***TASK*** the task is to summarize an input biomedical literature in six sentences 
    ***INPUT*** the input is a biomedical literature 
    ***OUTPUT*** the output is the summary of an input biomedical literature in six sentences 
    ***DOCUMENTATION*** 
    ***EXAMPLES*** 
    Input: Abstract . Glucocorticoid-induced osteoporosis has been reported to be caused by enhanced bone resorption and suppressed bone formation . To clarify whether administration of vitamin K , which enhances bone formation , prevents prednisolone-induced loss of bone mineral density ( BMD ) , a r and omized , prospect i ve , controlled study was conducted on 20 patients with chronic glomerulonephritis scheduled for treatment with prednisolone .  All patients were initially treated with 0.8 mg/kg body weight/day of prednisolone ( maximum of 40 mg ) for 4 weeks , tapering to 20 mg/day over approximately 6 weeks . Ten patients received prednisolone alone ( Group 1 ) , and the other 10 patients received prednisolone plus 15 mg of menatetrenone , vitamin K , three times per day ( Group 2 ) . BMD of the lumbar spine measured by dual-energy X-ray absorptiometry ( DXA ) and biochemical markers of bone metabolism in blood and urine were evaluated before and 10 weeks after administration of prednisolone alone or with menatetrenone . In Group 1 , treatment with prednisolone significantly reduced BMD of the lumbar spine from 1.14 ± 0.12 to 1.10 ± 0.11 g/cm2 ( P= 0.0029 ) . Serum intact osteocalcin and procollagen type I C-peptide ( PICP ) concentrations , biochemical markers of bone formation , were markedly reduced . A biochemical marker of bone resorption , urinary excretion of deoxypyridinoline , was significantly reduced . In Group 2 , prednisolone-induced  reduction of BMD was prevented by menatetrenone administration ( 1.09 ± 0.09 to 1.07 ± 0.07 g/cm2 , P= 0.153 ) . Menatetrenone prevented reduction of PICP concentration  by prednisolone but not in serum intact osteocalcin concentration and urinary excretion of deoxypyridinoline . Thus , treatment with prednisolone result ed in loss of BMD of the lumbar spine associated with suppression of both bone formation and bone resorption . Menatetrenone is a useful agent in preventing prednisolone-induced loss of BMD We have recently demonstrated that glucocorticoid ( GC ) suppresses bone formation and enhances bone resorption , with result ant bone loss . This altered bone turnover is not due to the action of parathyroid hormone ( PTH ) , but appears to be related to the suppression of osteoprotegerin ( OPG ) . As vitamin K2 ( menatetrenone ) has been used for the treatment of osteoporosis , the present study was carried out to evaluate the effect of vitamin K2 on GC-induced bone loss . Twenty patients with chronic glomerulonephritis treated with GC for the first time were chosen for this study . Ten patients received GC alone  ( group A ) and the other 10 patients each received 15 mg of vitamin K2 per day in addition to GC ( group B ) . Markers of bone metabolism , including serum OPG , osteocalcin ( OC ) , bone-specific alkaline phosphatase activity ( BAP ) , PTH , tartrate-resistant acid phosphatase ( TRAP ) , and bone mineral density ( BMD ) , were measured before and during the treatment . OPG was significantly decreased in group A ( P < 0.001 ) , while no significant change was seen in group B. TRAP was markedly increased in both groups , more particularly in group A ( P < 0.01 ) . PTH was decreased in group A , but was increased in group B. OC was decreased at month 1 but subsequently increased until month 12 in both groups . BAP had decreased at month 3 in group A ( P < 0.05 ) , but not in group B. BMD of the lumbar spine was significantly reduced after 6 months ( P < 0.01 ) , and 12 months ( P < 0.001 ) of treatment in group A , whereas there was no remarkable change in group B. The present study demonstrated that the inhibition exerted by vitamin K2 of the reduction in OPG induced by GC may , at least in part , play a role in the prevention and treatment of GC-induced  bone loss The purpose of this study was to evaluate the influence of gamma-glutamyl transferase ( GGCX ) gene polymorphisms on the response of serum undercarboxylated osteocalcin ( ucOC ) and bone turnover markers 3 months after treatment with menatetrenone .  One hundred and forty postmenopausal Thai women were enrolled and assigned to receive 45 mg/day treatment of menatetrenone ( MK-4 ) concurrently with calcium 1.2 g and vitamin D 400 IU for 3 months . Demographic characteristics , GGCX genotyping , serum bone turnover markers and ucOC levels were obtained from all participants at baseline . We evaluated the reduction of ucOC at 3 months and the reduction of beta-CTx and P1NP at 1 and 3 months . The responses were compared between the different genotypes of GG and GA + AA groups . There was a significant reduction of serum ucOC , beta-CTx and P1NP from the baseline at 3 months ( p < 0.001 ) though there was no significant difference between genotypes ( GG vs. GA + AA ; p > 0.05 ) . Nonetheless , a subgroup analysis of postmenopausal women who 65 years of age or over ( N = 37 ) revealed a significant difference between the two groups in the reduction of ucOC .  Menatetrenone significantly reduced serum ucOC as well as beta-CTX and P1NP from the baseline . GGCX polymorphism appeared to have an influence over the reduction of ucOC especially in older women ( age ≥65 ) . Furthermore , the groups which have “ A ” allele trend to being more efficient in reducing the serum ucOC level than the group which does not have it Vitamin K contributes to bone health , probably through its role as cofactor in the carboxylation of osteocalcin . Intervention studies in adults have demonstrated that markedly higher osteocalcin carboxylation is obtained by intakes of vitamin K well above the current recommended dietary intake . However , the relationship between increased vitamin K2 intake and enhanced osteocalcin carboxylation has never been shown in healthy children . The objective was to study the effect of 45 microg menaquinone-7 ( MK-7 ; one of the vitamin K2 species ) on the circulating levels of undercarboxylated osteocalcin ( ucOC ) and carboxylated osteocalcin ( cOC ) in healthy prepubertal children . We hypothesised that MK-7 supplementation will reduce the ucOC : cOC ratio ( UCR ) , indicating an improved vitamin K status . The present study is a double-blind r and omised placebo-controlled trial examining the effect of 8 weeks MK-7 supplementation on the carboxylation of osteocalcin in healthy children ( n 55 ) .  Serum levels of ucOC , cOC and MK-7 were measured at baseline and after 8 weeks , together with bone markers and coagulation parameters . The UCR was used as an indicator of vitamin K status . In the MK-7-supplemented  group ( n 28 ) , the circulating concentration of inactive ucOC reduced and the UCR improved whereas the concentration of MK-7 increased . Within the placebo group , ucOC , cOC , UCR and MK-7 did not significantly change over time . In both groups , bone markers and coagulation parameters remained constant over time . These findings demonstrate that in healthy , prepubertal children , modest supplementation with MK-7 increases circulating concentrations of MK-7 and increases osteocalcin carboxylation It has been previously shown that the level of circulating undercarboxylated osteocalcin ( ucOC ) is elevated in elderly women in comparison with young , healthy , premenopausal ones . To underst and the mechanism of the increase in the ucOC in the elderly and to assess its potential consequences on bone fragility , we have measured  ucOC  in the sera of 195 elderly institutionalized women 70 - 101 yr of age . In 45 women ( 23 % ) serum ucOC was above the upper limit of the normal range for young women . The level of ucOC was negatively correlated with 25OHD ( r = -0.32 , P < 0.001 ) even after excluding the effect of age , parathyroid hormone ( PTH ) , and creatinine by partial correlation ( r = -0.24 , P < 0.002 ) . During an 18-mo follow-up , 15 women sustained a hip fracture and their baseline ucOC level was higher ( P < 0.01 ) in women who subsequently sustained hip fracture than in the nonfracture group contrasting with no significant differences for serum calcium , phosphate , alkaline phosphatase , creatinine , PTH , 250HD , and total and carboxylated OC . The risk of hip fracture was increased in women with elevated ucOC ( relative ratio 5.9 , 99.9 % Cl 1.5 - 22.7 , P < 0.001 ) . During 1 yr of calcium/vitamin D2 treatment , ucOC decreased ( P < 0.05 ) , especially in those with the initially increased values ( from 2.22 + /- 0.35 to 1.41 + /- 0.29 ng/ml , P < 0.005 ) contrasting with an increase in the placebo group ( P < 0.05 ) . In conclusion , the increase in ucOC in the elderly reflects not only some degree of vitamin K deficiency but also their poor vitamin D status , suggesting that vitamin D may be important , either directly or indirectly through its effect on bone turnover , for achieving a normal gamma-carboxylation of OC . The ucOC , but not conventional calcium metabolism parameters , predicts the subsequent risk of hip fracture , suggesting that serum ucOC reflects some changes in bone matrix associated with increased fragility BACKGROUND Vitamin K mediates the gamma-carboxylation of glutamyl residues on several bone proteins , notably osteocalcin . High serum concentrations of undercarboxylated osteocalcin and low serum concentrations of vitamin K are associated with lower bone mineral density and increased risk of hip fracture . However , data are limited on the effects of dietary vitamin K. OBJECTIVE We investigated the hypothesis that high intakes of vitamin K are associated with a lower  risk of hip fracture in women . DESIGN We conducted a prospect i ve analysis within the Nurses ' Health Study cohort . Diet was assessed in 72327 women aged 38 - 63 y with a food-frequency question naire in 1984 ( baseline ) . During the subsequent 10 y of follow-up , 270 hip fractures result ing from low or moderate trauma were reported . RESULTS Women in quintiles 2 - 5 of vitamin K intake had a significantly lower age-adjusted relative risk ( RR : 0.70 ; 95 % CI : 0.53 , 0.93 ) of hip fracture than women in the lowest quintile ( < 109 microg/d ) . Risk did not decrease between quintiles 2 and 5 and risk estimates were not altered when other risk factors for osteoporosis , including calcium and vitamin D intakes , were added to the models . Risk of hip fracture was also inversely associated with lettuce consumption ( RR : 0.55 ; 95 % CI : 0.40 , 0.78 ) for one or more servings per day compared with one or fewer servings per week ) , the food that contributed the most to dietary vitamin K intakes . CONCLUSIONS Low intakes of vitamin K may increase the  risk of hip fracture in women . The data support the suggestion for a re assessment of the vitamin K requirements that are based on bone health and blood coagulation Vitamin K is required for the carboxylation of Gla-proteins in the liver ( coagulation factors ) and extra-hepatic tissues , such as bone ( osteocalcin , OC ) , and arterial wall ( matrix Gla-protein , MGP ) . Although the coagulation factors are essentially fully carboxylated under normal conditions , 10 - 40 % of OC and MGP remains undercarboxylated . We were therefore interested to study the dose-response effects of extra intake of menaquinones on the carboxylation of the extra-hepatic Gla-proteins . A total of forty-two healthy Dutch men and women aged between 18 and 45 years were r and omised into seven groups to receive : placebo capsules or menaquinone-7 ( MK-7 ) capsules at a daily dose of 10 , 20 , 45 , 90 , 180 or 360 μg . Circulating uncarboxylated OC ( ucOC ) , carboxylated OC ( cOC ) and desphospho-uncarboxylated MGP were measured by ELISA  . The ucOC : cOC ratio was calculated from circulating ucOC and cOC values . Endogenous thrombin potential and peak height were determined by calibrated automated thrombography . To increase the statistical power , we collapsed the treatment groups into three dosage groups : placebo , low-dose supplementation ( doses below RDA , Commission Directive 2008/100/EC ) , and high-dose supplementation ( doses around RDA , Commission Directive 2008/100/EC ) . MK-7 supplementation at doses in the order of the RDA ( Commission Directive 2008/100/EC ) increased the carboxylation 
    Output:
    
A meta- analysis study , but not a systematic review study , showed efficacy against vertebral and non-vertebral fractures mainly in postmenopausal women with osteoporosis .
There was no available evidence for men with osteoporosis .
The present review of the literature revealed some evidence of a positive effect of menatetrenone on the skeleton of postmenopausal women and in patients treated with glucocorticoid .
EXPERT OPINION Menatetrenone is considered to be a second-line medicine for postmenopausal osteoporotic women with an increased risk for vertebral fractures