Tuesday, 18 April 2017

NHS England: Even Longer Delays for Total Joint Replacements! What’s the solution?

A recent statement issued by NHS England’s Simon Stevens has caused concern that some patients awaiting elective knee and hip replacement operations may have to wait longer than is presently recommended to receive treatment. Current constraints on NHS funding and an increase in demand means budgets are having to be redirected to focus on A&E and cancer care.  The NHS has also stipulated that GPs should considerably reduce the number of people being referred to secondary care Consultants. 

Here are links to articles on this issue:



Are there any therapeutic options open to clinicians which may help alleviate the problems that some patients will face as a result of these changes?

It has been recognised for many years that Viscosupplementation can offer a valuable bridge between conservative care and surgery. Clinical studies have consistently shown intra-articular hyaluronic acid (HA) injections to be safe, efficacious and cost-effective (1-3). 

Before the introduction of the single injection HA OSTENIL® PLUS, OSTENIL® injections were usually administered as a course of up to 5 weekly injections. Mathies et al - in a seminal examination of the relationship between Viscosupplementation and the quality of synovial fluid - showed that Viscosupplementation could delay total knee replacements (TKR) by 4.5 to 6 months, and for some patients up to 12 months. His study also demonstrated that “OSTENIL® was safe and significantly improved symptoms in patients with painful advanced knee OA who were awaiting TKR, and that it improved the quality of life of these patients.” (4) In a larger study which examined the potential of HA for delaying knee arthroplasty, Altman demonstrated that “HA injection in patients with knee OA is associated with a dose-dependent increase in time-to-TKR” (7).

Since the introduction of OSTENIL® PLUS, patients have garnered the same symptom-reducing benefits from a single injection, and for the administering clinician - as well as the patient - the process is a lot more convenient. Significant symptomatic reduction and functional improvement was demonstrated in patients suffering moderate knee OA for up to 6 months following a single injection of OSTENIL® PLUS. (5,6). 

So why aren’t more OA patients in the UK being offered the option to help alleviate symptoms and potentially delay their joint replacement?

One of the major obstacles at present is the “Do not recommend intra-articular HA to treat osteoarthritis” in the current NIHCE guidelines on Knee OA. Although it is important to understand that the NIHCE Guidelines (CG177) DO NOT prohibit clinicians from using OSTENIL. In fact, OSTENIL® PLUS DOES meet the QLY cost to benefit criteria quoted by CG177.

Given the current climate in relation to treating degenerative joint change, clinicians and their patients have a limited number of options left open to them: simple analgesics, NSAIDs, and corticosteroid injections, none of which are entirely benign with prolonged use. Physiotherapy alone is not always an option if the joint has degenerated to such an extent that it makes exercise too painful. All this means that the impact on quality of life due to longer waiting times will be felt even more by an ageing and increasingly overweight population.

If you as an injecting physiotherapist/MSk specialist are receiving an increasing number of referrals of patients suffering symptomatic OA from GPs, have you considered Viscosupplementation as an option?

OSTENIL® injections do not require a Consultant to administer. Instead, local MSk triage services can offer a cost effective solution, providing GPs with an alternative patient treatment pathway, helping avoid unnecessary secondary care referrals - and the associated tariff fee - which would more than cover the cost of an OSTENIL® PLUS injection. As a result, not only would the ever growing demand on secondary care be ameliorated, patient waiting times could be reduced, and clinical outcomes improved. 

If you would like more information or chat to one of our representatives, please contact us on info@trbchemedica.co.uk. You can also visit our website here: ostenil.trbchemedica.co.uk, or call us on 0845 330 7556. 


1. Möller I et al. Presented at the 6th World Conference of the Osteoarthritis Research Society International 2001; poster PB22
2. Tsvetkova E et al. Ann Rheum Dis 2010;69(Suppl3):281
3. Funk L et al. Presented at the 9th World Conference of the Osteoarthritis Research Society International 2004; poster P338
4. Mathies B et al. Presented at the 5th Symposium of the International Cartilage Repair Society. May 26–29, 2004; poster 397.
5. Borràs Verdera A et al. Poster presented at the XXV triennial world congress of the International Society of Orthopedic and Traumatology. September 6-9, 2011.
6. K Frobenius “A new high-dose treatment with intra-articular hyaluronic acid facilitates the management of osteoarthritis”. Orthopädische Praxis 46, 5, 2009
7. Altman R, Lim S, Steen RG, Dasa V (2015) “Hyaluronic Acid Injections Are Associated with Delay of Total Knee Replacement Surgery in Patients with Knee Osteoarthritis: Evidence from a Large U.S. Health Claims Database. PLoS ONE 10(12): e0145776. doi:10.1371/journal.pone.0145776

Wednesday, 12 April 2017

Why consider topical Sodium Hyaluronate (HA) in the treatment of tendinopathy?

Firstly, the difference between HA and other glycosaminoglycans is that it is non-sulfated, forms in the plasma membrane instead of the Golgi apparatus, and can be very large, with its molecular weight often reaching the millions1. HA is considered to be a key molecule in the tissue regeneration process. It has been shown to modulate via specific HA receptors, inflammation, cellular migration, and angiogenesis, which are the main phases of wound healing7.

In relation to tendinopathies, hyaluronic acid modulates a variety of cellular functions: anti-inflammatory activity, enhanced cellular proliferation and collagen deposition. Studies have shown a link between the inhibition of fibroblast proliferation, with a reduction in the formation of adhesions at the tendon healing site; by limiting the proliferation of fibroblasts, HA may reduce the risk of adhesions.2

It has sometimes been assumed, in relation to tendinopathic change, that because there is an excess of GAGs detectable within the local bio-chemical environment, there is an excess of hyaluronan, which is not necessarily the case. For example, the activity of hyaluronidase (enzymes that catalyse the degradation of hyaluronan) has been shown to increase during the healing of equine superficial digital flexor tendon injuries6.

Multiple studies analysing tendon healing have confirmed that HA reduces the formation of scars and granulation tissue, and also prevents adhesions2. Importantly, HA forms part of the extracellular matrix as a major component of ground substance, giving structure for other GAGs and proteoglycans3. In tendon healing, the GAGs provide a temporary structure in the early stages of the wound4. So without the presence of HA, there is evidence to suggest that other GAGs are of limited use. Also, high levels of HA are thought to be instrumental in scar-less healing by facilitating the movement and proliferation of fibroblasts, and by regulating the production and type of collagen5.

HA also plays an important role as a hydrating agent, being able to absorb 3,000 times its own weight in water4. HA appears to inhibit the expression of key intermediaries for the inflammatory signalling pathways (NF-kB), by reducing the expression of pro inflammatory factors, exogenous HA may reduce the fragmentation of endogenous HA and further stimulate synthesis of endogenous HA.7,8.


1.       Fraser JR, Laurent TC, Laurent UB (1997). "Hyaluronan: its nature, distribution, functions and turnover" (PDF). J. Intern. Med. 242 (1): 27–33. doi:10.1046/j.1365-2796.1997.00170.x. PMID 9260563.
2.       Michele Abate, Cosima Schiavone, and Vincenzo Salini, “The Use of Hyaluronic Acid after Tendon Surgery and in Tendinopathies,” BioMed Research International, vol. 2014, Article ID 783632, 6 pages, 2014. doi:10.1155/2014/783632.
3.       Bertolami, C.N. (1984)Glycosaminoglycan interactions in early wound repair. In: Hunt, T.K., Heppenstall, R.B., Pines., Rovee, D. (eds). Soft and Hard Tissue Repair: Biological and clinical aspects. Eastbourne: Praeger Scientific.
4.       Snyder, R.J. (1999)Wound management: a global perspective. Ostomy/Wound Management 45: 9, 26-30.
5.       Desai, H. (1997)Ageing and wounds, part 2: healing in old age. Journal of Wound Care 6: 5, 237-239.
6.       J. W. Foland, G. W. Trotter, B. E. Powers, R. H. Wrighley, and F. W. Smith, “Effect of sodium hyaluronate in collagenase-induced superficial digital flexor tendinitis in horses,” American Journal of Veterinary Research, vol. 53, no. 12, pp. 2371–2376, 1992.
7.       Litwiniuk M., Krejner A., Grzela T. (2016). Hyaluronic acid in inflammation and tissue regeneration. Wounds 28, 78–88.
8.       Litwiniuk, Malgorzata, Alicja Krejner, and Tomasz Grzela. "Hyaluronic Acid In Inflammation And Tissue Regeneration". Wounds 28.3 (2016): n. pag. Print.