Diabetes affects millions of people around the globe, and much of the discussion centers around blood glucose regulation, but one complication is both silent and devastating and occurs at the feet.
Limited joint mobility in the diabetic foot is a condition that affects how freely the joints in your feet and ankles are able to move, and is far more serious than it sounds.
Stiff joints alter how pressure is distributed across the foot with each step, and this can lead to a cascade of problems including ulcers, deformity, and even amputation in some cases.
This article will give an outline of how this condition occurs, how it worsens foot health, and what can be done to address it.
How Limited Joint Mobility in Diabetic Foot Develops
An understanding of how diabetes can lead to limited joint mobility may not be immediately obvious, but the mechanisms involved are quite straightforward.
Prolonged elevated serum glucose results in a process known as glycation (in essence, attachment of sugar molecules to collagen fibers in the body), which causes a stiffening and cross-linking in the proteins.
The key tissue affected are tendons, ligaments, and joint capsules as they are all composed of collagen fibers.
Cross linking in these tissues becomes stiff, transmitting abnormal force within the tissues and limiting the range of motion.
The ankle joint and subtalar joint are most commonly affected, along with the terminal dorsals of the toes.
Connective Tissue Changes Lead to Reduced Range of Motion:
It takes time to develop glycation, where serum glucose levels are abnormal from elevated long term hyperglycaemia, this typically takes on the order of years so significant limited joint mobility occurs in those who have had diabetes ten years or more.
Advanced glycation end-products (above called AGEs) are laid down in the connective tissues giving them a leathery consistency and reducing their flexibility.
This process is not isolated to the foot however, and affects the entire body including hands, shoulders, and the rest of the joints. The feet however, bear the brunt of these changes due to the greater amounts of matter they support all day, and weightbearing forces involved walking and standing.
Impact of Ankle Dorsiflexion Deficiency:
The ankle joint is often the first area of deficiency. It is not just that the joint itself stiffens, but that ankle dorsiflexion as a result reduces.
Arthokinematic function is altered as the anterior tibia translates forward on the talus, reducing dorsiflexion of the ankle.
This change results in compensations through the gait cycle, increasing load on the forefoot.
The narrower the angle of dorsiflexion, the higher the loading on the forefoot and increased local pressure under the forefoot during walking.
Diabetic Foot Damage from Limited Joint Mobility
Knowing that forefoot pressure and ulceration is increased by restricted joint movement explains why clinicians pursue this so seriously. Limited joint mobility in the diabetic foot does not adequately receive impact forces from the ground on each step, as normal feet should do.
Instead, pressure in these feet is often focused on specific areas, most often the heel, area beneath the first meta-fora, and clawed toe tips.
Untreated pressure areas can convert into blisters, subsequent breakdown, ulceration, and then deep infection which can result in a potentially fatal charcot process. When nerve sensation is reduced, these pressure related injuries are insidious and prevent diagnosis until the damage becomes huge.
Deforming factors include Charcot, ulcer, and other structural changes:
Fortunately, not all who suffer from limited joint mobility in this manner will develope charcot – the process of diabetic neuroarthropathy (often called charcot foot) destroying the bones – and the deformity process is complex.
Increased pressure on the midfoot stimulates a breakdown in the subchondral bone which then weakens.
Socketing the deformity into a rocker-bottom shape reduces the pressure, but dramatically increases the loads elsewhere in the architecture of the foot and alters walking significantly. – which then predisposes to ulcer formation most commonly under the first met and lesser toes, corresponding to the areas with prolonged increased stress.15-17 The persistent thickening of the skin, called hyperkeratosis, results from pressure and shear forces, acting as a protective response by thickening of the epidermis.
Calluses over a bony prominence are a warning sign of underlying increased mechanical stress, whilst those over bony prominences can turn into ulcerated pockets under the callus and current or emerging infection.
Regular callus removal in the clinic has been shown to impact outcomes in the diabetic foot pathologically, as a treatment modality.
Practical Strategies to reverse or reduce joint stiffness:
While it is ideally best to prevent ligamentous calcification from happening in the first place, even small decreases in joint restriction can impact dramatically on forefoot pressure and risk of ulcer in the at risk foot.
By stretched, stretched with myofascial work, and an optimally fitted pair of shoes and custom insoles, reduced joint range of motion can be minimized. The earlier that the pain and clamp down on the joint can be addressed, the better the outcome both short and long-term.
Myofascial Stretches:
Importantly, calf stretching exercises including gastrocnemius and soleus stretches are some of the most effective stretching techniques for improving ankle dorsiflexion and decreasing abnormal joint range of motion long-term. Nine-patient case series have demonstrated that with adherence to this, significant decreases in ankle range of motion can be achieved within weeks to months.15-20 Successful therapy techniques can involve manual therapy from a physical therapist, deep stretches position for twenty seconds followed by ankle circles and toe flaps-27 repetitions and then held again for thirty second holds.
For these to be successful they need to be performed consistently, thereby enhancing the effectiveness of the stretch rather than one occasional stretch every 3 days in a week Long.
Shoes, Insoles, and Offloading:
The foot structure can be supported with extra depth shoes and then custom insoles to offload specific areas, alleviating pressure and will help limit hyperstatic tissue response.
Customized shoes, injection, or total contact casting may be necessary when a patient with a stiff joint lands on an ulcer or Charcot foot. These same support structures are the pivotal offloading moments for the at risk patient home, from the angle of ankle dorsiflexion to diminished.
Blood glucose regulation in this situation is still the overriding long-term basis for success.
Supply: limiting glycation by maintaining as near normal glucose levels as possible will slow the development of CTN and allow all other therapies to be more successful in controlling the diabetic foot.