Craniofacial Muscles

98 M. Lewis et al.
Studies suggest MMP-2 is secreted by MPCs and the interstitial fi broblasts
(Kherif et al. 1999 ) and is expressed in healthy skeletal muscle where it is localised
to the perivascular regions, nerves and neuromuscular junctions (NMJs) (Lewis
et al. 2001 ). MMP-9, a product of in fl ammatory cells (Lewis et al. 2000 ; Schoser
et al. 2002 ) , is not expressed in normal adult non-cranial skeletal muscles, but it is
upregulated after muscle injury or disease, where it is located next to the blood
vessels, nerves, and NMJs (Kherif et al. 1999 ) . Interestingly, it is also expressed
within myo fi bres in healthy human craniofacial muscle (Singh et al. 2000 ) . The
differences in location between the craniofacial and somite-derived muscles could
be the consequence of their different developmental origins. Speci fi cally within the
human masseter muscle, TIMP-1 appears to be consistently expressed. The very
low levels of TIMP-2, MMP-2 and MMP-9 expression support the low level of
ECM turnover in the craniofacial musculature (Tippett et al. 2008 ) . The gelatinases
facilitate MPC migration during development (Chin and Werb 1997 ) and regeneration,
and their important role has been clari fi ed by in vitro (Allen et al. 2003 ) and
in vivo (El Fahime et al. 2000 ) studies whereby overexpression facilitated substantially
greater migration and blocking activity was suf fi cient to prevent MPC migration.
MMP-9 expression within the craniofacial muscles increases just prior to MPC
fusion. In contrast, MMP-2 mRNA and protein expression occur during all stages of
MPC differentiation (Kherif et al. 1999 ; Lewis et al. 2000 ; Carmeli et al. 2004 ) .
Studies have also suggested a synergistic role of growth factors on MMP expression
(Allen et al. 2003 ) .
6.5 Regeneration and Adaptation
Satellite cells are present as mitotically quiescent, undifferentiated mononuclear
cells located between the sarcolemma of individual muscle fi bres and their associated
basal lamina sheaths (Mauro 1961 ; Muir et al. 1965 ) . These cells are a normal
constituent of all vertebrate skeletal muscle, regardless of age, fi bre type and location
(Schultz 1976 ) , and comprise 2–10 % of the nuclei associated with any particular
fi bre (Bischoff and Heintz 1994 ) . Of the total number of nuclei in mature muscle,
satellite cells make up 1–5 % (Allbrook 1981 ; Alameddine et al. 1989 ) . Interestingly,
satellite cells are in greater number within oxidative muscles as compared to glycolytic
muscles, regardless of species (Gibson and Schultz 1983 ; Schultz 1989 ) . The
size of the population is, in part, regulated directly or indirectly by innervation as
well as the muscle functional state (Schultz et al. 1984 ) . The fi bre type distribution
of the regenerated myo fi bres takes on the characteristics of the host muscle bed.
Hence, it follows that innervation, recruitment pattern, and ultimate fi bre type may
be important determinants of satellite cell distribution. The distribution along individual
fi bres is relatively even with the exception of the motor endplate regions
where cell density is increased (Wokke et al. 1989 ) . Several reasons have been
suggested for this, including preservation of the NMJ and synthesis of molecules
important for the structure or function of motor endplates (Wokke et al. 1989 ) .