Pathophysiology of OA and it's continuous progression may be the main reason behind this.

the following attachments may be useful to you.

and in addition to this please go through the following links:

http://www.ajol.info/index.php/ajbr/article/viewFile/50713/39405

http://www.ajol.info/index.php/sajaa/article/viewFile/69115/57162

Pathophysiology of OA and it's continuous progression is the main reason for this.

the following attachments may be very useful to you.

and in addition to this please go through the following links:

http://www.ajol.info/index.php/ajbr/article/viewFile/50713/39405

http://www.ajol.info/index.php/sajaa/article/viewFile/69115/57162

Since articular cartilage is aneural, these changes do not produce clinical signs unless innervated tissue becomes involved. Recent research advances demonstrate that synovitis and bone marrow lesions are important factors contributing to pain in osteoarthritis (1;2) Inflammation of the synovial tissue (i.e. synovitis) corresponds to clinical symptoms such as joint swelling and inflammatory pain. Bone marrow lesions may appear after acute injury (3) or after chronic excess loading (4) and are more often found in individuals with painful knee osteoarthritis than in individuals with non-painful osteoarthritis, thus suggesting a causal role in the development of pain (5;6). Neuroimaging has provided evidence of the contribution of the central brain network to pain perception in osteoarthritis. In a study by Baliki et al (2008) local treatment of the osteoarthritic knee resulted in reduction of brain activity, suggesting that central activation of the brain mediates pain during osteoarthritis (7). Moreover, data by Kulkarni et al propose that arthritic pain is associated with areas of the brain responsible for affect, aversive conditioning and motivation (8).

References:

1. Sellam J, Berenbaum F. The role of synovitis in pathophysiology and clinical symptoms of osteoarthritis. 2010;2010/10/07(11):625-35.

2. Sofat N, Ejindu V, Kiely P. What makes osteoarthritis painful? The evidence for local and central pain processing. 2011;2011/09/29.

3. Frobell RB, Le Graverand MP, Buck R, Roos EM, Roos HP, Tamez-Pena J, et al. The acutely ACL injured knee assessed by MRI: changes in joint fluid, bone marrow lesions, and cartilage during the first year. 2009;2008/09/02(2):161-7.

4. Felson DT, McLaughlin S, Goggins J, LaValley MP, Gale ME, Totterman S, et al. Bone marrow edema and its relation to progression of knee osteoarthritis. 2003;2003/09/11(5 Pt 1):330-6.

5. Felson DT, Chaisson CE, Hill CL, Totterman SM, Gale ME, Skinner KM, et al. The association of bone marrow lesions with pain in knee osteoarthritis. 2001;2001/04/03(7):541-9.

6. Sowers MF, Hayes C, Jamadar D, Capul D, Lachance L, Jannausch M, et al. Magnetic resonance-detected subchondral bone marrow and cartilage defect characteristics associated with pain and X-ray-defined knee osteoarthritis. 2003;2003/06/13(6):387-93.

7. Baliki MN, Geha PY, Jabakhanji R, Harden N, Schnitzer TJ, Apkarian AV. A preliminary fMRI study of analgesic treatment in chronic back pain and knee osteoarthritis. 2008;2008/10/28:47.

8. Kulkarni B, Bentley DE, Elliott R, Julyan PJ, Boger E, Watson A, et al. Arthritic pain is processed in brain areas concerned with emotions and fear. 2007;2007/03/30(4):1345-54.

I think the answers from Thomas are really extensive on our present knowledge on pain in osteoarthritis (OA). We also have performed a systematic review on structures in an OA knee (seen on MRI) that are associated with pain (Yusuf, et al. Annals of Rheumatic Diseases, 2011) and we found bone marrow lesion and synovitis are associated with pain. Yet, the level of evidence is not strong enough. So i believe that the pain is 'caused' by a combination of factors. Not only biological but also psychological (e.g. how to cope with pain).

Thanks Yusuf for your additional reference.

Recent work is showing that OA is a disease of the whole joint and mechanisms of pain include synovitis at different points of the disease, bone marrow lesions and sensitisation demonstrated by emerging neuroimaging studies. Further work is required now to evaluate the mechanisms driving such processes which could translate into future therapies.

We have found an very important factor that might trigger the process of so call "degeneration" in the knee joint. Our finding of "medial abrasion syndrome" (Ref. 3,5,6,7) initiated by impingement of medial plica and consequent repeated focal synovitis is an important source of pain in the very early stage of medial compartment knee OA. This factor might be the trigger of the cascades of cartilage degradation (Ref. 2). In the later stage, say K/L stage III or IV, when the destructed cartilage makes the knee deformed (varus in case of medial compartment OA), mechanical axis deviation becomes another factor for the deterioration of the disease process and also count for the bone marrow lesion and might become another source of pain. Therefore, our concept of treatment (i.e. KHPO, please see attached link) is based on these understandings. From 2001, we started to treat the "medial abrasion syndrome" by arthroscopic medial release (AMR, Ref. 4) at the early stage of OA knee and try to stop the disease process. Also, in later stage, we use another novel arthroscopic procedure (ACRFP, Ref. 1) to eliminate all detrimental factors in the knee joint to facilitate cartilage self repair. Our clinical outcomes revealed that we could reverse the natural course of OA knee in >80% of patients. The whole concept could be freely accessed online by the attached link.

References:

1. Lyu, S. R., Hsu, C. C., & Lin C. W., Arthroscopic cartilage regeneration facilitating procedure for osteoarthritic knee, BMC Musculoskeletal Disorders, 2012, 13:226, Free Online Access: http://www.biomedcentral.com/1471-2474/13/226

2. Wang, H. S., Kuo, P. Y., Yang, C. C., & Lyu, S. R. (2011), Matrix metalloprotease-3 expression in medial plica and pannus-like tissue in knees from patients with medial compartment osteoarthritis, Histopathology, 58(4), 593-600.

3. Lyu SR , Chiang JK, and Tseng CE, Medial plica in patients with knee osteoarthritis: a histomorphological study, Knee surgery, sports traumatology, Arthroscopy: official journal of the ESSKA 18(6):769-76, 2010 Jun

4. Shaw-Ruey Lyu, Arthroscopic medial release for medial compartment osteoarthritis of the knee, J Bone Joint Surg Br, September, 2008, Vol 90-B, issue 9, Pages 1186-1192

5. Shaw-Ruey Lyu, Relationship of medial plica and medial femoral condyle during flexion. Clinical Biomechanics, 2007, Volume 22, Issue 9, Pages 1013-1016

6. Shaw-Ruey Lyu, Jeh-En Tzeng, Chia-Yuan Kuo, Ai-Ru Jian, De-Shin Liu, Mechanical strength of mediopatellar plica - The influence of its fiber content. Clinical Biomechanics, Volume 21, Issue 8, October 2006, Pages 860-86

7. Lyu SR, Hsu CC, Medial plicae and degeneration of the medial femoral condyle. Arthroscopy. 2006 Jan;22(1):17-26.

http://www.intechopen.com/books/osteoarthritis-diagnosis-treatment-and-surgery/knee-health-promotion-option-for-osteoarthritic-knee-cartilage-regeneration-is-possible