arthritic joint stiffness

JOINT stiffness can arise from several sources, and is often associated as much with structures around the joint as within the joint itself.
Focusing on cartilage, Wright (1960 & 1969)  made a most  interesting observation when attributing stiffness to ‘articular gelling’, but, apparently, never pursued in detail.
The articular cartilage has been described in the light of recent studies as a 'proteoglycan-rich hydrated gel' supported on a collagen matrix.The gels such as this is highly consist of hydrogen bonds, are highly likely to fuse together, supporting the concept of 'articular gelling'.
Overlaying the surface of articular cartilage is an amorphous membranous layer of surface-active phospholipids (SAPLs). The lining of SAPL is shown to possess the capability to reduce friction to the very low levels recorded in the normal joint, and to do so under high load (Hills,1989) . Moreover, this lining has been shown to be deficient in osteoarthritis (Hills, 1998). In normal articular cartilage, SAPL acts as a good release agent and can inhibit or prevent gel fusion, including articular gels.
Therefore, the question is whether deficiency of SAPL in arthritic articular cartilage potentially contributes to joint stiffness which is a typical/diagnostic feature of osteoarthritis.
From Hills' study (1998), the authors have concluded Samples of human articular cartilage excised from osteoarthritic hips and knees during total joint replacement showed a 55% greater tendency to fuse together than normal bovine articular cartilage. Hence, joint stiffness can be attributed, in part, to a deficiency in the lubricating layer of SAPL lining the normal articular surface where it can inhibit articular gelling/gel fusion, possibly imparting other desirable physiological functions.

This is mainly quoted from:
Hills B.A., & Thomas K. (1998) Joint stiffness and 'articular gelling': Inhibition of the fusion of articular surfaces by surfactant. British Journal of Rheumatology. 1998 37:5 (532-538). 

now, as for me, a question arises here. Usually patients complain of morning stiffness or general joint stiffness after prolonged immobilisation (e.g. prolonged sitting) which goes away after moving about for a while. 

so does the friction coefficient gradually decrease as the synovial membrane secretes synovial fluid which potentially assists in increasing lubrication of the joint surfaces when you move around??

My guess is that there are many possible factors contribute to this phenomenon and i have to further investigate into this matter soon. Please let me know and share your experiences  if you are knowledgeable in this field