PubMed · 3409277
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J Zák, V Pacovský. 1988-06-17. [Bone remodeling].. https://pubmed.ncbi.nlm.nih.gov/3409277/
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Calcium deficiency is a major etiological determinant of rickets in Nigerian children and is accompanied by undermineralization of the developing bone matrix which is composed largely of type I collagen. We have assessed types I and III collagen metabolism by measuring the circulating concentrations of teh N- and C-terminal pro-peptides (intact PINP and PICP) and the C-terminal telopeptide (ICTP) of type I collagen, and the N-terminal pro-peptide (PIIINP) of type III collagen in 94 healthy Nigerian children and in 44 children aged 1-5 years with active calcium-deficiency rickets. In active rickets the mean levels of the four collagen metabolites were approximately twofold higher than in the healthy children, despite a wide variation of individual values. Mean intact PINP was 812 +/- 279 versus 403 +/- 189 microg/liter; PICP was 573 +/- 265 versus 348 +/- 299 microg/liter; PIIINP was 16.8 +/- 8.6 versus 10.8 +/- 3.6 microg/liter, and ICTP was 28.4 +/- 17.2 versus 11.9 +/- 4.1 microg/liter (all P < 0.001), in rachitic and healthy children, respectively. Healthy children younger than 3 years had higher levels of all the collagen metabolites than those between 3 and 5 years (all P < 0.05). Alkaline phosphatase was greater in rickets than in the healthy group (P < 0.001) whereas mean osteocalcin levels were slightly lower (P = 0.009). 1,25(OH)2D correlated with all the collagen propeptides, but not with ICTP in the healthy children. No such correlations were found in rickets, where there was a poor inverse correlation between 1,25(OH)2D and ICTP. These data suggest that collagen turnover is elevated in cases of calcium-deficiency rickets, where vitamin D status is adequate, possibly indicating increased turnover of undermineralized osteoid.
Although the initial versions of the functional matrix hypothesis (FMH) theoretically posited the ontogenetic primacy of "function," it is only in recent years that advances in the morphogenetic, engineering, and computer sciences provided an integrated experimental and numerical data base that permitted recent significant revisions of the FMH--revisions that strongly support the primary role of function in craniofacial growth and development. Acknowledging that the currently dominant scientific paradigm suggests that genomic, instead of epigenetic (functional) factors, regulate (cause, control) such growth, an analysis of this continuing controversy was deemed useful. Accordingly the method of dialectical analysis, is employed, stating a thesis, an antithesis, and a resolving synthesis based primarily on an extensive review of the pertinent current literature. This article extensively reviews the genomic hypothesis and offers a critique intended to remove some of the unintentional conceptual obscurantism that has recently come to surround it.
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