website – https://subchondralsolutions.com/
Even today in the world of orthopedics, many conditions remain under-served, particularly those that contribute to pain and the progression of osteoarthritis. One such challenge lies in the often-overlooked interface between cartilage and bone. This interface plays a crucial role in joint health, and its failure can lead to the cascade of osteoarthritis, a condition affecting millions worldwide. Recognizing this, a small startup named Subchondral Solutions, Inc. is stepping up to address this issue with their innovative S-Core® implant platform. The initial idea for Subchondral Solutions, Inc. S-Core® implant platform was developed in 2012 by Derek Dee MD, fellowship trained in sports medicine. At the time, he was performing the widely accepted procedures that were considered the “gold standard” to treat osteochondral disease and osteochondrosis including Osteochondral Autograft, Allograft and Microfracture for smaller lesions.
As the literature suggests, these procedures eventually fail. The literature shows that this failure can happen in as early as 12 months even with good disease management. Dr. Dee was disappointed that even with good surgical outcomes combined with a disciplined post-operative rehabilitation protocol, that his patients were returning with problems similar to what the literature suggests.
Dr. Dee hypothesized that maybe osteochondral disease is not isolated to the cartilage and began a full review of the literature to see what other things may be affecting the joint. In this review, he found that if the interface between the cartilage and the bone was compromised then that could be the underlying cause for the failures in the current repairs.
I was in Lake Tahoe just after a winter storm, my knees sore from top-to-bottom powder runs. I thought about my patients who were locals, many with knee issues from skiing. My fellowship training in orthopedic sports medicine was coming to an end, finally, my 6th year of orthopedic training after medical school. But I was concerned that the procedures I had learnt were inadequate or missing the full picture. Outcomes of common procedures we were performing for cartilage damage – debridement (cleaning out debride from cartilage wear fragments), chondroplasty (smoothing damaged cartilage), microfracture (puncturing the exposed bone to make it bleed), and cartilage grafts were temporary or inconsistent, and did not seem to limit the progression towards full joint failure and arthritis. We had the technology to harvest cartilage tissue and transplant grafts or plugs to “fill” the defects, or we could actually “grow” cartilage in a petri-dish and re-implant it. But these all ]had varying results. What were we missing?
Years earlier at the start of medical school, we learned history and physical, or H&P, also referred to as the SOAP note – subjective, objective, assessment, and plan. It is both a note and mode of thought, organized sequentially to arrive at a diagnosis (assessment) and appropriate treatment plan. It starts with the “chief complaint”. The chief complaint of our patients was typically pain. Cartilage has no nerves; bone does. Was our diagnosis correct? Was it solely cartilage damage and disease? We commonly notice osteophytes (growth of bone around joints) on radiographs as arthritis progresses – why? No one seemed to offer me a good explanation. With the advent of MRI, we could also see so much more, and often there were changes in the subchondral bone associated with cartilage defects. Why was this?
If bone was a potential source of pain, how about the role of cartilage and bone biomechanically? Was cartilage the main shock absorber of joints? It was surely a specialized tissue, a smooth, avascular gliding surface, smoother than ice-on-ice – but did it function on it’s own? The orthopedic surgery and sports journals we frequently reviewed and read didn’t seem to offer adequate answers. I started to delve into basic science, biomechanics, and other journals. Many of these articles were hard to find. They weren’t all on the internet. I spent a weekend at the UCSD medical library xeroxing stacks of articles.
What they revealed was fascinating. There had been much research starting 20 years ago on the role of the subchondral bone in the initiation and progression of arthritis. Buried in this literature were also theories that the bone dissipated the majority of the impact stresses of a joint – not the cartilage – or at least was a major contributor. So perhaps the bone was a significant shock absorber? In the last decade, studies have continued to confirm the importance of the subchondral bone as a significant roleplayer with cartilage in joint health. Cartilage acts to convert shear and tangential stresses to compression, transferring these loads through the osteochondral junction (the interface between cartilage and bone, which is dimpled like a golf ball) to the underlying subchondral bone to further dissipate. Bone is most stable in compression, it fails in shear and tangential stresses. When bone fails it interferes with both the structural and metabolic support of overlying cartilage. Recent research points to a sophisticated network of vascular chambers in the bone, the trabecular bone, the surface area of which is 10x greater than your lungs – to absorb and dissipate stress via a series of vascular release valves. The list goes on.
Joints must function to dissipate a spectrum of mechanical energy – from vibrational or repetitive to shock-type impact forces. Akin to structures placed atop skis to dampen forces or on tennis racquets – could we improve the function of joints by bolstering the structures responsible for dissipating much of the forces, the subchondral bone? As bone becomes damaged, there is also an interference of the vascular and metabolic role of the bone to the cartilage. Could we create a device to bolster both properties of the bone – structural shock dissipation, and maintenance of vascularity – with a versatile and durable surgical implant? These were the questions that continued to push me towards finding an answer. The more I dug, the more I found evidence that corroborated these theories.
As orthopedic surgeons, we are mechanical engineers of the body – screws, plates, devices. Bones and joints are subject to repetitive stresses, which can collectively cause failure termed fatigue failure. A stress crack or fracture. Bone, unlike cartilage, undergoes constant remodeling on the cellular level – cells to take away damaged or dysfunctional bone, osteoclasts, and cells to build bone – as long as the rate of repair exceeds the rate of damage, you have a healthy organ, homeostasis. It is when this is disrupted – when the rate of damage exceeds the ability of the body to repair, that you get progressive joint disease. Specifically, it is a breakdown of cartilage that converts shear stresses to compressive – which bone is able to handle – shear and tangential stresses will eventually lead to fatigue failure, a stress fracture, of the subchondral bone, that will in turn cause further damage to overlying structures.
I began to submit and write the patents 2010-12, and formed the company in 2014, known as Subchondral Solutions. We now have a product that performs as we had anticipated – immediate relief of pain, and durability for patient return to work and recreation, from the 68 year-old retired veterinarian hiker from San Jose, to the pro beach volleyball player enjoying the latter part of her career, after countless previous surgeries, to the 65 year-old snow skier from Tahoe that would do anything it took to get another powder day. The challenge has been to steer a large ship, composed of both industry and physicians, that have been focused on the top portion of the iceberg, while the keel of the iceberg, that which keeps it upright, lies beneath the surface.
For more information contact: Tom Kinder, CEO of Subchondral Solutions, at kinderthomas@subchondralsolutions.com.