Bone cells are connected to one another in a network, via their dendritic cellular processes. Previously, we hypothesized that these processes could be ruptured by microcracks. We proposed this as a mechanism by which osteoctyes could detect the presence of microcracks. In order for this mechanism to be effective, the number of ruptured processes would have to increase with microcrack length and also with the applied cyclic stress. This paper presents for the first time experimental data, which shows that this is indeed the case. We examined samples of bovine, ovine and murine bone ex vivo and observed processes passing across crack faces: some were still intact whilst others had ruptured. The number of intact processes per unit crack length decreased significantly with increasing crack length and also decreased in samples, which had been tested in vitro at higher stress levels. A theoretical model that we had developed previously was able to predict the overall magnitude and general trends in the experimental data. This work has provided further support for our "scissors" model, which proposes that microcracks can be detected because they disturb the osteocyte network, specifically by rupturing cellular processes where they pass across the crack faces.