title: Changes in bone mass and bone turnover following ankle fracture.
abstract: Bone loss and increased bone turnover are recognized local changes after a fracture, but the exact patterns of these changes after different fractures are unclear. We aimed to investigate the changes in bone density and biochemical markers following ankle fracture. Fourteen subjects (7 postmenopausal women and 7 men, mean age 63 years) were recruited following fracture of the distal tibia and fibula. Bone mineral density (BMD) of the ankle and proximal femur were measured by dual-energy X-ray absorptiometry (DXA) and quantitative ultrasound (QUS) of the calcaneus at 0, 6, 12, 26 and 52 weeks after fracture. Serum and urine samples were collected at 0, 3 and 7 days and at 2, 4, 6, 12, 26 and 52 weeks after fracture to measure markers of bone turnover. For bone formation we measured: bone alkaline phosphatase (iBAP), osteocalcin (Oc), procollagen type I N-terminal propeptide (PINP); and for bone resorption: tartrate-resistant acid phosphatase (TRAcP), deoxypyridinoline (iFDpd), N-telopeptides of type I collagen (NTx). We used the nonfractured limb to calculate values for baseline BMD and QUS. There was a significant decrease in BMD at the ultradistal ankle (p<0.001), the trochanteric region of the hip (p<0.01) and QUS of the heel after ankle fracture. This bone loss was maximal for ultradistal ankle BMD by 6 weeks at 13% (p<0.001) and for the trochanter by 26 weeks at 3% (p<0.01). The ankle BMD returned to baseline at 52 weeks but the trochanter BMD did not. Velocity of sound (VOS) decreased at 6 weeks by 2% (p<0.01) and broadband ultrasound attenuation (BUA) by 15% (p<0.01). VOS recovered completely by 52 weeks, but BUA did not return to baseline. Bone formation markers increased significantly between 1 and 4 weeks by 11-78% (p<0.01), and iBAP returned to baseline at 52 weeks but PINP and Oc remained elevated. Bone resorption markers did not increase and NTx was decreased at 52 weeks. We conclude that BMD decreased distal and immediately proximal to the fracture line when measured with DXA and QUS. Ankle BMD and heel VOS recovered at 52 weeks (trochanteric BMD and heel BUA did not) and the bone turnover markers returned toward baseline.
authors.affiliation: Bone Metabolism Group, Section of Medicine, Division of Clinical Sciences, University of Sheffield, UK.
authors.forename: B M
authors.initials: BM
authors.lastname: Ingle
authors.forename: S M
authors.initials: SM
authors.lastname: Hay
authors.forename: H M
authors.initials: HM
authors.lastname: Bottjer
authors.forename: R
authors.initials: R
authors.lastname: Eastell
mesh_terms: D015502:Absorptiometry, Photon; D000135:Acid Phosphatase / Q000032:analysis; D000368:Aged; D000369:Aged, 80 and over; D000469:Alkaline Phosphatase / Q000032:analysis; D000596:Amino Acids / Q000032:analysis; D000704:Analysis of Variance; D016512:Ankle Injuries / Q000150:complications / Q000503:physiopathology*; D015415:Biomarkers / Q000032:analysis; D015519:Bone Density; D016723:Bone Remodeling; D003094:Collagen / Q000032:analysis; D024042:Collagen Type I; D005260:Female; D050723:Fractures, Bone / Q000150:complications / Q000503:physiopathology*; D006801:Humans; D007527:Isoenzymes / Q000032:analysis; D008297:Male; D008875:Middle Aged; D015675:Osteocalcin / Q000032:analysis; D010446:Peptide Fragments / Q000032:analysis; D010455:Peptides / Q000032:analysis; D011347:Procollagen / Q000032:analysis; D012019:Reflex Sympathetic Dystrophy / Q000209:etiology / Q000503:physiopathology; D018709:Statistics, Nonparametric; D000071681:Tartrate-Resistant Acid Phosphatase; D013997:Time Factors
chemical_list: D000596:Amino Acids; D015415:Biomarkers; D024042:Collagen Type I; D007527:Isoenzymes; D010446:Peptide Fragments; D010455:Peptides; D011347:Procollagen; C052929:collagen type I trimeric cross-linked peptide; C047202:procollagen Type I N-terminal peptide; D015675:Osteocalcin; C015484:pyridinoline; D003094:Collagen; D000469:Alkaline Phosphatase; D000135:Acid Phosphatase; D000071681:Tartrate-Resistant Acid Phosphatase