Levels In Bone Research Articles

Organ-wide profiling in mouse reveals high editing levels of Filamin B mRNA in the musculoskeletal system

ABSTRACTAdenosine to inosine RNA editing in protein-coding messenger RNAs (mRNAs) potentially leads to changes in the amino acid composition of the encoded proteins. The mRNAs encoding the ubiquitously expressed actin-crosslinking proteins Filamin A and Filamin B undergo RNA editing leading to a highly conserved glutamine to arginine exchange at the identical position in either protein. Here, by targeted amplicon sequencing we analysed the RNA editing of Filamin B across several mouse tissues during post-natal development. We find highest filamin B editing levels in skeletal muscles, cartilage and bones, tissues where Filamin B function seems most important. Through the analysis of Filamin B editing in mice deficient in either ADAR1 or 2, we identified ADAR2 as the enzyme responsible for Filamin B RNA editing. We show that in neuronal tissues Filamin B editing drops in spliced transcripts indicating regulated maturation of edited transcripts. We show further that the variability of Filamin B editing across several organs correlates with its mRNA expression.

Lead poisoning

Lead is not known to have any physiological role in the body but is ubiquitous in nature. In our country there are many sources of lead exposure, in particular paints and recycling of batteries. Lead is a persistent metal and is present in water, soil and dust. After being absorbed through the gastrointestinal tract (GIT) or respiratory system, it is stored in soft tissues as well as bones. Lead tends to affect many organ systems in the body particularly the nervous system and kidneys. There are no safe levels and data suggests that low level exposure to lead may also affect health of individuals. The diagnosis of lead toxicity can be done by measuring blood lead levels and K x ray fluorescence (KXRF) instruments which measure lead levels in bone. The treatment consists of chelating agents like BAL, EDTA & DMSA. Eliminating lead from potential sources of exposure would go a long way in preventing effects of lead toxicity.

Effects of Gravity, Microgravity or Microgravity Simulation on Early Mammalian Development.

Plant and animal life forms evolved mechanisms for sensing and responding to gravity on Earth where homeostatic needs require responses. The lack of gravity, such as in the International Space Station (ISS), causes acute, intra-generational changes in the quality of life. These include maintaining calcium levels in bone, maintaining muscle tone, and disturbances in the vestibular apparatus in the ears. These problems decrease work efficiency and quality of life of humans not only during microgravity exposures but also after return to higher gravity on Earth or destinations such as Mars or the Moon. It has been hypothesized that lack of gravity during mammalian development may cause prenatal, postnatal and transgenerational effects that conflict with the environment, especially if the developing organism and its progeny are returned, or introduced de novo, into the varied gravity environments mentioned above. Although chicken and frog pregastrulation development, and plant root development, have profound effects due to orientation of cues by gravity-sensing mechanisms and responses, mammalian development is not typically characterized as gravity-sensing. Although no effects of microgravity simulation (MGS) on mouse fertilization were observed in two reports, negative effects of MGS on early mammalian development after fertilization and before gastrulation are presented in four reports that vary with the modality of MGS. This review will analyze the positive and negative mammalian early developmental outcomes, and enzymatic and epigenetic mechanisms known to mediate developmental responses to simulated microgravity on Earth and microgravity during spaceflight experiments. We will update experimental techniques that have already been developed or need to be developed for zero gravity molecular, cellular, and developmental biology experiments.

On the Relation of Bone Mineral Density and the Elastic Modulus in Healthy and Pathologic Bone.

Osteoporosis could lead to the bone mechanical failure. To examine the bone health, mechanical properties are often estimated from the images of the bone density. Here, we review the relationships that have been experimentally determined between mineral density and the elastic modulus and factors that affect these relationships. Studies, which have investigated the relation between the elastic modulus and bone mineral at the bulk scale, have shown that approximately 70% of variations in the elastic modulus can be explained based on the amount of mineral in bone. At the tissue level, however, higher resolution techniques are used to characterize the density and modulus more locally, and this leads to the correlation of mineral with modulus to be not as strong as that of the bulk level and often times, insignificant. This observation indicates the importance of structural hierarchy and mineral crystal organization in determining the local stiffness of the bone tissue. At the bulk level in bone (cm scale), modulus (E) is related to density (ρ) through a power law relationship (E ∝ ρα). At the tissue level (μm-mm scale), the relationship between the modulus and density is weak, likely due to the effect of microstructural features at small length scales.

Osteopontin levels in plasma, muscles, and bone in patient with non-healing diabetic foot ulcers: A new player in wound healing process?

BackgroundThe present study was designed to investigate the impact of osteopontin (OPN) in different tissue (e.g., plasma, muscles and bone) on amputation rate (in-hospital and during one year follow-up) for non-healing diabetic foot ulcers (DFUs). MethodsThis pilot study consisted of 30 diabetic patients, hospitalized due to non-healing DFUs. Patients were divided into two groups: Group 1 included 14 patients who underwent limb-preserved debridement procedure without amputation; Group 2 included 16 subjects who underwent amputation. Additionally, recurrent amputation rate during 1 year follow-up was investigated. ResultsPlasma OPN was higher and bone OPN was lower in Group 2 compared to Group 1 (p = 0.016 and p = 0.004, respectively). In the logistic regression analysis, bone OPN emerged as a significant independent predictor of amputation (OR = 0.042, 95% CI 0.003–0.699, p = 0.027). Plasma OPN was also associated with amputation such that each unit increase in plasma OPN was associated with an increase in odds of amputation of 17.7% (95% CI 0.997–1.388, p = 0.045). During 1 year follow-up 11 patients underwent recurrent amputation. Plasma OPN were higher and bone osteopontin was lower in patients who underwent amputation compared to patients who did not need amputation at one year follow-up. However, in GLM analysis bone OPN was only marginally associated with one year amputation (OR 0.001, 95% CI 0.000–2.0, p = 0.076). ConclusionsDecreased levels of OPN in bone and increased plasma OPN are independently associated with in-hospital amputation. Consequently, plasma OPN may be relevant in the routine assessment of amputation risk in this patient population.

Osteopontin levels in plasma, muscles and bone in patient with non-healing diabetic foot ulcers: a new player in wound healing process?

Osteopontin levels in plasma, muscles and bone in patient with non-healing diabetic foot ulcers: a new player in wound healing process?

Postnatal Skeletal Deletion of Dickkopf-1 Increases Bone Formation and Bone Volume in Male and Female Mice, Despite Increased Sclerostin Expression.

The Wnt antagonist Dickkopf-1 (Dkk1) is a negative regulator of osteoblast function and bone mass. However, because of the lack of appropriate models, many aspects of its role in the regulation of postnatal bone turnover and its cellular source have remained unknown. In this study, we deleted Dkk1 postnatally and in different cell types using various Cre-drivers (Rosa26-ERT2-Cre, Osx-cre, Dmp1-Cre) and assessed to which extent cells of the osteoblastic lineage contribute to the effects of Dkk1 on bone turnover and homeostasis. Female and male mice were examined at 12 weeks of age. Mice with a global or cell type-specific deletion of Dkk1 showed a two- to threefold higher bone volume compared with their Cre-negative littermates. The mineral apposition rate and the bone formation rate were increased two- to fourfold in all three mouse lines, despite a significant increase in systemic and skeletal levels of sclerostin. Dkk1 deletion further reduced the number of osteoclasts about twofold, which was accompanied by a strong decrease in the receptor activator of nuclear factor-κB ligand/osteoprotegerin mRNA ratio in femoral bone. Despite similar increases in bone mass, the deletion of Dkk1 in osterix-expressing cells reduced circulating Dkk1 significantly (males, -79%; females, -77%), whereas they were not changed in Dkk1fl/fl ;Dmp1-Cre mice. However, both lines showed significantly reduced Dkk1 mRNA levels in bone. In summary, we show that lack of Dkk1 in cells of the osteoblastic lineage leads to high bone mass with increased bone formation, despite increased levels of sclerostin. Moreover, the majority of systemic Dkk1 appears to originate from osteoprogenitors but not from mature osteoblasts or osteocytes. Nevertheless, the amount of Dkk1 produced locally by more mature osteogenic cells is sufficient to modulate bone mass. Thus, this study highlights the importance of local Wnt signaling on postnatal bone homeostasis. © 2018 American Society for Bone and Mineral Research.

English

Plants hormones are widely used in agriculture to alter plant characteristics as growth regulators. Gibberellic acid (GA3) plays important role in promoting plant growth, and cell differentiation. This work was performed to investigate the relationship between lipooxidative damage marker (HEL) and bone damage induced by GA3 in adult albino rats. This study was carried out on 20 adult albino rats for 4 weeks treated 6 days/week. The rats were distributed into 2 groups of 10 rats each: Groups I (control) and II (GA3); each rat was treated by GA3 oral gavage (75 ppm) once daily. There was an increase in body and femur weights and length as compared to controls. GA3 caused a decrease in calcium and phosphorus levels in bone while calcium increased and the phosphorus decreased in the plasma. Lipid peroxidation markers caused high femur malondialdehyde levels with decrease in superoxide dismutase, catalase and glutathione peroxidase activities confirmed by histological changes. Immunohistochemical examination for expression of Nε-HEL in bone tissues showed strong positive brown reaction in GA3 treated group when compared with control group that showed negative reaction. GA3 toxicity induced bone damage in adult albino rats. It is recommended to increase public awareness regarding the health impact of gibberellic acid. Key words: Bone, gibberellic acid, lipid per oxidation, Nε-hexanoyl Lysine. &nbsp

Liraglutide exerts a bone-protective effect in ovariectomized rats with streptozotocin-induced diabetes by inhibiting osteoclastogenesis.

Liraglutide, a glucagon-like peptide-1 receptor agonist, is an anti-diabetic medicine associated with a reduced risk of fracture in diabetic patients. In the present study, rats with streptozotocin (STZ)-induced diabetes and/or bilateral ovariectomy (OVX) were treated with liraglutide for eight weeks. Liraglutide treatment increased insulin secretion and managed blood glucose levels in the rats following STZ-induced diabetes. In addition, STZ- and OVX-induced reduction of femoral bone mineral density and destruction of bone microarchitecture were alleviated by liraglutide. STZ decreased, whereas OVX increased, serum osteocalcin (OC) level (a bone formation marker) and osteoblast counts in the trabecular bone. OVX, however not STZ, markedly increased the level of serum c-terminal telopeptide of type 1 collagen (CTX-1, a bone resorption marker) and osteoclast counts in the trabecular area. Liraglutide treatment significantly increased serum OC levels in all three osteoporotic models, however had minimal effects on osteoblast counts. Furthermore, liraglutide significantly decreased serum CTX-1 level and osteoclast numbers in OVX and STZ+OVX rats. Furthermore, the present study examined the mRNA expression and serum concentrations of osteoprotegerin (OPG) and receptor activator of nuclear factor-κB ligand (RANKL), and liraglutide significantly decreased the RANKL/OPG ratio compared with the untreated rats, indicating that osteoclastogenesis was inhibited by liraglutide. In summary, the results suggested that liraglutide ameliorates STZ+OVX-induced bone deterioration in the rat model, primarily through the inhibition of osteoclastogenesis. These preliminary findings propose a potentially beneficial effect of liraglutide on the bone health of postmenopausal diabetic patients.

Stężenie chromu w materiale kostnym człowieka a czynniki biologiczne i środowiskowe

ABSTRAKTWstęp: Celem pracy było poznanie i porównanie stężenia chromu (Cr) w trzech rodzajach materiału kostnego: chrząstce, kości zbitej i kości gąbczastej, pobranego z głowy kości udowej. Ponadto oceniono wpływ czynników ogólnobiologicznych i środowiskowych na stężenie Cr w badanych próbkach.Materiały i metody: Z głowy kości udowej pobranej od pacjentów (n = 37) poddanych alloplastyce stawu biodrowego odseparowano chrząstkę, kość zbitą i gąbczastą, które wysuszono do stałej masy, zmineralizowano w stężonych kwasach i w których oznaczono stężenie Cr metodą spektrofotometrii absorpcji atomowej (ICP-AES).Wyniki: Stężenie Cr w analizowanych próbkach kostnych można ułożyć w następujący malejący szereg: chrząstka < kość zbita < kość gąbczasta. Nie odnotowano zależności pomiędzy wiekiem i płcią badanych pacjentów a stężeniem Cr w próbkach kostnych. U osób pracujących w przemyśle ciężkim wartość stężenia Cr była prawie 30% większa niż u pracowników innych działów gospodarki. Wykazano zależność pomiędzy liczbą wypalanych papierosów (<10 lub ≥20) a stężeniem Cr w kości zbitej. Osoby wypalające ≥20 papierosów dziennie miały znacznie większe stężenia Cr w badanym materiale niż osoby wypalające <10 papierosów dziennie. Nie zaobserwowano istotnych różnic pomiędzy spożyciem dziczyzny, ryb i owoców morza a stężeniem Cr w analizowanych próbkach.Wnioski: Wiele wskazuje na to, że wielkości stężenia chromu w kościach pacjentów poddanych alloplastyce stawu biodrowego mogą być powiązane z czynnikami ogólnobiologicznymi i środowiskowymi, ale niezbędne są szersze i liczniejsze badania w tym zakresie, także w innych krajach Europy Środkowej.

Inducible Wnt16 inactivation: WNT16 regulates cortical bone thickness in adult mice.

Substantial progress has been made in the therapeutic reduction of vertebral fracture risk in patients with osteoporosis, but non-vertebral fracture risk has been improved only marginally. Human genetic studies demonstrate that the WNT16 locus is a major determinant of cortical bone thickness and non-vertebral fracture risk and mouse models with life-long Wnt16 inactivation revealed that WNT16 is a key regulator of cortical thickness. These studies, however, could not exclude that the effect of Wnt16 inactivation on cortical thickness might be caused by early developmental and/or growth effects. To determine the effect of WNT16 specifically on adult cortical bone homeostasis, Wnt16 was conditionally ablated in young adult and old mice through tamoxifen-inducible Cre-mediated recombination using CAG-Cre-ER; Wnt16flox/flox (Cre-Wnt16flox/flox) mice. First, 10-week-old Cre-Wnt16flox/flox and Wnt16flox/flox littermate control mice were treated with tamoxifen. Four weeks later, Wnt16 mRNA levels in cortical bone were reduced and cortical thickness in femur was decreased in Cre-Wnt16flox/flox mice compared to Wnt16flox/flox mice. Then, inactivation of Wnt16 in 47-week-old mice (evaluated four weeks later) resulted in a reduction of Wnt16 mRNA levels, cortical thickness and cortical bone strength with no effect on trabecular bone volume fraction. Mechanistic studies demonstrated that the reduced cortical bone thickness was caused by a combination of increased bone resorption and reduced periosteal bone formation. In conclusion, WNT16 is a crucial regulator of cortical bone thickness in young adult and old mice. We propose that new treatment strategies targeting the adult regulation of WNT16 might be useful to reduce fracture risk at cortical bone sites.

Bone tissue aging affects mineralization of cement lines.

Cement lines are known as thin peripheral boundaries of the osteons. With a thickness below 5 μm their composition of inorganic and organic compounds has been a matter of debate. Here, we hypothesized that cement lines become hypermineralized and their degree of mineralization is not constant but related to the tissue age of the osteon. Therefore, we analyzed the calcium content of osteons and their corresponding cement lines in a range of different tissue ages reflected by osteonal mineralization levels in femoral cortical bone of both postmenopausal women with osteoporosis and bisphosphonate-treated cases. Quantitative backscattered electron imaging (qBEI) showed that cement lines are hypermineralized entities with consistently higher calcium content than their corresponding osteons (mean calcium content: 29.46 ± 0.80 vs. 26.62 ± 1.11 wt%; p < 0.001). Micro-Raman spectroscopy complemented the qBEI data by showing a significantly higher phosphate/amide I ratio in the cement lines compared to the osteonal bone (8.78 ± 0.66 vs. 6.33 ± 0.58, p < 0.001), which was both due to an increased phosphate peak and a reduced amide I peak in cement lines. A clear positive correlation of cement line mineralization and the mineralization of the osteon was observed (r = 0.839, p = 0.003). However, the magnitude of the difference between cement line and osteonal calcium content decreased with increased osteonal calcium content (r = -0.709, p < 0.001), suggesting diverging mineralization dynamics in these osseous entities. The number of mineralized osteocyte lacunae per osteon bone area correlated positively with both osteonal and cement line calcium content (p < 0.01). The degree of mineralization of cement lines may represent another tissue-age related phenomenon, given that it strongly relates to the osteonal mineralization level. Understanding of the cement lines' mineralization and their changes in aging and disease states is important for predicting crack propagation pathways and fracture resistance mechanisms in human cortical bone.

WNT16 overexpression partly protects against glucocorticoid-induced bone loss.

Therapeutic use of glucocorticoids (GCs) is a major cause of secondary osteoporosis, but the molecular mechanisms responsible for the deleterious effects of GCs in bone are only partially understood. WNT16 is a crucial physiological regulator of bone mass and fracture susceptibility, and we hypothesize that disturbed WNT16 activity might be involved in the deleterious effects of GC in bone. Twelve-week-old female Obl-Wnt16 mice (WNT16 expression driven by the rat procollagen type I α1 promoter) and wild-type (WT) littermates were treated with prednisolone (7.6 mg·kg-1·day-1) or vehicle for 4 wk. We first observed that GC treatment decreased the Wnt16 mRNA levels in bone of female mice (-56.4 ± 6.1% compared with vehicle, P < 0.001). We next evaluated if WNT16 overexpression protects against GC-induced bone loss. Dual-energy X-ray absorptiometry analyses revealed that GC treatment decreased total body bone mineral density in WT mice (-3.9 ± 1.2%, P = 0.028) but not in Obl-Wnt16 mice (+1.3 ± 1.4%, nonsignificant). Microcomputed tomography analyses showed that GC treatment decreased trabecular bone volume fraction (BV/TV) of the femur in WT mice ( P = 0.019) but not in Obl-Wnt16 mice. Serum levels of the bone formation marker procollagen type I N-terminal propeptide were substantially reduced by GC treatment in WT mice (-50.3 ± 7.0%, P = 0.008) but not in Obl-Wnt16 mice (-3.8 ± 21.2%, nonsignificant). However, the cortical bone thickness in femur was reduced by GC treatment in both WT mice and Obl-Wnt16 mice. In conclusion, GC treatment decreases Wnt16 mRNA levels in bone and WNT16 overexpression partly protects against GC-induced bone loss.

Citrate Improves Collagen Mineralization via Interface Wetting: A Physicochemical Understanding of Biomineralization Control.

Biological hard tissues such as bones always contain extremely high levels of citrate, which is believed to play an important role in bone formation as well as in osteoporosis treatments. However, its mechanism on biomineralization is not elucidated. Here, it is found that the adsorbed citrate molecules on collagen fibrils can significantly reduce the interfacial energy between the biological matrix and the amorphous calcium phosphate precursor to enhance their wetting effect at the early biomineralization stage, sequentially facilitating the intrafibrillar formation of hydroxyapatite to produce an inorganic-organic composite. It is demonstrated experimentally that only collagen fibrils containing ≈8.2 wt% of bound citrate (close to the level in biological bone) can reach the full mineralization as those in natural bones. The effect of citrate on the promotion of the collagen mineralization degree is also confirmed by in vitro dentin repair. This finding demonstrates the importance of interfacial controls in biomineralization and more generally, provides a physicochemical view about the regulation effect of small biomolecules on the biomineralization front.

Expression of adiponectin in the subchondral bone of lumbar facet joints with different degrees of degeneration

BackgroundOsteoarthritis research has been most commonly performed in the setting of the articular cartilage of the knee. To the best of our knowledge, no studies have evaluated the role of adiponectin in osteoarthritis of the lumbar facet joint (FJOA). Therefore, in this study, we explored whether adiponectin was expressed in the lumbar facet joints and evaluated the role of adiponectin in FJOA.MethodsWe enrolled patients who underwent lumbar computed tomography (CT) and magnetic resonance imaging (MRI) at the Orthopedic Department of the First Affiliated Hospital of Nanchang from May 2015 to June 2016. Lumbar facet joints were obtained from 135 patients at the time of lumbar fusion surgery and divided into three groups according to the Weishaupt grade. Cytokine levels in the subchondral bones were evaluated by enzyme-linked immunosorbent assays (ELISAs), and adiponectin levels were determined by immunohistochemistry, western blotting, and quantitative polymerase chain reaction (qPCR).ResultsBy ELISA, adiponectin levels were examined in the subchondral bone for lumbar facet joint, and adiponectin was found to be negatively correlated with BMI in 52 patients (p < 0.001, r = −0.861). By immunohistochemistry analysis, adiponectin was found to be expressed in the subchondral bone of the lumbar facet, whereas the cartilage area was negative for adiponectin expression. Immunostaining intensity and area was related to the degeneration of the lumbar facet joint, and, in our research, considerably decreased staining intensity and area were observed in more severely degenerated lumbar facet joints. Furthermore, the expression of adiponectin was also reduced in degenerated lumbar facet joints, and the level of decline corresponded to degeneration detected by western blotting and qPCR analysis (n = 27, p < 0.0001).ConclusionsAdiponectin expression was observed in the subchondral bone of the lumbar facet joint and decreased as the degree of degeneration increased. Thus, the results of this study provide new insights into the relationship between adiponectin and osteoarthritis.

Studying hepcidin and related pathways in osteoblasts using a mouse model with insulin receptor substrate 1‑loss of function.

Hepcidin is one of the most important proteins in iron metabolism. In the present study, its role in iron metabolism and the associated signaling pathways involved was investigated in a mouse model with insulin receptor substrate 1‑loss of function (IRS‑/‑), and osteoblasts in the iron overload condition. Protein expression levels of hepcidin, interleukin 6 (IL‑6), bone morphogenetic protein receptor 1α and ferritin demonstrated a significant increase in the liver of the IRS‑/‑ mice compared with the IRS+/‑ and IRS+/+ mice. Hepcidin levels in the jaw bone were also increased in the IRS‑/‑ mice (although not significantly). Furthermore, mRNA expression levels of bone morphogenetic protein 6 (BMP6) and ferroportin (FPN) were significantly increased in the liver of the IRS‑/‑ mice compared with the other two models, but no significant differences were observed in the transferrin receptor mRNA expression levels. Additionally, the mRNA expression of hepcidin, FPN and IL‑6 was upregulated in osteoblasts after ferric ammonium citrate exposure, while the mRNA expression of BMP6 was inhibited. Collectively, the results of the present study indicated that hepcidin is involved in iron metabolism in IRS‑1‑/‑ mice via the signaling pathways involving BMP6 and IL‑6. Furthermore, hepcidin is also involved in iron metabolism in osteoblasts under iron overload conditions. Therefore, hepcidin and its associated signaling pathway proteins may represent potential targets for the treatment of conditions associated with iron overload.

Expression of the deubiquitinase cylindromatosis in articular cartilage and subchondral bone is associated with the severity of knee osteoarthritis.

Cylindromatosis (CYLD) is a deubiquitinating enzyme that regulates multiple key signaling pathways involved in the pathophysiology of knee osteoarthritis (KOA). Previous studies have indicated that the expression of CYLD in the articular cartilage of patients with KOA is significantly higher than in healthy controls. However, limited data are available regarding the association between CYLD expression and the severity of KOA. The aim of the present study was to investigate the association between CYLD expression in joint tissues and the severity of KOA. A total of 156 individual tibial plateau samples were obtained between January 2011 and January 2016 from patients that had undergone total knee arthroplasty due to KOA or from healthy controls. The severity of KOA was evaluated using the Kellgren Lawrence (KL) and Mankin scoring systems. Additionally, CYLD expression in the articular cartilage and subchondral bone was analyzed using immunohistochemistry. Compared with the healthy controls, patients with KOA exhibited significantly increased CYLD levels in the articular cartilage (6.53±2.01 vs. 28.69±13.23, P<0.001) and significantly decreased CYLD levels in the subchondral bone (11.46±2.34 vs. 3.50±2.54, P<0.001). Correlation analysis indicated that CYLD expression in the articular cartilage was positively correlated with the KL (r=0.837, P<0.001) and Mankin scores (r=0.925, P<0.001), while its expression in the subchondral bone was negatively correlated with the KL (r=−0.802, P<0.001) and Mankin scores (r=−0.844, P<0.001). The results of the present study demonstrate that CYLD levels in the articular cartilage and subchondral bone are associated with the severity of KOA. Thus, CYLD may be a potential diagnostic and predictive biomarker for KOA and a novel target in its treatment.

Investigation of the effect of astaxanthin on alveolar bone loss in experimental periodontitis.

Astaxanthin is a keto-carotenoid that has a strong antioxidant effect. The purpose of this study was to evaluate the effects of astaxanthin on alveolar bone loss and histopathological changes in ligature-induced periodontitis in rats. Wistar rats were divided into four experimental groups: non-ligated (C, n=6); ligature only (L, n=6); ligature and astaxanthin (1mg/kg/day astaxanthin, AS1 group, n=8); ligature and astaxanthin (5mg/kg/day astaxanthin, AS5 group, n=8). Silk ligatures were placed at the gingival margin of lower first molars of the mandibular quadrant. The study duration was 11days and the animals were killed at the end of this period. Changes in alveolar bone levels were clinically measured and tissues were immunohistochemically examined, osteocalcin, bone morphogenic protein-2, inducible nitric oxide synthase, Bax and bcl-2 levels in alveolar bone and tartrate-resistant acid phosphatase-positive osteoclast cells, osteoblast and inflammatory cell counts were determined. Alveolar bone loss was highest in the L group and the differences among the L, AS1 and AS5 groups were also significant (P<.05). Both doses of astaxanthin decreased tartrate-resistant acid phosphatase-positive+ osteoclast cell and increased osteoblast cell counts (P<.05). The inflammation in the L group was also higher than those of the C and AS1 groups were (P<.05) indicating the anti-inflammatory effect of astaxanthin. Although inducible nitric oxide synthase, osteocalcin, bone morphogenic protein-2 and bax staining percentages were all highest in the AS5 group and bcl-2 staining percentage was highest in the AS1 group, values were close to each other (P>.05). Within the limits of this study, it can be suggested that astaxanthin administration may reduce alveolar bone loss by increasing osteoblastic activity and decrease osteoclastic activity in experimental periodontitis model.

Utrata kości wokół implantów z łącznikiem stożkowym lub heksagonalnym – przegląd piśmiennictwa

Based on a review of topical literature, the paper presents the results of studies concerning marginal bone loss around dental implants. The paper provides a detailed description of the process of bone loss around dental implants with conical implant-abutment connection generally used in implant prosthetic treatment. The reviewed articles reported experimental studies involving animals, as well as clinical research in humans. The results concerning bone loss around the hexagonal implant-abutment interface are cited only to provide the historical background, as implants with internal connections are generally available and currently used in oral implantology. The research on bone loss around implants conducted over the years has allowed for the assessment of the relationships between various factors that may affect the process of bone loss around implants and, consequently, influence the final result of the treatment and therapeutic success. The researchers focused on the effect of such factors as: differences in implant structure, types of surfaces, shapes and materials. In addition, bone loss is dependent on prosthetic treatment: implants may be placed at different locations in the alveolar process bone and at different levels in the hard bone; open or closed methods of healing are used; types of prosthetic restorations loaded after implantation vary, as also varies the time from implantation to loading (early or late loading), types of cementing material and cementing techniques. The paper discusses also the presence of a microgap and its colonization by microorganisms as factors that negatively affect the process of osseointegration.

Cytoprotective Effects of the Red Marine Alga Chondrus canaliculatus Against Maneb-Induced Hematotoxicity and Bone Oxidative Damages in Adult Rats

The current study aimed at evaluating the ability of a mineral and antioxidant-rich extract from Chondrus canaliculatus to improve maneb (MB)-induced toxicity in adult rat. The animals were divided into four groups: group 1 used as a control group, group 2 received MB, group 3 received MB + C. canaliculatus extract, and group 4 received only the algal extract. MB, a Mn-containing ethylene-bis-dithiocarbamate fungicide, induced oxidative stress damages, mineral perturbations in the plasma, urine, and bone, and genotoxicity in rats. Hematological analysis revealed in the MB-treated group a disruption in the number of red blood cells, platelets, and white blood cells associated with a striking genotoxicity. Interestingly, a significant increase in malondialdehyde and advanced oxidation protein product levels in erythrocytes and bones were found. On the other hand, an impairment of the antioxidant status in both tissues was occurred. Along, our results revealed that MB injection caused a striking drop and disruption in bone's mineral rates, especially calcium and phosphorus. These biochemical results were in accordance with the histological and molecular changes. However, co-treatment with C. canaliculatus extract showed, for the first time, that this alga was effective against MB-induced hematotoxicity, genotoxicity, and oxidative stress in the blood and bone and maintained osteomineral metabolism and bone histo-architecture. Such observations might be explained by the strong in vitro antioxidant and antibacterial activities exhibited by the alga, as well as by its high levels in several minerals: calcium, phosphorus, sodium, potassium, magnesium, iron, and zinc.