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Objectives: This study aimed to determine the optimal dose of quercetin (plant origin) on growth performance, nutrient digestibility, meat composition, shank mineralization, and production costs in broilers. Materials and Methods: A total of 180 day-old, mixed-sex Ross 308 chicks were randomly assigned to four dietary groups, with five replicates of nine birds per group. The corn-soy-based basal diet provided 2998 kcal metabolizable energy (ME)/kg and 22.94% crude protein (CP) in the starter diet and 3120 kcal ME/kg and 21.25% CP in the grower diet. The basal diet was supplemented with quercetin at 0.00, 0.40, 0.80, or 1.20 gm/kg, corresponding to the 0.00Q (control), 0.40Q, 0.80Q, and 1.20Q groups, respectively. Results: Quercetin supplementation at increasing levels improved feed intake and body weight gain, increased conversion ratios (feed, CP, and ME), and increased meat fat content, with the 1.20Q group showing the greatest effects (p ≤ 0.05). However, there were no significant differences among the quercetin-supplemented groups. Moreover, quercetin supplementation had no impact on broiler dressing yield (DY), drip loss, meat components (dry matter (DM), CP, and ash), shank DM, and ash percentages (p > 0.05). Shank dry weight, DM, ash yield, and nutrient digestibility were significantly improved in the 1.20Q group compared to the control and 0.40Q groups (p < 0.05). Quercetin supplementation at increasing levels significantly increased feed and quercetin costs but improved profit and the benefit-cost ratio (BCR), with the 1.20Q group showing the greatest improvement (p < 0.05). Conclusions: Supplementation at 1.20 gm quercetin/kg diet improved growth performance, digestibility, shank mineralization, and BCR, but had no significant effect on DY and meat composition except for fat content.

The present study investigated the effect of Azomite (AZO) on the growth performance, nutrient utilisation, and bone mineralisation of broilers fed low protein diet. A total number of 180 one-day-old male chicks were randomly distributed to three treatment groups having six replicates of 10 birds each. Experimental diets included; positive control (PC) with 21.5% CP (starter) and 19.0% CP (finisher), negative control (NC) with 2% lower CP than PC in each period and treatment group (AZO-0.25) in which NC was supplemented with 0.25% AZO. Azomite significantly (p < .05) improved live body weight, average daily gain and feed conversion ratio, but not the feed intake, as compared to NC. Eviscerated, breast muscle and leg muscle percentages were significantly (p < .05) higher in the birds fed AZO-0.25 than NC, while abdominal fat (AF) percentage was significantly (p > .05) higher in NC. Azomite improved the digestibility of dry matter (DM), crude protein (CP), apparent metabolisable energy (AME), calcium (Ca) and phosphorus (P) (p < .05) compared to the NC. Trypsin activity was increased (p < .05) in birds fed diet with AZO-0.25 compared with NC. Blood creatinine, growth hormone (GH) and calcitonin (CT) was also higher (p < .05) in birds supplemented with AZO-0.25. Treatment also affected (p < .05) the tibia breaking strength (TBS), ash, Ca and P contents. Overall, AZO improved the growth performance, nutrient utilisation and tibia mineralisation in broilers fed with low CP diet, which looks an economically promising approach. HIGHLIGHTS The dietary supplementation of Azomite improved the growth and nutrient utilisation in broiler chicken. The efficiency of digestive enzymes and digestibility was enhanced by dietary Azomite. Dietary Azomite improved the tibia breaking strength and bone mineralisation in broiler chicken.

Coccidial infections reduce fat-soluble vitamin status and bone mineralisation in broiler chickens. We hypothesised that broilers infected with Eimeria maxima would benefit from increased dietary supplementation with vitamin D (vitD) or with 25-hydroxycholecalciferol (25(OH)D3 or 25D3). Broilers were assigned to diets with low (L) or commercial (M) vitD levels (25 v. 100 μg/kg) supplemented as cholecalciferol (D3) or 25D3. At day 11 of age, birds were inoculated with water or 7000 E. maxima oocysts. Pen performance was calculated over the early (days 1–6), acute (days 7–10) and recovery periods (days 11–14) post-infection (pi). At the end of each period, six birds per treatment were dissected to assess long bone mineralisation, plasma levels of 25D3, Ca and P, and intestinal histomorphometry. Parasite replication and transcription of cytokines IL-10 and interferon-γ (IFN-γ) were assessed at day 6 pi using quantitative PCR. Performance, bone mineralisation and plasma 25D3 levels were significantly reduced during infection (P < 0·05). M diets or diets with 25D3 raised plasma 25D3, improved performance and mineralisation (P < 0·05). Offering L diets compromised feed efficiency pi, reduced femur breaking strength and plasma P levels at day 10 pi in infected birds (P < 0·05). Contrastingly, offering M diets or diets with 25D3 resulted in higher parasite loads (P < 0·001) and reduced jejunal villi length at day 10 pi (P < 0·01), with no effect on IL-10 or IFN-γ transcription. Diets with M levels or 25D3 improved performance and mineralisation, irrespective of infection, while M levels further improved feed efficiency and mineralisation in the presence of coccidiosis.

The aim of studywas to compare efficacy of 1-α(OH)D3 alone or in combination with phytase and 1-α(OH)D3 in combination of phytase and different concentration of cholecalciferol on performance, tibia parameters, andplasma minerals of quails fed Ca-P deficient diet. A total of 280 mixed sex 5-d-old quails were allocated to 7 treatments with 5 replicates. The vitamin supplement which incorporated to basal diet did not contain cholecalciferol. The dietary treatments were as follows: Ca-P deficient diet (basal diet); basal diet + 500 FTU phytase/kg of diet; basal diet + phytase + 5 μg of 1-α(OH)D3 kg-1 of diet;basal diet + phytase + 5 μg of 1-α(OH)D3 and 250, 500, 750 and 1,000 IU of cholecalciferol kg-1of diet. The highest final body weight and the best feed conversion ratioobtained in the group supplemented with 1,000 IU cholecalciferol kg-1 of diet (p < 0.05). Supplementation of 1-α(OH)D3 alone or in combination with phytase and phytase and different concentration of cholecalciferol could improve tibia parameters (p < 0.05). In conclusion, supplementation of 1-α(OH)D3 alone to Ca-P deficient diet could maximize tibia mineralization, whereas it couldn't maximize performance, performance criteria were maximized by supplementation of 1,000 IU cholecalciferol kg-1 of diet.

Bone metabolism fluctuates throughout the reproductive cycle of sows to enable foetal growth and milk production. Although increased bone mineralisation is conceivable in sows during reproduction, a study of mineralisation in function of parity has not been performed. This study evaluated the fluctuations of markers for bone metabolism in primiparous and multiparous sows throughout a reproductive cycle. The experiment included ten multiparous and five primiparous commercial hybrid sows from one herd. The sows were monitored for one reproductive cycle and fed according to commercial dietary standards. Blood samples were taken in the morning before feeding at fixed time intervals before (day -5) and during gestation (insemination (day 0), 21, 42, 63, 84), around parturition (day 108, 112, parturition (115), 118), and during lactation (day 122, 129, 143). Serum osteocalcin (OC) concentration increased in early and mid-gestation (P=0.002) and decreased at the end of gestation (P=0.001), whereas crosslaps (CTX) concentration decreased during early and mid-gestation (P=0.002) and increased towards the end of gestation (P=0.001). Towards the end of lactation serum levels of both markers increased (P=0.007 and 0.013, respectively). For hydroxyproline (HYP) no significant fluctuation in function of the reproductive cycle was detected. Matrix metalloproteinase 2 (MMP2) concentration increased towards parturition for both primiparous and multiparous sows (P=0.001), whereas during lactation no significant fluctuations in function of the reproductive cycle were found. A parity effect was found for OC and CTX (P<0.010), but not for the other markers. These results demonstrate that bone metabolism differed between primiparous and multiparous sows, although in both groups a similar fluctuation throughout the reproductive cycle was observed.

Cortical bone structure is a crucial determinant of bone strength, yet for many years studies of novel genes and cell signalling pathways regulating bone strength have focused on the control of trabecular bone mass. Here we focus on mechanisms responsible for cortical bone development, growth, and degeneration, and describe some recently described genetic-driven modifications in humans and mice that reveal how these processes may be controlled. We start with embryonic osteogenesis of preliminary bone structures preceding the cortex and describe how this structure consolidates then matures to a dense, vascularised cortex containing an increasing proportion of lamellar bone. These processes include modelling-induced, and load-dependent, asymmetric cortical expansion, which enables the cortex’s transition from a highly porous woven structure to a consolidated and thickened highly mineralised lamellar bone structure, infiltrated by vascular channels. Sex-specific differences emerge during this process. With aging, the process of consolidation reverses: cortical pores enlarge, leading to greater cortical porosity, trabecularisation and loss of bone strength. Each process requires co-ordination between bone formation, bone mineralisation, vascularisation, and bone resorption, with a need for locational-, spatial- and cell-specific signalling pathways to mediate this co-ordination. We will discuss these processes, and a number of cell-signalling pathways identified in both murine and human genetic studies to regulate cortical bone mass, including signalling through gp130, STAT3, PTHR1, WNT16, NOTCH, NOTUM and sFRP4.

Abstract Osteogenesis imperfecta (OI) is a phenotypically and genetically heterogeneous skeletal dysplasia characterized by bone fragility, growth deficiency, and skeletal deformity. Previously known to be caused by defects in type I collagen, the major protein of extracellular matrix, it is now also understood to be a collagen-related disorder caused by defects in collagen folding, posttranslational modification and processing, bone mineralization, and osteoblast differentiation, with inheritance of OI types spanning autosomal dominant and recessive as well as X-linked recessive. This review provides the latest updates on OI, encompassing both classical OI and rare forms, their mechanism, and the signaling pathways involved in their pathophysiology. There is a special emphasis on mutations in type I procollagen C-propeptide structure and processing, the later causing OI with strikingly high bone mass. Types V and VI OI, while notably different, are shown to be interrelated by the interferon-induced transmembrane protein 5 p.S40L mutation that reveals the connection between the bone-restricted interferon-induced transmembrane protein-like protein and pigment epithelium-derived factor pathways. The function of regulated intramembrane proteolysis has been extended beyond cholesterol metabolism to bone formation by defects in regulated membrane proteolysis components site-2 protease and old astrocyte specifically induced-substance. Several recently proposed candidate genes for new types of OI are also presented. Discoveries of new OI genes add complexity to already-challenging OI management; current and potential approaches are summarized. Graphical Abstract Graphical Abstract

Over 200 million people suffer from osteoporosis worldwide. Individuals with osteoporosis have increased rates of bone resorption while simultaneously having impaired osteogenesis. Most current treatments for osteoporosis focus on anti-resorptive methods to prevent further bone loss. However, it is important to identify safe and cost-efficient treatments that not only inhibit bone resorption, but also stimulate anabolic mechanisms to upregulate osteogenesis. Recent data suggest that macrophage polarization may contribute to osteoblast differentiation and increased osteogenesis as well as bone mineralization. Macrophages exist in two major polarization states, classically activated macrophages (M1) and alternatively activated macrophage (M2) macrophages. The polarization state of macrophages is dependent on molecules in the microenvironment including several cytokines and chemokines. Mechanistically, M2 macrophages secrete osteogenic factors that stimulate the differentiation and activation of pre-osteoblastic cells, such as mesenchymal stem cells (MSC’s), and subsequently increase bone mineralization. In this review, we cover the mechanisms by which M2 macrophages contribute to osteogenesis and postulate the hypothesis that regulating macrophage polarization states may be a potential treatment for the treatment of osteoporosis.

Risedronate is used in osteoporosis treatment. Postmenopausal women enrolled in the Vertebral Efficacy with Risedronate Therapy trial received either risedronate (5 mg/day) or placebo for 3 years. Subjects received calcium and vitamin D supplementation if deficient at baseline. Lumbar spine bone mineral density (BMD) was measured at baseline and at 3 years. Quantitative back-scattered electron imaging (qBEI) was performed on paired iliac crest biopsies (risedronate, n = 18; placebo, n = 13) before and after treatment, and the mineral volume fraction in the trabecular bone was calculated. Combining dual-energy X-ray absorptiometric values with the mineral volume fraction for the same patients allowed us to calculate the relative change in trabecular bone volume with treatment. This showed that the effect on BMD was likely to be due partly to changes in matrix mineralization and partly due to changes in bone volume. After treatment, trabecular bone volume in the lumbar spine tended to increase in the risedronate group (+2.4%, nonsignificant) but there was a significant decrease (-3.7%, P < 0.05) in the placebo group. Calcium supplementation with adequate levels of vitamin D led to an approximately 3.3% increase in mineral content in the bone material independently of risedronate treatment. This increase was larger in patients with lower matrix mineralization at baseline and likely resulted from correction of calcium/vitamin D deficiency as well as from reduced bone remodeling. Combining BMD and bone mineralization density distribution data show that in postmenopausal osteoporosis 3-year treatment with risedronate preserves or may increase trabecular bone volume, unlike placebo. This analysis also allows, for the first time, separation of the contributions of bone volume and matrix mineralization to the increase in BMD.

This study aimed to analyze the morphology of bone graft granules, the presence of granule demineralization, and bone morphology in retrieved human maxillary sinus bone graft biopsies. Healthy patients underwent sinus bone augmentation using lateral access. Two different dimensions of the antrostomy were performed, a 4 mm or 8 mm height. After 6 months, all sites received one implant using a flap technique, crestal positioning, and submerged healing. Implant biopsies were retrieved after 3 months and were histologically processed. The ESEM analysis was performed on the entire portion of the peri-implant bone (up to 750 µm from the implant thread). Three different regions of interest (ROIs) were selected: the coronal, middle, and apical portions of the implant. In these areas, EDX was performed, and calcium (Ca), phosphate (P), nitrogen (N), and their atomic ratios (Ca/P, Ca/N, and P/N) were calculated. Different bone tissue electron-dense areas were detected through grayscale intensity quantification of ESEM images with different organic (N) or inorganic (Ca,P) compositions. A total of 16 biopsies from 16 healthy patients were analyzed. Bone graft granules were mostly detected in the apical ROI. New bone tissue bridges were detected in the apical and middle ROI. These structures, with lower Ca/N and P/N ratios, were connected and enveloped the bone graft granules. Cortical ROI revealed the most mineralized bone tissue. Conclusions: After 9 months, bone graft resorption was only partially completed and new bone tissue appeared less mineralized in the middle and apical ROI than in the coronal ROI.