Method of treating osteoarthritis

Abstract

A method of treating osteoarthritis by modifying the shape change of bone(s) underlying articular cartilage, comprising evaluating the bone shape of the patient's joint, injecting the patient with a peptide of SEQ ID No. 1 or applying other therapeutic interventions that can reduce the shape change of the bone(s) underlying articular cartilage, and thereafter evaluating the bone shape of the patient's joint is disclosed.

Description

FIELD OF THE INVENTION[0001]The invention relates generally to methods of treating osteoarthritis by modifying joint bone shape change, which is a pathology underlying onset and progression of osteoarthritis.BACKGROUNDOsteoarthritis[0002]Osteoarthritis is the most common disease of the joints, and one of the most widespread of all chronic diseases. In the US, osteoarthritis (OA) is second only to heart disease as a cause of work disability in men over 50 years of age. Globally, osteoarthritis is the 6th leading cause of years living with disability (Woolf 2003).[0003]Approximately 80% of OA patients need treatment in the knee. Within the knee joint of symptomatic individuals, the most common radiographic pattern is loss of articular (hyaline) cartilage and remodeling of adjacent bone, often with osteophyte formation at the joint margins. Both the tibiofemoral and patello-femoral compartments are commonly affected by degenerative changes. Patello-femoral arthritis due to loss of cart...

AI Technical Summary

Benefits of technology

The patent describes a method using MRI to diagnose and evaluate the treatment of osteoarthritis by measuring the cartilage and bone shape. By combining these measurements, the method can increase the sensitivity of evaluating treatment effects.

Problems solved by technology

Corticosteroid injections have been implicated in further cartilage degeneration in the knees (McAlindon 2017) limiting the willingness of clinicians to use this treatment modality.

While joint pain reduction may persist for weeks to months in some patients (Cohen 1998), multiple clinical trials have failed to demonstrate a clinically meaningful treatment effect.

Unfortunately, articular cartilage does not regenerate naturally, neither after trauma nor in the setting of chronic “wear and tear” of aging (Buckwalter 2002).

However, fibrocartilage has much less structural strength and stability than normal articular cartilage and degenerates more quickly.

Treatment failures are common, as is the need for additional surgery to manage complications.

Common complications include delamination, graft failure, and disturbed graft fusion (Niemeyer 2008).

The final option for patients with disabling knee OA is joint replacement surgery, an invasive and expensive option with potential for serious morbid complications.

However, average age of the patients who receive TKR has been falling.

While numerous drugs believed to inhibit cartilage degeneration in knee OA have been tested in controlled clinical trials, thus far none has been successful in slowing or stopping cartilage loss.

However, clinical observations have led some researchers to question whether cartilage degeneration may follow changes in other parts of the joint.

On the other hand, many OA patients experience severe pain and functional limitations when their articular cartilage has little measurable degeneration.

. . there are several ongoing issues with developing such products, including the multifactorial and complex etiopathogenesis of the disease, the well-recognized discordance between structural changes and signs / symptoms / function, the lack of standard definitions of disease progression, and, correspondingly, the absence of endpoints to reliably assess the ability of a product to alter OA disease progression.” (FDA 2018)

Specifically, changes in cartilage thickness may not be sufficient to explain the disease of OA as patients experience it; nor can cartilage thickness increases be assumed to modify clinical outcomes of OA unless they are persuasively linked to patient benefit.

Their efficacy in stabilizing or strengthening subchondral bone has not been demonstrated clinically, and significant adverse effects have dampened enthusiasm for these agents.

For example, strontium ranelate was found to increase the risk of myocardial infarction and its use has been limited by the European Medicines Agency.

There have been epidemiology reports that high bone mass or high bone mineral density is associated with increased risk of knee OA or joint replacement (Nevitt 2010, Hardcastle 2013).

Combining these with the bisphosphonate data above, bone mass increase or strengthening does not necessarily improve or reduce the risk of OA.

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