Spondyloarthropathies consist of chronic inflammatory disorders genetically linked with each other through HLA-B27 molecules, and are connected with the destruction of periarticular bone and also with systemic bone loss in many cases. Expected molecular mechanisms behind these conditions overlap the functions of Hsp70s, a group of major molecular chaperones and cytokines. Hsp70s may control disease progression via inhibition of unfolded HLA-B27 protein accumulation and alteration of ER stress signaling. Further, Hsp70s may improve disease related malfunction of antigen presentation, and may induce nitric oxide (NO) release from macrophages which probably protective against spondyloarthropathies as well. Considering premised possible influence of Hsp70s on core mechanisms of spondyloarthropathies it may be expected that, increased expression of Hsp70s advantageously retards disease progress, or may lead to remission. On the other hand Hsp70s as danger signals induce the secretion of proinflammatory cytokines playing major role in the progression of spondyloarthropathy induced bone loss. Consequently, the effect of Hsp70s on the progression of spondyloarthropathic bone loss is "Janus-faced" in some respect: increase of Hsp70s' level is likely advantageous regarding to the core of disorder; but it may facilitate existing bone resorption processes.