Table 1 Summary of the experts group consensus

1

At the present time there is no evidence that glucosamine modulates ageing phenotype and no studies have been performed on the effects of glucosamine on aged cartilage.

2

New and more focused studies are clearly needed to determine if GlcN can affect oxidative stress, mitochondrial function, autophagy and responsiveness to cytokines and growth factors.

3

Chondrocytes have the capacity to biosynthesize glucosamine from glucose in health and disease. There is no evidence that chondrocyte glucosamine requirement is modified with age or pathological situation.

4

The endogenous level of glucosamine is comprised between 1μM and 2μM, and reach to 10 μM after oral administration of a therapeutic dose (1500 mg);

5

There is no information about the optimal dose use and no information of the interference of diet, age and other gastrointestinal comorbidities or association with other nutraceuticals most particularly with chondroitin sulfate on the GlcN phamarcokinetic profile.

6

Glucosamine might contribute to the maintenance of healthy joints, but this should be confirmed in clinical trials designed to investigate its effects on healthy subjects with high risk of osteoarthritis and using parameters, which establish the link between consumption of glucosamine and maintenance of joints (e.g. biochemical markers and/or MRI).

7

In vitro and ex vivo studies on normal and OA chondrocytes demonstrated stimulating effect of GlcN with supra-pharmacological concentrations on the synthesis of cartilage matrix components and inhibiting potencies on pro-catabolic and pro-inflammatory factors.

8

Prophylactic evidence has been shown in some animal models, but not in human.

9

More research is necessary to explore possible beneficial effects of GlcN in healthy subjects or on risk factors of OA.