Previous studies reported consistent results that the proteoglycan content of articular cartilage changed first in the early OA, decreasing gradually from the surface to the deeper layers with the degeneration [ 22, 23].
Histologically, diffuse white matter abnormalities on MR imaging have correlated with deep white matter vacuolar degeneration and with adjacent axonal injury in normal-appearing white matter [22].
A preferential degeneration of deep CA1 pyramidal cells was also observed during early postnatal development in rabbits as a consequence of pilocarpine-induced seizures (Towfighi et al. 2004).
There are, however, many reasons to assume that degeneration of deep grey matter structures, besides the hippocampus and the amygdala, may also occur in the process of Alzheimer's disease and may contribute to cognitive deterioration.
However, possible degeneration of the deep cartilage and subchondral bone remains undetected.
The lichenoid reactions showed a widespread vacuolar basal epidermic degeneration with a deep dermal lymphohistiocytic infiltrate into a lichenoid pattern, associated with deposition of exogenous pigment.
Notably, early vasoregression was mostly seen in midcapillary areas of the network suggesting that the initial degeneration starting in the deep capillary layer.
In addition to confirming the well-known presence of decreased global grey matter and hippocampal volumes in Alzheimer's disease, this study investigated whether deep grey matter structure also suffer degeneration in Alzheimer's disease, and whether such degeneration is associated with cognitive deterioration.
According to these results, it can be suggested that changes in histomorphometric parameters of subchondral bone are secondary to cartilage damage and proceed deeper into subchondral bone with increasing cartilage degeneration.
In the dog sham group and in the Active 1 group, one animal in each group showed focal degeneration and gliosis in the deeper parenchyma with no direct connection to implant site.
