Minimodeling Reduces the Rate of Cortical Bone Loss in Patients With Secondary Hyperparathyroidism

Yajima, Aiji; Inaba, Masaaki; Tominaga, Yoshihiro; Ito, Akihiro

doi:10.1053/j.ajkd.2006.11.045

Cited by 26 publications

(30 citation statements)

References 25 publications

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“…Nevertheless, there have been few clinical studies about the role of the osteocyte in patients with chronic kidney disease (CKD) . It is likely that bone fragility in CKD patients suffering from renal hyperparathyroidism increases as a result of increased hypomineralized bone area caused by impaired mineralization by osteocytes, increased woven bone area, and the reduced cortical bone area caused by cortical thinning and increased cortical porosity . The long‐term reduction of osteocyte numbers generally leads to increased fracture risk …”

Section: Introductionmentioning

confidence: 99%

“…(4)(5)(6)(7) It is likely that bone fragility in CKD patients suffering from renal hyperparathyroidism increases (8,9) as a result of increased hypomineralized bone area caused by impaired mineralization by osteocytes, (10,11) increased woven bone area, (12,13) and the reduced cortical bone area caused by cortical thinning and increased cortical porosity. (14,15) The long-term reduction of osteocyte numbers generally leads to increased fracture risk. (16) Parathyroidectomy is an important treatment option for hyperparathyroid bone disease caused by renal hyperparathyroidism (17,18) because this procedure is completed in approximately 1 hour with little bleeding.…”

Section: Introductionmentioning

confidence: 99%

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The Importance of Biologically Active Vitamin D for Mineralization by Osteocytes After Parathyroidectomy for Renal Hyperparathyroidism

et al. 2019

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Hypomineralized matrix is a factor determining bone mineral density. Increased perilacunar hypomineralized bone area is caused by reduced mineralization by osteocytes. The importance of vitamin D in the mineralization by osteocytes was investigated in hemodialysis patients who underwent total parathyroidectomy (PTX) with immediate autotransplantation of diffuse hyperplastic parathyroid tissue. No previous reports on this subject exist. The study was conducted in 19 patients with renal hyperparathyroidism treated with PTX. In 15 patients, the serum calcium levels were maintained by subsequent administration of alfacalcidol (2.0 μg/day), i.v. calcium gluconate, and oral calcium carbonate for 4 weeks after PTX (group I). This was followed in a subset of 4 patients in group I by a reduced dose of 0.5 μg/day until 1 year following PTX; this was defined as group II. In the remaining 4 patients, who were not in group I, the serum calcium (Ca) levels were maintained without subsequent administration of alfacalcidol (group III). Transiliac bone biopsy specimens were obtained in all groups before and 3 or 4 weeks after PTX to evaluate the change of the hypomineralized bone area. In addition, patients from group II underwent a third bone biopsy 1 year following PTX. A significant decrease of perilacunar hypomineralized bone area was observed 3 or 4 weeks after PTX in all group I and II patients. The area was increased again in the group II patients 1 year following PTX. In group III patients, an increase of the hypomineralized bone area was observed 4 weeks after PTX. The maintenance of a proper dose of vitamin D is necessary for mineralization by osteocytes, which is important to increase bone mineral density after PTX for renal hyperparathyroidism. © 2019 The Authors. JBMR Plus published by Wiley Periodicals, Inc. on behalf of American Society for Bone and Mineral Research.

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Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

The Importance of Biologically Active Vitamin D for Mineralization by Osteocytes After Parathyroidectomy for Renal Hyperparathyroidism

et al. 2019

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“…There are few reports of studies of cortical bone histology in either patients with or animal models of chronic kidney disease (CKD) . Clinical fractures generally initiate in cortical bone, therefore, a clearer understanding of the histomorphometry of cortical bone would be very important to devise methods to prevent fractures.…”

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Impact of Lanthanum Carbonate on Cortical Bone in Dialysis Patients with Adynamic Bone Disease

et al. 2013

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Among the most serious problems in patients with chronic kidney disease (CKD) is fragility of cortical bone caused by cortical thinning and increased cortical porosity; the cortical fragility is sometimes irreversible, with fractures generally initiating from cortical bone. Therefore, development of treatments for problems of cortical bone is urgently desired. Cortical bone has the three surfaces, including the periosteal surface, intracortical spaces and endocortical surface. Bone turnover at the endocortical surface and intracortical resorption spaces are increased as compared with that at cancellous surface. Bone growth sometimes depends on apposition at the periosteal surface. We treated hyperphosphatemia in two hemodialysis patients with adynamic bone disease with 750-1500 mg/day of lanthanum carbonate, which is a non-calcium containing phosphate binder; the treatment resulted in a decrease of the serum phosphorus levels (P levels), without significant change of the serum intact parathyroid hormone levels. We now report that treatment of these patients with lanthanum carbonate increased mineralization of the periosteal surface, increased bone mass within the intracortical resorption spaces and increased mineralization of the minimodeling surface at the endocortical surface. In addition, woven bone volume in cortical bone was decreased and mineralization of bone units, namely, osteons, was increased. Although these findings were not observed across all surfaces of the cortical bone in the patients, it is expected that lanthanum carbonate would increase the cortical stability in CKD patients, with consequent reduction in the fracture rate in these patients.

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“…These changes may compensate for the decrease in bone mineral contents and serum Ca levels if the serum level of 1, 25(OH) 2 D 3 was within the normal range. Bone formation without prior bone resorption, or “minimodeling”, compensates for bone loss in both cancellous bone and cortical bone following suitable exercise [31], [32].…”

Section: Discussionmentioning

confidence: 99%

Is Gastrectomy-Induced High Turnover of Bone with Hyperosteoidosis and Increase of Mineralization a Typical Osteomalacia?

et al. 2013

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Gastrectomy (GX) is thought to result in osteomalacia due to deficiencies in Vitamin D and Ca. Using a GX rat model, we showed that GX induced high turnover of bone with hyperosteoidosis, prominent increase of mineralization and increased mRNA expression of both osteoclast-derived tartrate-resistant acid phosphatase 5b and osteocalcin. The increased 1, 25(OH)2D3 level and unchanged PTH and calcitonin levels suggested that conventional bone and Ca metabolic pathways were not involved or changed in compensation. Thus, GX-induced bone pathology was different from a typical osteomalacia. Gene expression profiles through microarray analysis and data mining using Ingenuity Pathway Analysis indicated that 612 genes were up-regulated and 1,097 genes were down-regulated in the GX bone. These genes were related functionally to connective tissue development, skeletal and muscular system development and function, Ca signaling and the role of osteoblasts, osteoclasts and chondrocytes. Network analysis indicated 9 genes (Aldehyde dehydrogenase 1 family, member A1; Aquaporin 9; Interleukin 1 receptor accessory protein; Very low density lipoprotein receptor; Periostin, osteoblast specific factor; Aggrecan; Gremlin 1; Angiopoietin-like 4; Wingless-type MMTV integration site family, member 10B) were hubs connected with tissue development and immunological diseases. These results suggest that chronic systemic inflammation might underlie the GX-induced pathological changes in bone.

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Minimodeling Reduces the Rate of Cortical Bone Loss in Patients With Secondary Hyperparathyroidism

Cited by 26 publications

References 25 publications

The Importance of Biologically Active Vitamin D for Mineralization by Osteocytes After Parathyroidectomy for Renal Hyperparathyroidism

The Importance of Biologically Active Vitamin D for Mineralization by Osteocytes After Parathyroidectomy for Renal Hyperparathyroidism

Impact of Lanthanum Carbonate on Cortical Bone in Dialysis Patients with Adynamic Bone Disease

Is Gastrectomy-Induced High Turnover of Bone with Hyperosteoidosis and Increase of Mineralization a Typical Osteomalacia?

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