Elsevier

Clinical Biomechanics

Volume 20, Issue 5, June 2005, Pages 532-539
Clinical Biomechanics

Does the thickening of Achilles tendon and plantar fascia contribute to the alteration of diabetic foot loading?

https://doi.org/10.1016/j.clinbiomech.2005.01.011Get rights and content

Abstract

Background. The diabetic foot often undergoes abnormal plantar pressures, changing in walking strategy, ulcerative processes. The present study focuses on the effects that diabetes-induced alterations of Achilles tendon, plantar fascia and first metatarso-phalangeal joint—both anatomical and functional—may have on foot loading.

Methods. Sixty-one diabetic patients, with or without neuropathy, and 21 healthy volunteers were recruited. Thickness of Achilles tendon and plantar fascia was measured by ultrasound. Flexion–extension of the first metatarso-phalangeal joint was measured passively. Main biomechanic parameters of foot–floor interaction during gait were acquired and related to the above measurements.

Findings. Plantar fascia and Achilles tendon were significantly (P < 0.05) thicker in diabetics than in controls; mean values (SD) for controls, diabetics without and with neuropathy were 2.0 mm (0.5), 2.9 mm (1.2) and 3.0 mm (0.8) for plantar fascia, respectively, and 4.0 mm (0.5), 4.6 mm (1.0) and 4.9 mm (1.7) for Achilles tendon, respectively. Flexion–extension of the first metatarso-phalangeal joint was significantly (P < 0.05) smaller in diabetics than in controls; mean values (SD) for controls, diabetics without and with neuropathy were 100.0° (10.0), 54.0° (29.4) and 54.9° (17.2), respectively. The increase in the vertical force under the metatarsals was strongly related (R = 0.83, explained variance = 70.1%) to the changes in the three above parameters.

Interpretation. Thickening of plantar fascia and Achilles tendon in diabetics, more evident in the presence of neuropathy, concurs to develop a rigid foot, which poorly absorbs shock during landing (performs the physiological impact force absorption during landing). More generally, an overall alteration of the foot–ankle complex motion likely occurs throughout the whole gait cycle, which partly explains the abnormal loading under the forefoot.

Introduction

Diabetes mellitus is a diffuse endocrine disease characterised by metabolic abnormalities and long-term complications. Plantar ulcers due to the alteration of gait are hard-to-heal, recurrent wounds in diabetics, and can lead to the amputation of the minor or major foot joints. Great attention is therefore paid to the treatment of the diabetic foot and the prevention of ulcers (Kwon and Mueller, 2001).

Severe damages to both locomotor structures and functions of diabetic patients come from the onset of peripheral neuropathy, which is responsible for sensory deficiencies of the most distal parts of the body (Kwon and Mueller, 2001). In particular, the motor control of gait is compromised by the diminished feedback from the somatosensory system (Cavanagh et al., 1998), and nerve degeneration may also compromise the performance of gait (Schoenhaus et al., 1991). Abundant scientific documentation has been produced, that deals with diabetic neuropathy, both of sensory and motor origin (Boulton, 1991, Edmons et al., 1986, Uccioli et al., 1992). Most of these studies addressed the diabetic neuropathy as the almost only cause for the onset of the ulceration processes, thus delaying the development of clinical interest and basic research towards previous and/or concurrent causes. As a result, the setup of screening and treatment for the prevention of neuropathic ulcers is still poorly effective.

A different approach to the investigation of all the potential causes of the plantar ulceration process comes from the observation that the common sign of the distinct diabetic syndromes is hyperglycaemia, which promotes glycosilation of proteins and the consequent accumulation of advanced glycosilation end-products in most human tissues (Barbagallo et al., 1993). This means that muscles, cartilages, tendons, ligaments, all might experience structural changes even before the onset of diabetic neuropathy, and might then concur to alter the overall function of the foot–ankle complex during gait. As a result, several factors significantly contribute to the ulceration of the diabetic neuropathic foot according to linear or more complex laws (Boulton, 1994). Among those factors, attention should be paid to the modifications of main tendons and ligaments that manage the foot.

The thickening of tendinous and ligamentous structures of diabetic patients’ hands and feet—due to the abnormal storage of collagenous layers in the tissue—has been clinically observed since 1950s (Lundbeak, 1957), even though this does not necessarily entail significant changes in their elastic properties (Duffin et al., 2002).

Physiologically, Achilles tendon and plantar fascia play an important role in the biomechanics of the foot (Grant et al., 1997, Arangio et al., 1998). Together with the metatarso-phalangeal joints, they synergically work to absorb shock and prevent the collapse of the longitudinal arch of the foot during landing, when plantar fascia acts like a truss, and to lock the midtarsal bones and stabilise the arch during propulsion, when plantar fascia acts like a beam. This last stabilising mechanism was described by Hicks as the Windlass mechanism (Hicks, 1954, Perry, 1983): in a healthy subject it should take place at the beginning of heel rise, when Achilles tendon contributes to talus supination and to plantar fascia tightening. The plantar ligament is further tightened by the flexion at the metatarso-phalangeal joints, and maintains the longitudinal arch high and rigid to efficiently perform the propulsion.

From an experimental point of view some authors proved the described anatomical link of Achilles tendon, plantar fascia and metatarso-phalangeal joints by measuring the strain in the plantar fascia under various loading conditions of the Achilles tendon and under different angular positions of the metatarso-phalangeal joints (Carlson et al., 2000, Snow et al., 1995). Most of these studies, however, were conducted in vitro and only focused on the effects each single cited structure has on the others.

On the basis of the above observations, it is reasonable to hypothesize that, once the main foot tendinous and ligamentous structures are significantly modified, as it occurs in diabetic patients, the overall foot function is compromised. Among the bulk of the possible experimental investigations, the present study addresses the in vivo examination of the foot loading during gait in the presence of structural alterations of Achilles tendon and plantar fascia—namely changes of tissue thickness at different levels of neuropathy, and altered motion of the first metatarso-phalangeal joint. The hypothesis, in fact, is that, together with the atrophy of the intrinsic muscles of the foot secondary to motor neuropathy, the overall thickening of the above structures does contribute to the maintenance of the foot in a cavus configuration, thus hardly accomplishing foot landing and propulsion. This phenomenon might then contribute to the occurrence of abnormal loading in the areas at risk of ulceration (metatarsal heads).

Section snippets

Recruited population

Patients were recruited from the outpatients clinic of the Metabolic Diseases Department at the University of Rome “Tor Vergata”. Main exclusion criteria were: (i) age over 70 years; (ii) history of peripheral vascular, neurological (other than those of diabetic aetiology), musculo-skeletal, or rheumatic disease; (iii) any major or minor amputation; (iv) peripheral vascular diseases with ankle brachial pressure index <0.85; (v) Charcot neuroarthropathy and hallux rigidus due to previous traumas.

Results

The demographic data of the recruited population are provided in Table 1. There were no significant differences between groups for age, BMI, metabolic control or diabetes duration.

As for the measurements which dealt with the structural and functional impairing factors hereby observed, a progressive reduction of IMPJ was observed throughout the pathologic classes with respect to controls. The reduction became statistically significant for DN and DPNU groups (Table 2). Ultrasound examination

Discussion

In diabetic patients, peripheral neuropathy (sensory and motor) is responsible for remarkable changes in both structure and function of the foot. Atrophy and reduced volume of intrinsic muscles, deformities of the foot structure such as claw toes and prominent metatarsal heads, reduced strength of the lower limb muscles, alterations of plantar soft tissue and denervation of tendinous and ligamentous structures have been reported in clinical observations and experimental studies (Andersen et

Conclusions

Even though neuropathy is still considered as the major responsible for the ulceration of the diabetic foot, we believe that several other factors should be investigated and monitored, in the attempt of preventing the formation of such severe wounds.

In the present study we observed structural alterations of the main tendinous and ligamentous structures of the foot–ankle complex in presence of mild-to-severe diabetic neuropathy. Range of motion of the first metatarso-phalangeal joint in the

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