Biochemical Markers of Bone Metabolism

Serum total and bone alkaline phosphatase levels and their correlation with serum minerals over the lifespan of sheep

“…The pattern of variation of serum BALP along the sheep lifetime (growing, mature, old, lactating, dry, pregnant) was similar to that described for total ALP, presenting a continuous decline of its serum levels along the sheep lifespan, namely in mature and older sheep (3 to 5 years old or older), probably indicating decreased bone turnover associated with ageing and metabolism. In the human population and also in dogs, a similar pattern was found not only for BALP but also for other bone formation markers such as OC, PINP and PICP, and also for bone resorption markers (Allen et al, 1998;Allen et al, 2000;Cremers et al, 2008).…”

Bone turnover markers for early detection of fracture healing disturbances: A review of the scientific literature

“…BTMs are products of bone cell activity and are generally subdivided into three categories: bone resorption markers, bone formation markers and osteoclast regulatory proteins (Leeming et al 2006). The markers of bone resorption result from degradation of the type-I collagen such as the C-terminal telopeptide (CTX), the N-terminal telopeptide (NTX) of type-I collagen, the CTX -matrix metalloproteinase (ICTP), hydroxyproline (HYP), the collagen crosslinks [pyridinoline (PYD), deoxypyridinoline (DPD)], and the enzymes secreted by the osteoclasts, namely tartrate-resistant acid phosphatase (TRAP) 5b isoform (Cremers et al 2008). Bone formation markers derive from the osteoblastic activity, formed during the different stages of osteoblasts proliferation, differentiation and of osteoid synthesis (Aubin 2008, Cremers et al 2008, Seibel 2000, namely the bone alkaline phosphatase (BALP), osteocalcin (OC), N-terminal propeptide (PINP) and C-terminal propeptide (PICP) of type-I procollagen (Cremers et al 2008).…”

“…The markers of bone resorption result from degradation of the type-I collagen such as the C-terminal telopeptide (CTX), the N-terminal telopeptide (NTX) of type-I collagen, the CTX -matrix metalloproteinase (ICTP), hydroxyproline (HYP), the collagen crosslinks [pyridinoline (PYD), deoxypyridinoline (DPD)], and the enzymes secreted by the osteoclasts, namely tartrate-resistant acid phosphatase (TRAP) 5b isoform (Cremers et al 2008). Bone formation markers derive from the osteoblastic activity, formed during the different stages of osteoblasts proliferation, differentiation and of osteoid synthesis (Aubin 2008, Cremers et al 2008, Seibel 2000, namely the bone alkaline phosphatase (BALP), osteocalcin (OC), N-terminal propeptide (PINP) and C-terminal propeptide (PICP) of type-I procollagen (Cremers et al 2008). Osteoclast regulatory proteins include the receptor activator of nuclear factor NF-κB ligand (RANKL) produced by osteocytes, osteoblasts and immune system cells, which are responsible for osteoclast activation, differentiation and survival (Li et al 2000, Teitelbaum and Ross 2003, Komori 2013 and also its membrane-bound receptor (RANK) in the osteoclast precursor cells (Asagiri and Takayanagi 2007).…”

Serum total and bone alkaline phosphatase and tartrate-resistant acid phosphatase activities for the assessment of bone fracture healing in dogs

“…Bone formation markers are enzymes or proteins secreted by osteoblasts during the bone formation process, such as bone-specific isoform of alkaline phosphatase (BALP), serum osteocalcin (OC) and serum procollagen type I C-and N-terminal propeptides. Bone resorption markers are those resulting from the breakdown of type I collagen during the bone resorption process and specific enzymes expressed in boneresorbing osteoclasts, namely tartrate-resistant acid phosphatase (TRAP), serum carboxyterminal telopeptide of type I collagen and urinary collagen type I cross-linked C-and N-telopeptide (Cremers et al, 2008).…”