Biomechanics of the Foot in

Diabetes Mellitus
Some Theoretical Considerations

CRAIG B. PAYNE, DipPod(NZ), MPH*

Although diabetes mellitus is a biochemical disease, it has biomechan-

ical consequences for the lower extremity. Numerous alterations occur
in the function of the foot and lower extremity in people with diabetes.
This article evaluates biomechanical alterations of the foot in the pres-
ence of neuropathy in patients with diabetes in the context of several
theoretical concepts. Further study of these hypotheses will result in a
better understanding of how diabetes causes elevated plantar pres-
sures and the potential of strategies to prevent these changes so that
the burden of diabetic foot disease can be reduced. (J Am Podiatr Med
Assoc 88(6): 285-289, 1998)

Diabetes mellitus imposes a large economic burden
on society and the individual. Complications of the
foot are a significant contributor to this burden.1 Dia-
betes mellitus is a biochemical disease, but a large
number of lower-extremity complications of the dis-
order are due to biomechanical dysfunction. Dia-
betes not only alters the biomechanics of the lower
extremity, it also complicates any preexisting biome-
chanical dysfunction. Reviews of the biomechanics
of the foot in patients with diabetes are available
elsewhere,2-7 so the discussion here will focus on re-
viewing recent data and thought on foot biomechan-
ics in patients with diabetes in the context of a num-
ber of theoretical considerations.
A key feature of the foot in people with diabetes is
that dynamic plantar pressures are higher than in
those without diabetes. This feature is independent
of body weight.8 Issues concerning measurement of
plantar pressures have been adequately dealt with
elsewhere.9, 10 The causes of higher plantar pressure11
are generally assumed to be bony deformity, clawing
of the toes, pes cavus, lack of soft-tissue cushioning,
callus formation, and limited joint mobility. A loss of
protective sensation in the foot due to peripheral
sensory neuropathy permits undetected injury from
mechanical insults to occur to the foot when higher
*Lecturer, Department of Podiatry, La Trobe University,
Bundoora, Victoria 3083, Australia.
plantar pressures are present. Brand12 first elucidat-
ed the mechanical causes of plantar ulcers in neuro-
pathic feet.
Limited Joint Mobility
Limited joint mobility has been widely documented
in patients with diabetes.13-15 It is probably due to a
nonenzymatic glycosylation of collagen from the
chronic hyperglycemia, resulting in a stiffening of the
joint ligaments and other structures around joints.
Delbridge et al16 found a significant decrease in the
range of subtalar joint motion in diabetic patients
with a history of foot ulceration compared with con-
trol groups. Fernando et al17 showed that diabetic pa-
tients with limited joint mobility had higher plantar
pressures.
In 1949, Hiss18 suggested that a limitation in joint
mobility results in an alteration of the progression of
forces through the foot, which alters weightbearing.
It is generally assumed that limited joint mobility in-
creases plantar pressures owing to restriction of pro-
nation at the subtalar joint16 based on the traditional
understanding of the foot19 as a “mobile adaptor.”
Pronation at the subtalar joint when the foot con-
tacts the ground is assumed to allow the foot to ab-
sorb shock. However, recently several of the concepts
of Root et al19 have been questioned,20, 21 and one pos-

Volume 88 • Number 6 • June 1998 285

sible alternative, the sagittal-plane facilitation of mo-
tion model, has been proposed.22 It is also difficult to
accept that mobility of the subtalar joint allowing the
foot to absorb shock during the contact period of the
gait cycle could be related to increased pressures
under the forefoot during propulsion. Recently Ying-
ling et al23 demonstrated that there was no increase
in the impulse wave at the level of the tibia when
subtalar joint pronation was restricted, which raises
a question about subtalar joint pronation absorbing
impact shock.
The sagittal-plane facilitation of motion model22
suggests that normal foot function is dependent on
an adequate range of motion at the first metatar-
sophalangeal joint during dynamic function (which is
independent of the range of motion of the joint dur-
ing clinical examination) so that the windlass mecha-
nism24 can be established. This allows the foot to ad-
equately resist the stress applied to the foot during
the propulsive phase of gait. If this mechanism and
other autosupportive mechanisms22 are not estab-
lished owing to a functional hallux limitus or an inap-
propriate direction of “weight flow” through the foot
or to limited joint mobility affecting dorsiflexion of
the first metatarsophalangeal joint and plantarflexion
of the first ray, a number of compensatory mecha-
nisms are predicted by the model to occur.22 One of
these is an “off-loading” of the medial side of the
forefoot and an increase in weightbearing under the
lateral side of the forefoot. While other mechanisms
or structural changes may increase plantar pressures
under the first metatarsophalangeal joint, such as a
limited range of motion of the first ray,25 the model
offers another alternative theoretical explanation for
the correlation between limited joint mobility and in-
creased plantar pressures.
A restricted range of motion at the first metatar-
sophalangeal joint has been shown to be more com-
mon in patients with diabetes compared with con-
trols.26 One of the findings of Stokes et al27 was a
more lateral distribution of plantar pressures in the
diabetic group compared with controls. Stess et al28
showed that plantar pressures increased more in
those with a history of diabetic ulcers compared with
the diabetic control group, with the highest pressure
noted on the lateral side of the plantar forefoot. St
Zimney et al29 also reported a greater increase in
plantar pressures under the fourth and fifth metatar-
sal heads. These reported findings are consistent
with what would be predicted by the sagittal-plane
model; however, Ctercteko et al30 showed a medial
shift in the increase of plantar pressures. Schaff and
Cavanagh31 reported that a rocker-bottom shoe re-
duced pressures by over 30% under the medial fore-
286
foot, but increased pressures on the lateral side of
the forefoot. The sagittal-plane facilitation of motion
model would predict that the rocker sole would pre-
vent the autosupportive mechanisms of the foot from
being established owing to a lack of dorsiflexion of
the first metatarsophalangeal joint, resulting in an in-
crease in lateral plantar pressures.
The presence of limited joint mobility in patients
with diabetes raises the possibility of therapeutic in-
terventions to increase the mobility of the joints of
the foot, with the aim of reducing plantar pressures.
In a small uncontrolled trial, Curran et al32 used phys-
ical therapy on a group of diabetic patients with lim-
ited joint mobility for 6 weeks; the result was an in-
crease in the range of motion of the subtalar joint
from 14.5° to 24.5° and an increase in that of the mid-
tarsal joint from 17.6° to 31.4°. The peak plantar pres-
sures decreased from 10.1 to 7.2 kg/cm2. It is unclear
what exercises were used and which other joints
were mobilized, but this hypothesis is promising and
needs further investigation by means of prospective
clinical trials.
Sensory-Attenuation Hypothesis
The sensory-attenuation hypothesis, originally pro-
posed by Robbins et al 33-36 in relationship to athletic
footwear, states:
In humans, avoidance of uncomfortable or painful but
locally innocuous plantar cutaneous tactile stimuli
moderates shock on subsequent impacts when hu-
mans walk, run, or jump repetitively. This feedback
control circuit is optimized in terms of protection for
mechanical interaction of the bare foot and natural
surfaces. Eventually learning allows anticipatory
avoidance. Modern athletic footwear is unsafe be-
cause it attenuates plantar sensations that induce the
behavior required to prevent injury.33(p218)
This hypothesis is not without controversy,37, 38 but it
suggests that some plantar discomfort on impact is
required for optimal shock absorption, which is at-
tenuated by soft footwear. When impact is sensed,
some impact-moderating behavior takes place. If im-
pact is attenuated by soft footwear or if sensory neu-
ropathy is present, there is a perceptual illusion of
less plantar impact than actually exists, which re-
duces impact-moderating behavior.
As a consequence, the model predicts that more
weight is borne by the metatarsal heads and less by
the toes, which was demonstrated by Robbins and
Hanna39 in those who habitually wear soft running
shoes. Ctercteko et al30 showed a similar effect in pa-
tients with sensory neuropathy with a reduced toe
loading and increased metatarsal head pressures.
Journal of the American Podiatric Medical Association
Similar findings have been reported by Stokes et al27
and Boulton et al.35 Frykberg 5 attributed these report-
ed changes to intrinsic muscle atrophy and claw toe
development in patients with diabetic neuropathy;
however, it is proposed here that the sensory-attenu-
ation hypothesis offers an alternative explanation.
If this hypothesis can be demonstrated by pro-
spective studies to apply to the lower extremities of
those with sensory neuropathy, it raises a question
about the use of soft cushioning on orthoses or in
footwear in those who have not yet developed a sen-
sory neuropathy or are in the early stages of one. If
plantar sensations are further attenuated, this may
alter foot morphology and function in a detrimental
way. Further prospective investigations are needed
to test this hypothesis.
Structural Changes
The putative effects of motor neuropathy and ampu-
tations on foot function are adequately dealt with
elsewhere6 and are not considered here. The signifi-
cance of structural changes was demonstrated by
Cavanagh et al,40 who demonstrated that static struc-
tural variables are significant predictors of dynamic
foot function in walking. Measurements from stan-
dardized radiographs explained approximately 35%
of the variance of dynamic plantar pressures under
the first metatarsal and the heel. The two most domi-
nant factors in the predictions of pressures for both
regions were soft-tissue thickness and inclination of
the first metatarsal. For each 1° increase in first
metatarsal inclination, heel pressures increased by
17 kPa and first metatarsal head pressure increased
by 47 kPa.
In the hand, limited joint mobility causes a con-
tracture of the palmar aponeurosis that results in the
characteristic “prayer sign,” in which the patient can-
not oppose the palmar surfaces. It has been generally
assumed that this contracture does not occur in the
foot because of the weightbearing forces on the plan-
tar aponeurosis. However, in a dynamic situation, Kidd
and Kidd41 hypothesized that glycosylation of the col-
lagen-rich plantar aponeurosis would result in a con-
tracture of the plantar truss structures, leading to an
accentuated arch height via first ray plantarflexion
and the windlass mechanism. The result would be a
more rigid, high-arched foot with prominent metatarsal
heads. In support of this theory, pes cavus has been
shown to be more common in those with diabetes
than in nondiabetic controls,26 whereas the preva-
lence of pes planus was the same in the two groups.
The characteristic “intrinsic minus foot,”7 with
claw toes, anterior advancement of the plantar foot
Volume 88 • Number 6 • June 1998
pads, and depressed metatarsal heads, has generally
been considered to result from intrinsic muscle atro-
phy and dominance of the long flexor muscles. How-
ever, the hypothesis proposed by Kidd and Kidd and
the sensory-attenuation hypothesis discussed above
could also account for these structural changes.
Mechanism of Tissue Damage
It has been well documented that elevated pressures
are associated with tissue damage,42 but the mecha-
nism of the tissue damage has not been clearly eluci-
dated. Landsman et al 43 proposed a cellular model
that shows that high rates of tissue deformation may
cause elevated intracellular calcium concentrations,
resulting in cellular death, while comparable loads
gradually applied do not. They hypothesized that ulcer
formation is a result of high-strain-rate deformation
rather than the actual peak threshold. They further
hypothesized that a reduction in the rate of loading,
rather than the reduction of peak loads, will lead to
healing and minimize the recurrence of foot ulcera-
tion. Strength in the anterior compartment of the leg
will be reduced because of the motor neuropathy, re-
sulting in a “foot slap” and a higher rate of forefoot
loading. They proposed that an ankle-foot orthosis
will reduce foot slap. No data can be found linking
the velocity of foot strike and anterior-compartment
weakness in those with plantar ulcers. Anderson et
al44 found a 21% reduction in strength of the ankle
dorsiflexion muscle group in insulin-dependent dia-
betic patients compared with controls, which would
support the hypothesis presented above. However,
Anderson and Mogensen45 showed that peak velocity
at the ankle was lower in patients who had been in-
sulin-dependent for a long time, presumably owing to
a slower cadence.
Most of the literature has focused on elevated
plantar pressure, probably because of the limitations
inherent in the equipment used to measure shear
stress under the foot. The consequences of combined
shear and vertical pressures are likely to be much
greater than those of vertical pressures alone. Ul-
brecht et al9 discussed the issues surrounding the
variability in the reported threshold of vertical pres-
sures at which tissue damage occurs. Some of the
variability may be due to shear stresses. Dinsdale 46
was able to induce an ulcer in the skin of swine with
a verticle pressure of 290 mm Hg, but a pressure as
low as 45 mm Hg was sufficient when friction was
present. Davis 47 proposed the existence of a “wrin-
kled carpet” effect, with the tissues being either
“bunched up,” stretched, or sheared, depending on
the direction of slippage. Brand48 showed in a study
287
using pressure pads on pigs that when the pressure
was exerted over 5 to 7 hours, there was some tissue
destruction. The pressure was greatest at the center
of the pressure pads, but the greatest tissue damage
was at the periphery of the pads, where there is in-
creased shear stress between the area under pres-
sure and the area not under pressure. Brash et al 49
demonstrated a signal void (“dropout”) on magnetic
resonance imaging (MRI) evaluation indicating a mi-
croscopic hemorrhage in the subcutaneous fat in the
region of prior ulceration in diabetic subjects. Shear
stress may be responsible for the type of tissue dam-
age demonstrated by the MRI. Bojsen-Moller and
Lamoreux50 showed that dorsiflexion of the toes tight-
ens the connective-tissue framework of the ball of the
foot, which enables shear forces to be transferred to
the skeleton. Limited joint mobility will restrict this
process, and the glycosylation of tissues will also in-
terfere with this mechanism, further increasing the
potential for tissue damage.
Conclusion
This article has proposed several new theoretical
concepts regarding biomechanical alteration of the
foot in the presence of neuropathy in patients with
diabetes mellitus. As yet, these concepts are unsup-
ported. Further prospective study of these hypothe-
ses will result in a better understanding of how dia-
betes causes elevated plantar pressures and the po-
tential of strategies to prevent these changes and the
subsequent tissue damage. The proposed hypotheses
are not necessarily inconsistent with one another,
but each has different consequences for therapeutic
interventions. Appropriate prospective clinical inves-
tigations are needed to test the interventions. Strate-
gies that need to be implemented should be done so
in the wider context of appropriate intervention strat-
egies for the diabetic foot.51
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