Following intralesional resection of giant cell tumour local recurrence happens in up to 40% depending on type of treatment. Common plain radiography or Magnetic resonance tomography (MRI) often has the problem not to discriminate between scar and recurrent tumour tissue in the cement-tissue border of lesions treated with cement packing. The value of Positron emission tomography (PET) for diagnosis of tumour and recurrence was investigated in these patients.

In 19 patients with giant cell tumour dynamic PET using F18-Fluordeoxyglucose for estimation of FDG turnover was carried out. PET was performed before surgery and as follow up. In all patients giant cell tumour was treated by curettage followed by burring and cement packing. Giant cell tumour was shown by histology in all patients.

All giant cell tumours showed a specific PET pattern with a very high standard uptake value (SUV) of 4.8 in median. In follow up after surgery this value dropped to 0.3. In one case also pulmonary metastasis could be demonstrated. Recurrence was suspected in the follow up in 5 patients by MRI or plain radiography. In all these patients PET could show an elevated SUV above 4.0. In these 5 patients surgery was performed and recurrence could be proven by histology. In one patient MRI showed signs of recurrence but PET showed a SUV of 1.3. In the revision surgery no tumour could be found. In one patient MRI was negative but PET showed a SUV of 5.2 indicating re-recurrent tumour which could be demonstrated by histology.

We conclude that PET is a very helpful tool not only in the first line diagnosis of giant cell tumour but also in diagnosis of metastatic disease and especially for detection of recurrent tumour.

Common in vitro protocols for TGF-β driven chondrogenic differentiation of MSC lead to hypertrophic differentiation of cells. This might cause major problems for articular cartilage repair strategies based on tissue engineered cartilage constructs derived from these cells. BMPs have been described as alternate inductors of chondrogenesis while PTHrP and FGF-2 seem promising for modulation of chondrogenic hypertrophy. The aim of this study was to identify chondrogenic culture conditions avoiding cellular hypertrophy. We analyzed the effect of a broad panel of growth factors alone or in combination with TGF-β3 on MSC pellets cultured in vitro and after transplantation in SCID mice in vivo.

Chondrogenic differentiation in vitro was successful after supplementation of the chondrogenic medium with TGF-β3 as confirmed by positive collagen type II and alcian blue staining. None of the other single growth factors (BMP-2, -4, -6, -7, FGF-1, IGF-1) led to sufficient chondrogenesis as indicated by negative collagen type II and alcian blue staining. Each of these factors, however, allowed chondrogenesis in combination with TGF-β without suppressing collagen type X expression. Combination of TGF-β with PTHrP or FGF-2 suppressed ALP activity, induced MMP13 expression, and prevented differentiation to chondrocyte-like cells when added from day 0. Delayed addition of PTHrP or FGF-2 stopped chondrogenesis at the reached level and repressed ALP activity. The treatment of MSC constructs with FGF-2 or PTHrP in the last 3 weeks before transplantation did not prevent hypertrophy and calcification in vivo.

FGF-2 and PTHrP were potent inhibitors for early and late chondrogenic differentiation in contrast to BMPs. As soon as a developmental window of collagen type II positive and collagen type X negative pellet cultures can be created in this model, both seem to be potent factors to suppress hypertrophy and to generate stable chondrocytes for transplantation purposes.