The overgrowth-affected gingiva of patients treated with cyclosporin A after kidney transplant was examined with ultrastructural and histochemical methods to evaluate the involvement of connective tissue. Gingival overgrowth has the same clinical signs as local edema. The ultrastructural study showed that the dimensional increase was largely due to increased production of amorphous ground substance by fibroblasts, possibly resulting from an increased release of histamine by mast cells. The histochemical data revealed that the affected tissues contained higher levels of glycosaminoglycans and that cyclosporin A induced comparably high levels of glycosaminoglycans in in vitro cultures of fibroblasts obtained from normal gingiva. The combination of ultrastructural and histochemical data, therefore, strongly suggests that the response of the connective tissue in gingival overgrowth cannot be ignored and may be the main cause of the observed pathological condition.

The present work collected data on the ultrastructural features of the attached gingiva in kidney transplant patients who showed gingival hyperplasia following cyclosporin A (Cy A) treatment. Ultrastructural examination was carried out on biopsies of attached gingiva obtained from 8 male patients (30 to 60 years old) undergoing treatment at the Dental Clinic of the University of Ferrara. The data showed that, although many fibroblasts are present in Cy A-induced hyperplasia, there is a particular abundance of amorphous substance compared to fibrous, as well as marked plasma cell infiltration. On the basis of the data collected, we hypothesize that the morphological features of the dimensional increase in gingival tissue associated with Cy A treatment in kidney transplant patients may be considered local manifestations of a systemic phenomenon.

Focal or diffuse cerebral hypoperfusion was found in more than half of the neurologically asymptomatic SSc patients studied, paralleling the incidence of altered brain MRI. The hypoperfusion was not linked to ageing and possibly reflects the cerebral location of the microangiopathic process characterizing the disease.

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