF is associated with increased endothelial OPG expression without concomitant RANKL downregulation.
Autosomal dominant osteosclerosis, an entity previously labelled by various names, is clearly separate from Van Buchem disease; Van Buchem disease exhibits autosomal recessive inheritance. The clinical manifestation of autosomal dominant osteosclerosis is a widened and deepened mandible with increased gonial angle. Radiographic manifestations include endosteal sclerosis of the neurocranium with loss of the diploë, osteosclerosis and hyperostosis of the mandible with absence of the normal antegonial notches, endosteal sclerosis of the diaphyses of long bones (including metacarpals and metatarsals), and osteosclerosis of the pelvis.
We studied a family with autosomal dominant osteosclerosis associated with familial spinal canal stenosis. The propositus, a 44-year-old Japanese woman, had a 9-month history of occipitalgia and left tinnitus, and also had a 2-month history of pain and numbness of the right upper limb. Radiographic skeletal survey showed osteosclerotic changes in the neurocranium, diaphysis of the long bone, mandible, shoulder, clavicle, and ribs. Serum alkaline phosphatase was normal, and no periosteal excrescences were seen. The inheritance pattern was autosomal dominant. The propositus and her daughter, both with severe osteosclerosis, showed spinal canal stenosis, but her son, whose osteosclerosis was moderate, did not. This is the first report of autosomal dominant osteosclerosis associated with familial spinal canal stenosis.
Osteosclerosis of the subchondral bone was measured by densitometer on plain radiographs in 55 medial compartmental osteoarthritic knees of 40 patients who were treated with high tibial valgus osteotomy for correction of varus deformity. The ratio of the osteosclerosis value of the medial side of the knee to that of the lateral side (Medial/Lateral ratio) was calculated and used as a parameter. The Medial/Lateral ratio of osteosclerosis decreased rapidly within three years after osteotomy at the reference points of the femur and the tibia. Even 7 to 19 years after osteotomy, a decrease of the ratio was noted in 16 knees with a standing femorotibial angle (FTA) less than 168 degrees (12 degrees of anatomical valgus angulation). This was interpreted to mean that osteosclerosis of the medial condyle decreased compared with that of the lateral condyle after overcorrection of varus deformity. In the cases of more than 7 years after high tibial osteotomy, a positive straight regression line was drawn by calculation between Medial/Lateral ratio and postoperative limb alignment expressed by standing femorotibial angle, with coefficient of correlation (gamma) of 0.295 (p < 0.01).
Bone mineral density (BMD) was evaluated in 52 patients with HbS/beta-thalassemia. Seventeen (32%) patients had osteopenia/osteoporosis and 30 (57%) had osteosclerosis. Bone resorption was diminished in patients with osteosclerosis and increased in those with osteopenia/osteoporosis. The sRANKL/osteoprotegerin ratio was elevated in the osteosclerotic group. Osteoporosis patients had mild renal impairment and their BMD correlated with osteoprotegerin, and bone resorption markers. Osteosclerosis patients had multiple infarctions in the studied bones that led to reduced osteoclast activity and increased BMD. In conclusion, HbS/beta-thalassemia patients may develop osteopenia/osteoporosis mainly due to marrow expansion or osteosclerosis because of ischemia after a vaso-occlusive crisis. The RANKL/ osteoprotegerin axis participates in these phenomena.
Osteosclerosis of the subchondral bone was measured by densitometry on plain roentgenograms in 55 medial compartmental osteoarthritic knees of 40 patients who underwent high tibial osteotomy for correction of varus deformity. The osteosclerosis value of the medial side of the knee to that of the lateral side (Medial/Lateral ratio) was calculated and used as a parameter. Medial/Lateral ratios of the osteosclerosis were increased from 0.90 +/- 0.15 preoperatively to 0.99 +/- 0.20 (p < 0.05) postoperatively in 2 mm proximal area from the joint surface of the femur, from 0.95 +/- 0.15 to 1.04 +/- 0.21 (p < 0.05) in 7 mm proximal area from the joint surface of the femur, and from 0.87 +/- 0.14 to 0.95 +/- 0.13 (p < 0.05) in 2 mm distal area from the joint surface of the tibia within 3 years. The increase of the ratio was noted more than 7 years after osteotomy in the cases with standing femoro-tibial angle (FTA) less than 165 degrees. This is interpreted to mean that osteosclerosis of the medial chondyle decreased as compared with that of the lateral condyle after correction of varus deformity. More than 7 years after high tibial osteotomy, minus straight line relationship was found between Medial/Lateral ratio and FTA in 2 mm proximal area from the joint surface of the femur of the case with FTA less than 175 degrees with coefficient of correlation -0.408 (p < 0.05) and in 2 mm distal area from the joint surface of the tibia with coefficient of correlation -0.437 (p < 0.01). From these results, the sufficient correction of varus deformity is considered to be one of the most important factor in the treatment of osteoarthritis of the knee.