Elastic discontinuity due to ectopic calcification in a human fibrous joint

Disease can alter natural ramp-like elastic gradients to steeper step-like profiles at soft–hard tissue interfaces. Prolonged function can further mediate mechanochemical events that alter biomechanical response within diseased organs. In this study, a human bone–tooth fibrous joint was chosen as a model system, in which the effects of bacterial-induced disease, i.e. periodontitis, on natural elastic gradients were investigated. Specifically, the effects of ectopic biomineral, i.e. calculus, on innate chemical and elastic gradients within the cementum–dentin complex, both of which are fundamental parameters to load-bearing tissues, are investigated through comparisons with a healthy complex. Complementary techniques for mapping changes in physicochemical properties as a result of disease included micro X-ray computed tomography, microprobe micro X-ray fluorescence imaging, transmission electron and atomic force microscopy (AFM) techniques, and AFM-based nanoindentation. Results demonstrated primary effects as derivatives of ectopic mineralization within the diseased fibrous joint. Ectopic mineralization with no cementum resorption, but altered cementum physicochemical properties with increasing X-ray attenuation, exhibited stratified concretion with increasing X-ray fluorescence counts of calcium and phosphorus elements in the extracellular matrix in correlation with decreased hygroscopicity, indenter displacement, and apparent strain-relieving characteristics. Disease progression, identified as concretion through the periodontal ligament (PDL)–cementum enthesis, and sometimes the originally hygroscopic cementum–dentin junction, resulted in a significantly increased indentation elastic modulus (3.16 ± 1.19 GPa) and a shift towards a discontinuous interface compared with healthy conditions (1.54 ± 0.83 GPa) (Student’s t-test, P < 0.05). The observed primary effects could result in secondary downstream effects, such as compromised mechanobiology at the mechanically active PDL–cementum enthesis that can catalyze progression of disease.