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Years of suffering with AS have left my bones quite weak from demineralization and this is due, as were my kidney stones, to a lack of calcium.

That view doesn't seem to be supported by the scientific literature. As per the study I previously cited, bone mineral density of subjects with AS is decreased, in spite of normal calcium homeostasis and bone remodeling indices. As you mention, the role of inflammation and other factors such as OPG are supported by many studies.

"About 74% of AS patients have reduced BMD and this change reflects disease activity. Serum sRANKL levels and sRANKL/OPG ratios are up-regulated in patients with AS and have relationship with BMD and radiological changes. These results suggest that the imbalance between RANKL and OPG might be involved in the pathogenesis and clinical courses of osteoporosis in AS." - http://rheumatology.oxfordjournals.org/content/45/10/1197.short

"A role for inflammatory cytokines has received support from several studies. Inflammation of the entheses and synovium may result in increased release of proinflammatory cytokines, whose deleterious effects on bone metabolism have been established. Tumor necrosis factor alpha (TNFα), interleukin-1, and interleukin-6, which play a pivotal role in inflammation, as well as nitric oxide, induce bone metabolism imbalances in animals and humans [35]. Thus, in several studies, significant correlations were found between bone turnover markers (pyridinoline, deoxypyridinoline, C- and N-telopeptide crosslinks, and osteocalcin) and the levels of proinflammatory cytokines or their markers (erythrocyte sedimentation rate and C-reactive protein) used in clinical practice [36]." (Osteoperosis & Ankylosing Spondylitis - http://www.sciencedirect.com/science/article/pii/S1297319X03001878)

And when inflammation is reduced, bone density increases. "TNFα has been shown to increase bone resorption and decrease bone formation. This study, in which inhibition of TNFα resulted in a decrease in systemic inflammation, and in an increase in bone density, adds some evidence in favour of the hypothesis of bone loss mainly due to systemic inflammation through direct effects of TNF on bone."

So if you can stop the inflammatory process it appears that you can stop bone loss. "In two longitudinal studies a decrease in BMD was seen only in patients with SpA with persistent active disease." - http://ard.bmj.com/content/62/4/347.abstract

The scientific literature appears to support the idea that inflammation and not calcium deficiency plays a key role in both depression and bone demineralisation associated with AS. Reducing inflammation through medications, diet or lifestyle are likely to improve these parameters.