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At least 19 recordsLinked to original sources
PubMedDate not supplied

Ionophores. Chemistry, physiology and potential applications to bone biology.

Ionophores are substances which facilitate the movement of ions into and/or through organic phases. The two major classes of compounds are the neutral ionophores, which form charged clathrate complexes with ions, and the carboxylic polyether ionophores which are neutral in the complexed state. Many of the ionophores exclusively bind organic monovalent cations. Selectivity for divalent metal cations or for anions is less common. One carboxylic polyether, X-537A, forms complexes with small organic cations as well as a variety of metals. Ionophores selective for monovalent cations have been used primarily for studies of mitochondrial metabolism. Compounds like X-537A and A23187, which show high affinity for biologically active divalent cations, are being widely used as tools to study the physiologic roles of these cations. These studies have confirmed the central role of calcium in many biological processes. The major problem encountered with X537A is a lack of selectivity. A23187 has produced variable results in studies of bone as well as other tissues. Despite these difficulties, the ionophores offer promise of being useful tools in studies of bone metabolism.

Animals↗
PubMed1978

The effects of root shape and biology on bone growth.

A statistical study was carried out on the influence of root surfaces on adjacent cellular activity. This activity is indeed affected by both the shape and the biology of those surfaces. Flat surfaces tend to inhibit, nicked surfaces tend to stimulate bone formation in a bone-growing environment. A biologic effect is exerted by the matrix of diseases roots. They contain an inhibitory principle which is not present in healthy roots. This factor is masked by the apatite structure and is destroyed by heat.

Animals↗
PubMed2025

Membrane Palmitoylated Protein 7 is Required for Osteogenesis and is Linked with Bone Mineralization and Osteoporosis: The Functional Evaluation of GEFOS GWAS Hit.

Genome-wide association studies have identified multiple loci associated with bone mineral density, a major determinant of osteoporotic fracture risk. At one such locus, genetic, bioinformatic, and zebrafish knockout data strongly prioritize membrane palmitoylated protein 7 (MPP7) as a candidate gene, although its precise role in bone biology remains poorly defined. MPP7 encodes a member of the p55 Stardust family of membrane-associated guanylate kinase proteins, which are key regulators of epithelial cell polarity and junctional organization. Here, we investigated the functional role of MPP7 in bone biology. We found that MPP7 expression was significantly reduced-by approximately twofold-in bone tissue from osteoporotic patients compared with osteoarthritic patients and non-osteoporotic controls. Furthermore, we generated a CRISPR/Cas9-mediated MPP7 knockout in the human osteosarcoma HOS cell line and demonstrated that MPP7 deletion impairs osteogenic differentiation and completely abrogates mineralization through downregulation of ALPL expression. Knockout cells also displayed altered morphology, suggesting that MPP7 influences osteoblast function via effects on cell polarity and adhesion. Collectively, our findings, together with zebrafish genetic evidence, indicate that MPP7 plays a critical role in osteoblast differentiation and mineralization and may contribute to osteoporosis susceptibility in humans.

Humans↗
PubMed1977

Preprosthetic bone graft augmentation with allogeneic bone: a preliminary report.

Allogeneic bone biologically interacts with host tissues at a graft site. Addition of autogenous cancellous bone and marrow to allogeneic bone enhances the osteogenic activity of the graft. These observations have been confirmed by noninvasive, quantitative radionuclide methods. The process of freeze-drying greatly reduces and, from the standpoint of clinical significance, essentially eliminates the antigenicity of allogeneic bone. Judged by the results of 14 cases that are under continuous follow-up, allogeneic bone graft augmentation of the denture-bearing area is a possible alternative to autogenous grafting. The process of obtaining and preparing the blanked bone for surgery is reasonable although some questions remain, such as the desirable length of time for tissue reconstitution and the need for culturing or adding antibiotics to the reconstitution solution, or both. It appears that the addition of autogenous cancellous bone and marrow is desirable in most instances unless the dimension of the area to be augmented is quite small or an iliac osteotomy is precluded for medical reasons. The occurrence of complications such as infection and dehiscence during the postoperative course is similar to that in patients with autogenous grafts. Dehiscence can be expected although it appears that if the graft has been supplemented with autogenous cancellous marrow the incidence and extent are dminished. It should be emphasized that dehiscence does not signify failure of the graft-allogeneic bone is not sloughed in toto after being exposed to the oral cavity. Secondary soft tissue procedures can be used in patients with allogeneic grafts; additional cases with long-term follow-up are still needed to establish this method.

Adult↗
PubMed1977

The use of freeze-dried bone as a biologic crib for ridge augmentation. A preliminary report.

Freeze-dried bank bone has been used as a biologic crib, packed with autogenous cancellous bone from the iliac crest, to augment mandibular and maxillary ridges. This technique entails little morbidity. It has been used in six patients, with good clinical success. Three of the patients who underwent mandibular augmentations began wearing dentures within 3 months after augmentation surgery. One patient had a soft-tissue breakdown overlying a graft to the maxilla and subsequently lost a portion (less than one third) of the graft; the other two patients are currently ungoing denture construction. Secondary procedures, such as vestibuloplasty, have been necessary in only two of the six patients. Long-term follow-up is needed, but clinical and radiographic evidence to date demonstrates good results.

Alveoloplasty↗
PubMed2024

Disassembly of the TRIM56-ATR complex promotes cytoDNA/cGAS/STING axis-dependent intervertebral disc inflammatory degeneration.

As the leading cause of disability worldwide, low back pain (LBP) is recognized as a pivotal socioeconomic challenge to the aging population and is largely attributed to intervertebral disc degeneration (IVDD). Elastic nucleus pulposus (NP) tissue is essential for the maintenance of IVD structural and functional integrity. The accumulation of senescent NP cells with an inflammatory hypersecretory phenotype due to aging and other damaging factors is a distinctive hallmark of IVDD initiation and progression. In this study, we reveal a mechanism of IVDD progression in which aberrant genomic DNA damage promoted NP cell inflammatory senescence via activation of the cyclic GMP-AMP synthase/stimulator of IFN genes (cGAS/STING) axis but not of absent in melanoma 2 (AIM2) inflammasome assembly. Ataxia-telangiectasia-mutated and Rad3-related protein (ATR) deficiency destroyed genomic integrity and led to cytosolic mislocalization of genomic DNA, which acted as a powerful driver of cGAS/STING axis-dependent inflammatory phenotype acquisition during NP cell senescence. Mechanistically, disassembly of the ATR-tripartite motif-containing 56 (ATR-TRIM56) complex with the enzymatic liberation of ubiquitin-specific peptidase 5 (USP5) and TRIM25 drove changes in ATR ubiquitination, with ATR switching from K63- to K48-linked modification, c thereby promoting ubiquitin-proteasome-dependent dynamic instability of ATR protein during NP cell senescence progression. Importantly, an engineered extracellular vesicle-based strategy for delivering ATR-overexpressing plasmid cargo efficiently diminished DNA damage-associated NP cell senescence and substantially mitigated IVDD progression, indicating promising targets and effective approaches to ameliorate the chronic pain and disabling effects of IVDD.

Humans↗
PubMed2026

ARID1A Mediates ROS-Induced Osteoclast Activation in TMJ Osteoarthritis.

Excessive osteoclast activation drives rapid subchondral bone destruction, serving as a critical early-stage event precipitating temporomandibular joint osteoarthritis (TMJ-OA). Although epigenetic remodeling is widely recognized as an important interface between pathological environmental signals and genomic response, the specific epigenetic mechanisms translating TMJ-OA-associated stimulation into pathological osteoclast activation remain to be elucidated. Here, using a mechanically induced TMJ-OA mouse model, we identify aberrant reactive oxygen species (ROS) accumulation as a critical upstream driver initiating excessive osteoclast activation and subsequent joint deterioration. By integrating transcriptomic and epigenomic analyses, we delineate the chromatin remodeler AT-rich interaction domain 1A (ARID1A) as an essential oxidative stress sensor within the osteoclast lineage. Mechanistically, ROS accumulation induces ARID1A upregulation and recruitment to the Src enhancer, transcriptionally activating Src and amplifying PI3K-AKT signaling to drive pathological osteoclastogenesis. Conditional knockout of Arid1a in myeloid cells effectively abrogates subchondral bone loss and cartilage destruction in TMJ-OA. Translating these mechanistic insights, we engineered an ROS-responsive, osteoclast-targeting hydrogel for the on-demand delivery of an ARID1A-dependent canonical BRG1/BRM-associated factor complex inhibitor, which successfully alleviates TMJ-OA progression. Our findings establish the epigenetic response to ROS accumulation as a key pathogenic mechanism in TMJ-OA and highlight ARID1A as a promising therapeutic target for early disease intervention.

biomaterial(s)↗
PubMed1979

Studies on the biology of fish bone. III. Ultrastructure of osteogenesis and resorption in osteocytic (cellular) and anosteocytic (acellular) bones.

The comparative ultrastructure of fish bone osteogenesis and resorption induced by scale removal was described in the osteocytic (cellular-boned) Carassius auratus and the anosteocytic (acellular-boned) Tilapia macrocephala. Osteocytes, present in osteocytic bone, were lacking in anosteocytic bone. In osteocytic bone the osteoblast secreted a collagenous preosseous matrix in which it became enmeshed and then was termed a preosteocyte. When the preosseous matrix mineralized, the preosteocyte was termed an osteocyte and was completely surrounded by bone. In anosteocytic bone the osteoblasts receded from the mineralizing front and never became trapped as osteocytes. During resorption, types A and B resorptive cells, present in both bone types, invaded the matrix and demineralized the osseous zone. These cells were characterized by large amounts of granular endoplasmic reticulum and intracellular inclusions containing crystal-like material. Although functionally similar to mammalian osteoclasts, these cells lacked a characteristic ruffled border and were not multinucleated. The osteocytes of cellular bone did not appear to be involved during demineralization.

Animals↗
PubMed1976

Morphological, biological, immunological and biochemical studies on bone tumors of animals and man.

Biological studies on FBJ osteosarcoma virus in tissue cultures have led to the isolation of murine sarcoma virus. Characteristic type C-MuLV particles were observed in bone tumors induced by the SD-MSV-M-virus in vitro and in vivo. The SD-MSV-M virus also induced bone tumors in rats of all strains tested, and it has a similar tumor-inducing property in hamsters. Immunoelectronmicroscopic studies showed that envelope antigens of MSV-SD virus in rat bone tumors can be distinguished from those found in hamster bone tumor cells. In tissue cultures of MSV-SD rat bone tumors, two separate cell lines have been established: one of them releases both MSV and MuLV and the other produces MuL virus only. The MuLV in this cell line acts as helper. The different interactions appear to support the concept of control mechanisms for the partial expression of genes which are responsible for neoplastic properties, virus replication, and synthesis of gs-antigens. Biochemical studies on structural rearrangement and subunit composition of RNA released from MSV-SD virus, have shown that there are two forms of the native genome RNA differing in their sedimentation coeffiiecients and in subunit composition. In human osteosarcoma tissue culture, type-C viruslike particles are found. In cocultures derived from human osteosarcoma with cells taken from the bone marrow or peripheral blood of patients with different types of leukemia, certain morphological changes are observed which resemble those induced in animal cells by RNA tumor viruses. In osteosarcomas where no cytoplasmic antigen could be proved by an immunofluorescence test, the antigen could be produced by cocultivation with antigen-positive leukemic bone marrow cells. Whole human embryo cells treated with fluid from leukemia bone marrow cultures showed the presence of the cytoplasmic antigen when tested with positive sera, but they showed no morphologic changes. In high molecular weight RNA species, sedimentation coefficients ranging from 62S to 68S are demonstrated by molecular hybridization techniques. In cross-hybridization experiments, annealing values were observed only with complementary DNA products synthesized from sarcoma viruses. Three particularly high molecular weight RNA species released from human sarcoma cell cultures showed no cross-hybridization with either the DNA product of Rauscher leukemia virus or that of Gross leukemia virus.

Adult↗
PubMedDate not supplied

[Bone in hepatic cirrhosis: morphometric and biological study (author's transl)].

Quantitative bone histomorphometry and evaluation of blood parameters have been performed in 24 patients with hepatic cirrhosis. 13 patients show osteoporosis which, in 8 of them, is associated with osteoclastic hyperactivity but without elevation of blood parathormon. All patients have hypocalcemia and 14 of them hyperosteidosis. These results are compared with data of the literature on bone morphometry and phosphocalcic metabolism during hepatic cirrhosis.

Bone and Bones↗
PubMed1979

Dialysis bone disease in childhood: treatment with 25-hydroxycholecalciferol.

The effect of 8 months of administration of moderate doses of 25-hydroxycholecalciferol (25 OH D3) on radiologic, biologic, and bone histologic changes was assessed in five children on chronic hemodialysis. Osteomalacia, defined by an increase in the thickness index of the osteoid seams and decrease of the calcification rate, was present on the initial bone biopsy of only one patient and improved with the treatment. Secondary hyperparathyroidism and its prints on bone tissue, noted in all five children, did not improve in the absence of adequate serum phosphorus control. Furthermore, cancellous bone volume diminished in two patients with the administration of 25 OH D3. This activity of the drug could be related to its inhibitory effect of osteoblastic apposition as demonstrated by the decrease in the calcification rates, while the thickness index of the osteoid seams remains normal. Despite the small number of patients studied, these results suggest the importance of limiting the prescription of 25 OH D3 to children suffering from renal osteodystrophy only after having assessed unequivocally an osteomalacic component by histodynamical criteria. Secondary hyperparathyroidism appears not to be improved with moderate doses of 25 OH D3 in the absence of adequate serum phosphorus control.

Adolescent↗