The Essentials of Charcot Neuroarthropathy: Biomechanics, Pathophysiology, and MRI Findings

By Claude Pierre-Jerome

The Essential Charcot Neuroarthropathy: Biomechanics, Pathophysiology, and MRI Findings provides a comprehensive analysis of Charcot neuroarthropathy (or Charcot Foot) in diabetic patients. All aspects are covered, including epidemiology, biomechanics, pathophysiology, socioeconomic impacts, radiological findings, and differential diagnosis, with an emphasis on MRI. Chapters address the challenges of pre-and-post surgical management of Charcot neuroarthropathy and the role of unconventional imaging modalities in diagnosis. The book presents an analysis of the normal biomechanics of the ankle and foot, the biomechanical derangements of the ankle-foot unit (including abnormal gait) caused by diabetes Type II, and more.

Finally, there is also a reference of the pathophysiology of diabetes-induced peripheral neuropathy and its direct link with the development of Charcot neuroarthropathy foot. Diabetes-induced Charcot foot is frequently misunderstood, misinterpreted and misdiagnosed which can lead to confusion and detrimental management with reported high morbidity.

• Presents a clear differentiation of Charcot neuroarthropathy with other conditions such as osteoarthritis, gout, psoriasis, rheumatoid arthritis, the Madura foot, and others
• Provides a state-of-art catalogue of all radiological features of Charcot neuroarthropathy with MRI
• Describes the pre-and post-surgical procedures used for the management of Charcot neuroarthropathy and their socioeconomic impacts
• Includes MRI color images of soft tissue damages for ease of understanding

• Language: English
• Publisher: Elsevier Science
• Release date: May 11, 2022
• ISBN: 9780323995788

Claude Pierre-Jerome

Dr. Pierre-Jerome has over 40 years of experience in Radiology and research including diabetes, skeletal muscle and bone marrow. Author of several publications in International Journals. Co-author of five books in Radiology. Reviewer for US and European Journals. Author of two novels. He’s a member of several Medical Associations and fluent in English, French, Spanish and Norwegian.?He was the visiting Associate Professor in University of Rochester, New York and worked as Faculty and Director of International Exchange Program for the Musculoskeletal Division at Emory University School of Medicine, Atlanta GA, USA.?Presently he is working at the Akershus University Hospital in Oslo, Norway.

Book preview

Front Cover for The Essentials of Charcot Neuroarthropathy - Biomechanics, Pathophysiology, and MRI Findings - 1st edition - by Claude Pierre-Jerome

The Essentials of Charcot Neuroarthropathy

Biomechanics, Pathophysiology, and MRI Findings

Claude Pierre-Jerome

Emory University, Atlanta, GA, United States

Oslo University, Oslo, Norway

Table of Contents

Cover image

Title page

Copyright

List of contributors

Acknowledgments

Introduction

Chapter 1. Biomechanics of the ankle-foot unit: derangements and radiological signs

Abstract

1.1 Basic biomechanics of the normal ankle-foot unit

1.2 The ankle-foot unit: anatomy and structural organization

1.3 The plantar arches of the foot: biomechanical functions

1.4 The gait and gait cycle, normal biomechanics in the gait cycle

1.5 The swing phase

1.6 Muscle involvement in the gait phases, rocker action of the ankle-foot unit

1.7 Gait abnormalities in the diabetic foot

1.8 Biomechanical derangements of the diabetic foot: Charcot joint disease and limitation of joint motility

1.9 Plantar pressure abnormalities in diabetic peripheral neuropathy

1.10 Diabetic peripheral neuropathy and structural changes in bones, joints, and soft tissues

References

Chapter 2. Diabetes and Charcot neuroarthropathy: pathophysiology

Abstract

2.1 Diabetes: definition and general considerations

2.2 Pathophysiology of diabetes mellitus type 1 and type 2

2.3 Diabetes-induced Charcot neuroarthropathy

2.4 Charcot foot syndrome versus Charcot neuro-osteoarthropathy or Charcot neuropathic-sarco-osteoarthropathy

2.5 Theories of Charcot neuroarthropathy: the German theory and the French theory

2.6 Prevalence of Charcot neuroarthropathy

2.7 Conditions that influence the advent of Charcot neuroarthropathy

2.8 Symmetrical and asymmetrical neuropathy in relation to Charcot neuroarthropathy

2.9 Autonomic neuropathy and neuropathic edema

2.10 Nondiabetic conditions producing Charcot foot or Charcot neuroarthropathy

2.11 Complications of Charcot neuroarthropathy (bones and soft tissues)

2.12 Complications affecting soft tissues

2.13 Signs of remission and recurrence of Charcot neuroarthropathy

2.14 Role of imaging in Charcot neuroarthropathy

2.15 Differential diagnosis or common conditions that resemble Charcot neuroarthropathy

2.16 Prognosis of Charcot neuroarthropathy

2.17 Conclusion

References

Chapter 3. Epidemiology and socioeconomic impact of diabetes and Charcot neuroarthropathy

Abstract

3.1 Introduction

3.2 Diabetes mellitus type 2: epidemiology and prevalence worldwide

3.3 Diabetes mellitus type 2: effect of rapid economic development and modernization

3.4 Prevalence of diabetes mellitus type 2 in some countries

3.5 Common risk factors for diabetes mellitus type 2 complications

3.6 General costs of diabetes mellitus type 2 in the United States

3.7 Diabetes-induced Charcot neuroarthropathy

3.8 Risk factors for Charcot neuroarthropathy

3.9 Foot ulcerations in Charcot neuroarthropathy

3.10 Infection

3.11 Cost of foot ulceration

3.12 Foot amputation in Charcot neuroarthropathy

3.13 Depression, anxiety, dementia, and sexual dysfunction in Charcot neuroarthropathy

3.14 Life expectancy and mortality in Charcot neuroarthropathy

3.15 Conclusion

References

Chapter 4. Charcot neuroarthropathy: historical analysis and characteristics

Abstract

4.1 Charcot neuroarthropathy (the diabetic foot): definition and characteristics

4.2 Historical perspectives of Charcot neuroarthropathy

4.3 Epidemiology, incidence, prevalence, and ethnicity of diabetic foot disease

4.4 Risk factors and disorders producing the Charcot Foot

4.5 Development and presentation of Charcot neuroarthropathy: the theories (acute inflammation theory and neurotraumatic and neurovascular theory) and predisposing factors

4.6 Clinical presentation and distribution of Charcot involvement and the concept of vicious cycle and equinus deformity of the Charcot foot

4.7 Stages of Charcot neuroarthropathy

4.8 Classifications of Charcot neuroarthropathy based on anatomic locations: a meta-analysis

4.9 New classification: a proposed classification based on anatomy, biomechanics, and magnetic resonance imaging findings in bones and soft tissues

References

Chapter 5. Normal bone, bone deformity, and joint dislocation in Charcot neuroarthropathy

Abstract

5.1 Normal bone: infrastructure and biomechanical properties of bone

5.2 Biomechanical properties of bone

5.3 Loading and off-loading of the ankle-foot unit: generalities

5.4 Loading and off-loading of the foot in diabetes

5.5 Pathomechanics of the midfoot: mechanism of bone deformity

5.6 Joint dislocations in Charcot neuroarthropathy

5.7 Diagnostic imaging

5.8 Complications of Lisfranc dislocation

5.9 Toe deformities

5.10 Second ray syndrome

References

Chapter 6. Biomechanical behavior of bone. Fractures in Charcot neuroarthropathy

Abstract

6.1 The normal bone: biomechanical characteristics

6.2 Bone elasticity: cortical bone versus trabecular bone

6.3 Biomechanical behavior of bone: role of the bone matrix

6.4 Muscular activity and effects on bone

6.5 Bone geometry and effects on biomechanical behavior

6.6 Bone changes with aging: deterioration of intrinsic and extrinsic resistance

6.7 Changes in trabecular bone with aging

6.8 Bone remodeling: mechanism and characteristics

6.9 Diabetes type 2: effects on bone infrastructure

6.10 Fractures of the ankle–foot unit in diabetes mellitus

6.11 Stress fractures of the ankle–foot unit

6.12 DMT2 therapeutics and effects on bones

References

Further reading

Chapter 7. Osteomyelitis in Charcot neuroarthropathy

Abstract

7.1 Osteomyelitis: definition and history

7.2 Osteomyelitis: clinical characteristics and risk factors

7.3 Ulceration and osteomyelitis

7.4 Diagnosis of osteomyelitis in Charcot neuroarthropathy

7.5 Osteomyelitis versus Charcot neuroarthropathy

7.6 Osteomyelitis: generalities and pathogenesis in diabetes-related Charcot neuroarthropathy

7.7 Imaging of osteomyelitis in Charcot neuroarthropathy

References

Chapter 8. Differential diagnosis in Charcot neuroarthropathy

Abstract

8.1 Introduction

8.2 Common inflammatory conditions that resemble Charcot neuroarthropathy

8.3 Rheumatoid arthritis and Charcot neuroarthropathy

8.4 Osteoarthritis, diabetes, and Charcot neuroarthropathy

8.5 Gout and Charcot neuroarthropathy

8.6 Psoriasis arthritis and Charcot neuroarthropathy

8.7 Pseudogout and Charcot Neuroarthropathy

8.8 Infectious conditions that resemble diabetes-induced Charcot neuroarthropathy

8.9 Human immunodeficiency virus infection and Charcot neuroarthropathy

8.10 Nondiabetic conditions with underlying neurogenic arthropathy

8.11 Covid-19 infection and diabetes

References

Further reading

Chapter 9. The articular cartilage: biomechanics and damage in diabetes-induced Charcot neuroarthropathy

Abstract

9.1 Introduction

9.2 Articular cartilage: function, composition, and structure

9.3 Biomechanical behavior of articular cartilage

9.4 Biomechanics of cartilage degeneration

9.5 Metabolism of the cartilage: role of the chondrocytes

9.6 The link between diabetes and osteoarthritis

9.7 Risk factors for diabetes mellitus type 2 and osteoarthritis

9.8 Effects of diabetes mellitus type 2 and hyperglycemia on cartilage

9.9 Effects of diabetes mellitus type 2 and hyperglycemia on tendons and ligaments

9.10 Relevance of the triad: diabetes, arthritis, and obesity

9.11 Diabetes, osteoarthritis, and subchondral bone lesion

9.12 Diabetes and association with loss of cartilage and impairment of fracture repair

9.13 Magnetic resonance imaging of articular cartilage

References

Chapter 10. The skin: anatomy and pathologies in diabetes

Abstract

10.1 Introduction

10.2 Layers of the skin

10.3 Blood supply to the skin of ankle and foot

10.4 Innervation of the skin of the ankle-foot unit

10.5 Skin diseases in diabetes: prevalence and pathogenesis

10.6 Skin ulceration

10.7 Sinus tracts

10.8 Diabetic blisters (bullosis diabeticorum)

10.9 Callus and corns

10.10 Skin xerosis

10.11 Eruptive xanthomatosis

10.12 Madura foot (mycetoma)

References

Further reading

Chapter 11. Plantar subcutaneous fat pad and Kager fat pad and changes in Charcot neuroarthropathy

Abstract

11.1 The foot fat pads: generalities

11.2 The plantar fat pad: function, anatomy, and histology

11.3 Biomechanics of the plantar fat pad

11.4 Plantar fat pad and pressure distribution

11.5 Plantar fat pad atrophy: causes and pathophysiology

11.6 Effects of diabetes and hyperglycemia on the plantar fat tissue

11.7 The calcaneal fat pad

11.8 Diabetes mellitus type 2-related lesions in the plantar fat pad

11.9 The Kager fat pad

References

Chapter 12. The plantar aponeurosis: anatomy, pathomechanics, imaging, and pathologies related to Charcot neuroarthropathy

Abstract

12.1 The plantar aponeurosis: anatomy

12.2 MR anatomy of the plantar aponeurosis: relationship with adjacent structures

12.3 Pathomechanics of plantar aponeurosis

12.4 Pathologies of plantar aponeurosis in relation with diabetes and Charcot neuroarthropathy

12.5 Plantar fibromatosis

References

Chapter 13. The intrinsic and extrinsic muscles: anatomy and pathologies in diabetes-related Charcot neuroarthropathy

Abstract

13.1 The intrinsic plantar foot muscles

13.2 The extrinsic muscles

13.3 Pathomechanics of the foot muscles

13.4 Pathologies of the muscles in diabetes-related Charcot neuroarthropathy

13.5 Conclusion

References

Further reading

Chapter 14. The Achilles tendon: anatomy biomechanics and changes in Charcot neuroarthropathy

Abstract

14.1 Introduction

14.2 Achilles tendon anatomy

14.3 Biomechanics of the Achilles tendon

14.4 Pathologies of the Achilles tendon

References

Chapter 15. The tendons and ligaments of the ankle-foot unit, the tarsal tunnel, the sinus tarsi, fascial compartments of the ankle-foot unit, and changes seen in Charcot neuroarthropathy

Abstract

15.1 Introduction

15.2 The tendons of the ankle-foot unit

15.3 Imaging considerations

15.4 Tendon pathology (tendinosis, tear, and tenosynovitis)

15.5 Pathophysiology of tendon disease in diabetes and Charcot neuroarthropathy

15.6 Tendinosis

15.7 Tenosynovitis

15.8 Tendon rupture

15.9 The ligaments of the ankle-foot unit

15.10 The tarsal tunnel

15.11 The sinus tarsi

15.12 Fascial compartments of the ankle-foot unit

References

Further reading

Chapter 16. The synovium and bursae of the ankle-foot unit: anatomy and pathologies in Charcot neuroarthropathy

Abstract

16.1 The synovium

16.2 The synovial joints and the functions of the synovium

16.3 The synovium and the tendon: functions of the synovium

16.4 Pathologies of the synovium at the ankle-foot unit

16.5 The bursa

16.6 Pathology of the bursa: imaging

References

Further reading

Chapter 17. The vascular system of the ankle-foot unit: anatomy and pathologies in Charcot neuroarthropathy

Abstract

17.1 Anatomy of the vascular system of the ankle-foot unit

17.2 Pathologies of the vascular system

17.3 Role of imaging in peripheral arterial disease

17.4 Monckeberg’s arteriosclerosis

17.5 Muscle infarction in diabetic foot

17.6 Necrosis in Charcot neuroarthropathy

References

Chapter 18. The nervous system: innervations of the skeleton; bone homeostasis; and peripheral neuropathies (Baxter’s neuropathy, tarsal tunnel syndrome, and peroneal neuropathy)

Abstract

18.1 Introduction

18.2 The nervous system and innervations of the skeleton

18.3 The peripheral nervous system: somatic innervation of bones

18.4 Peripheral nervous system: autonomic (sympathetic and parasympathetic) innervation of bones

18.5 Characteristics of the skeleton and regulation of bone homeostasis

18.6 Autonomic innervation of the bone marrow

18.7 The bone marrow niche

18.8 Clinical relevance of diabetic autonomic neuropathy

18.9 Diabetic peripheral neuropathy and bone disease

18.10 Influence of the peripheral nervous system on bone growth, fracture healing, denervation, and heterotopic bone formation

18.11 Pathophysiology of bone pain

18.12 Peripheral neuropathies of ankle-foot unit: Baxter’s neuropathy, tarsal tunnel syndrome, and peroneal neuropathy

18.13 Peroneal neuropathies

18.14 Conclusion

References

Chapter 19. The surgical management of the Charcot foot: physical examination of the foot prior to surgery, indications and criteria for amputation, and surgical techniques

Abstract

19.1 Examination of the Charcot neuropathic foot

19.2 Current conservative management of Charcot neuropathic foot

19.3 Indications and criteria for surgery

19.4 Current surgical management of Charcot neuropathic foot

19.5 Amputation

19.6 Conclusion

References

Chapter 20. The operated Charcot foot: biomechanics of the operated foot and foot ulcerations and their management

Abstract

20.1 Biomechanics of the operated foot

20.2 Ulcerations: management and follow-up

20.3 Preventive measures for Charcot foot deformity: the role of footwear

20.4 Complications of the deformed Charcot foot

20.5 Surgical management of the deformed Charcot foot: rehabilitation

20.6 Psychosocial implications of the Charcot foot

References

Chapter 21. The surgical approach and follow-up of the complicated Charcot foot: general considerations

Abstract

21.1 Physical examination of the Charcot neuroarthropathic foot (diabetic foot)

21.2 Classifications

21.3 Current conservative management of Charcot neuropathic foot, diabetic foot infections, and preventative measures for skin ulcerations

21.4 Risk factors for diabetic foot ulcers

21.5 Indications and criteria for surgery and amputation

21.6 Surgical management of the infected diabetic foot and surgical techniques and prognosis

21.7 Surgical management of the deformed Charcot foot: postsurgical recovery and rehabilitation

21.8 Future nonoperative developments and surgical techniques

21.9 Imaging techniques

21.10 Diabetic foot ulcers: new debridement methods and wound healing strategies

References

Further reading

Chapter 22. Imaging modalities in Charcot neuroarthropathy: indications and usefulness

Abstract

22.1 Introduction

22.2 Radiography: indications

22.3 Ultrasonography: indications in Charcot neuroarthropathy

22.4 Computed tomography: indications in Charcot neuroarthropathy

22.5 Nuclear medicine: use in Charcot neuroarthropathy

22.6 Magnetic resonance imaging in Charcot neuroarthropathy

22.7 Magnetic resonance imaging: protocol and indications

References

Chapter 23. Considerations of different imaging techniques in the evaluation of Charcot neuroarthropathy (MR spectroscopy, MR diffusion tensor imaging-tractography, MR elastography, and positron emission tomography/magnetic resonance imaging)

Abstract

23.1 Introduction

23.2 Ultrasonography (Doppler, tractography) in Charcot neuroarthropathy

23.3 Dual-energy spectral computed tomography and positron emission tomography computed tomography in Charcot neuroarthropathy

23.4 Nuclear imaging in Charcot neuroarthropathy

23.5 Advanced MR techniques in Charcot neuroarthropathy

23.6 Magnetic resonance imaging of skeletal muscle: qualitative and quantitative techniques (MR spectroscopy, MR diffusion tensor imaging-tractography, MR elastography, and positron emission tomography/magnetic resonance imaging)

23.7 Areas of research needed in the future

References

Index

Copyright

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List of contributors

Eildar Abyar,     University of Alabama, Birmingham, AL, United States

Dana M S Al Nuaimi,     Rashid Hospital, Dubai, United Arab Emirates

Usama M. AlBastaki,     Rashid Hospital, Dubai, United Arab Emirates

Reem Alketbi,     Rashid Hospital, Dubai, United Arab Emirates

Patrick Battaglia,     Logan University, Chesterfield, MO, United States

Arne S. Borthne,     Oslo University, Oslo, Norway

Sadaf Batool Faisal,     Rashid Hospital, Dubai, United Arab Emirates

Jonn Terje Geitung,     Oslo University, Oslo, Norway

Michael D. Johnson,     University of Alabama, Birmingham, AL, United States

Norman W. Kettner,     Department of Radiology, Logan University, Chesterfield, MO, United States

Hossameldin Ahmed Kotb,     Rashid Hospital, Dubai, United Arab Emirates

Haley McKissack,     University of Alabama, Birmingham, AL, United States

Johnny U.V. Monu,     University of Rochester, New York, NY, United States

Martin Jervis Nsubuga,     Oslo University, Oslo, Norway

Claude Pierre-Jerome

Emory University, Atlanta, GA, United States

Oslo University, Oslo, Norway

Acknowledgments

I am deeply thankful to Helene Lie, senior librarian at Akershus University Hospital Medical Library in Oslo, for her exceptional effort and times. Helene was responsible for the literature research. She provided an incredible amount of data that contributed to the elaboration of the book. Without Helene, the realization of this book would have been impossible.

Tusen takk skal du ha! Thank you very much!

I am extremely grateful to my late parents Ulda Josephine and Luc, to my sisters Yola and Circee, to my brothers Herns, Henry, Frantz, Yves for their patience and understanding. This academic work is the result of tremendous efforts and countless working times which could have been fruitless without their unconditional support.

Merci beaucoup. Thank you very much!

Introduction

Claude Pierre-Jerome

The human foot is one of the nature’s works of art and as such, it has not yet been fully recognized and explained. It will require a deal of scientific investigation before this structure is fully understood.

Georg Hohmann

These words from Georg Hohmann’s textbook Fuss und Bein: ihre Erkrankungen und deren Behandlung edited in 1923 are still relevant today. If the anatomy of the foot is known almost in its entirety, its biomechanics, and the pathophysiology of certain of its diseases are still under investigation. A classic example of the latter is the diabetic foot also called as the Charcot foot or Charcot neuroarthropathic foot. A better understanding of the diabetic foot requires not only a detailed knowledge of foot anatomy but also a comprehension of the biomechanical functions of the ankle and foot anatomical components, which constitute the ankle–foot unit.

From an anatomical and biomechanical standpoint, the ankle and the foot are closely related. They interact to provide for a harmonious and delicate functioning both during gait and while standing. Biomechanically, the ankle and the foot form the ankle–foot unit to which the authors constantly refer in the elaboration of this book. Functionally, the ankle–foot unit is made of three indivisible components: the hindfoot (or rearfoot), the midfoot, and the forefoot.

The incidence of diabetes mellitus has increased in the last two to three decades, as have its complications. Likewise, important progress has been achieved regarding its prevention, diagnosis, and treatment. Nevertheless, there are still challenges to overcome. When complications erupt from diabetes mellitus, the inconceivable may become reality. This is particularly true with changes that gradually, perhaps irreversibly, take place in the musculoskeletal system, especially in the lower extremity. For reasons not completely understood, diabetes mellitus can affect every anatomic structure of the musculoskeletal system: skin, fat, muscle, fascia, ligaments, tendons, synovium, hyaline cartilage, vasculature, nerves, and skeleton.

The changes that take place in the bone marrow of the diabetic patient deserve particular attention. Despite the advances of imaging technology, the bone marrow per se remains a vast domain of ambiguity and uncertainty. This is probably due to the histological complexity of the marrow which is composed of hematopoietic and fatty cells embedded in a net of trabecular bone. Frequently, although the prevalence is unknown, edema of the bone marrow is seen on magnetic resonance images (MRI) of the diabetic’s axial and appendicular skeleton. In the diabetic foot, whether the bone marrow edema is associated with infection or noninfected inflammation, the mechanism by which it is engendered remains enigmatic and controversial. Is the edema a manifestation of mechanical derangement? Or a sign neurovascular damage? Thorough scientific investigations by means of new imaging modalities such as MRI or molecular nuclear medicine imaging may provide a deeper understanding of the genesis and localization of the edema in the intra- or extra-cellular compartment.

The myriad of disorders that strike the muscles, fat tissues, and the joints of the foot are not better understood, but they are certainly as relevant. The radiological analysis of changes that occur in the diabetic foot requires both knowledge and experience. Understanding is a must. And the understanding of most changes seen in the diabetic foot cannot be complete if the basic knowledge of biomechanics of the ankle–foot unit and the prevailing pathophysiology are lacking.

There are several books and countless articles covering the social, epidemiological, dietetic, clinical, and therapeutic aspects of diabetes and its complications. From a radiological standpoint, there is a penury of publications and documents related to biomechanics, pathophysiology, and diversity of anatomical derangements seen in the diabetic foot. Radiologists, especially specialists in the musculoskeletal system, podiatrists, foot surgeons, diabetologists and others, should be aware of the biomechanics and biomechanical anomalies of the ankle–foot unit. Any study of the biomechanics of the foot must necessarily include the ankle, and vice versa, for both are integral parts of an indivisible unit. Likewise, imaging investigations of the diabetic foot must include the ankle joint, as the structures of the entire ankle–foot unit are doomed to damages resulting from diabetic neuroarthropathy. In the last five decades the rapid evolution of imaging technologies, especially the advent of MRI, has alleviated the painful task of understanding and interpreting complex pathologies such as the chronological phases of bleeding/hematoma. The visualization of the neuroarthropathic lesions of the diabetic foot has become easier amid the technological advances in radiology; nevertheless, the mechanism by which many of these neuroarthropathic lesions occur remains in the domain of the unknown.

Diabetes-induced Charcot neuroarthropathy (or diabetic foot) is a complex and poorly understood condition. Its understanding and interpretation constitute a challenge for radiologists, podiatrists, foot surgeons, osteopaths, primary care, and other health-care providers engaged in its prevention, diagnosis, and management. The diabetic foot is a pathological entity per se. It has its proper anatomical derangements, biomechanics, pathophysiology, morbidity, and costly socioeconomic impact. The main purpose of this book is to provide a wide spectrum of relevant information vis-à-vis diabetes-related Charcot neuroarthropathy.

This book is unique for several reasons. First, there is no dedicated book on the Charcot neuroarthropathy in the radiological literature. Secondly, the content (biomechanical, pathophysiological, and radiological aspects of diabetes-induced Charcot neuroarthropathy) provides a comprehensive analysis of the condition from a unique and complementary perspective. Thirdly, the book addresses a large audience of health-care specialists including family physicians, podiatrists, orthopedic foot surgeons, physical therapists, diabetologists, radiology residents, fellows, and radiologists.

Still many readers may find the book incomplete, for the information encountered in certain chapters may not reach their need. But understandably, due to the complexity of the subject, not all the aspects and variants of the diabetic foot can be covered in one book. A wide range of data is provided for the satisfaction of all readers regardless of their occupation or speciality.

Chapter 1

Biomechanics of the ankle-foot unit: derangements and radiological signs

Claude Pierre-Jerome¹,², Patrick Battaglia³ and Norman W. Kettner⁴,    ¹Oslo University, Oslo, Norway,    ²Emory University, Atlanta, GA, United States,    ³Logan University, Chesterfield, MO, United States,    ⁴Department of Radiology, Logan University, Chesterfield, MO, United States

Abstract

This chapter presents the essential of the biomechanics of the ankle-foot unit (rearfoot, midfoot, and forefoot). The gait phases are reviewed with an analysis of the normal and abnormal gait in diabetic patients. The load distributions in the ankle-foot unit are discussed. The locations and effects of the plantar pressures in diabetic patients are presented. The structural derangements associated with diabetes mellitus type II and peripheral neuropathy are also discussed. A catalog of magnetic resonance images and illustrations are provided for better understanding of the biomechanics of the ankle-foot unit and to facilitate the diagnosis of most bone and soft tissue changes consistent with diabetes-induced Charcot neuroarthropathy.

Keywords

Biomechanics; gait; structural changes; diabetes; peripheral neuropathy; Charcot neuroarthropathy

Teaching points

1. Biomechanical studies of the musculoskeletal (MSK) analyze the magnitude and nature of forces involved in various joints and muscles of the axial and appendicular skeleton.

2. Foot and ankle are interconnected anatomically and functionally. They are an inseparable entity the ankle-foot unit.

3. Load transmitted to the talar dome is distributed in equal measure posteriorly (to the calcaneus) and anteriorly to the medial and lateral segment of the midfoot and forefoot.

4. The calcaneus absorbs 50% of the weight. The central and medial compartments of the foot absorb 33% of the weight, while the lateral segment receives only 17%.

5. The metatarsals are major stabilizers of the foot; they absorb a considerable amount of stress.

6. The plantar aponeurosis (or plantar fascia) is indispensable for maintaining the shape and stability of the foot.

7. The calcaneonavicular ligament, or spring ligament, with its three components (superoplantar, medioplantar, and inferoplantar) assists in the stability of the ankle-foot unit.

1.1 Basic biomechanics of the normal ankle-foot unit

1.1.1 Basic biomechanics: definition

Biomechanics is, per definition, the study of the body in motion. It is considered a branch of biomedical engineering [1,2]. The biomechanical studies of the musculoskeletal system serve to analyze the magnitude and nature of forces involved in various joints and muscles of the axial and appendicular skeleton. The latter comprises the upper and lower extremities, including the pelvis. The foot and the ankle are interconnected anatomically and functionally, they are an inseparable entity forming the so-called ankle-foot unit. Therefore the study of the biomechanics of the foot necessarily involves the ankle, as the biomechanical assessment of the ankle must include the foot (Fig. 1.1).

Figure 1.1 (A) Plain radiograph. Frontal view of both feet displaying the osseous structures and joints of the midfoot and forefoot. (B) Plain radiograph. Lateral view of the right ankle-foot unit displaying the tibiotalar joint, talonavicular joint, subtalar joint, intertarsal joints, tarsometatarsal joints, metatarsophalangeal joints, and interphalangeal joints. (C) MR T1W sagittal image showing the tibiotalar joint (1), posterior aspect of the subtalar joint (2), sinus tarsi (3), calcaneocuboid joint (4), plantar fascia (5), and Achilles tendon (6).

1.1.2 The biomechanics of the ankle-foot unit

The understanding of the biomechanics of the ankle-foot unit is important for the study of the normal static and dynamic functions of the whole lower extremity. From proximal to distal, the lower extremity is made of three biomechanical units: the hip joint, the knee joint, and the ankle-foot unit.

Biomechanically, any change in position of one of these units automatically involves a change in the position of the other two units. For instance, in the upright posture, considering the frontal plane of the body, the neck of the femur forms a posteriorly open angle of approximately 20 degrees. The direction of the axis of the hip joint corresponds accurately to the connection of the inner-malleolus (medial malleolus) with the outer-malleolus (lateral malleolus) of the ankle joint. Normally, in relation to the frontal plane of the body, the two malleoli adopt an external rotation of approximately 20 to 30 degrees. Therefore there is a constant conformity between the hip axis and the ankle axis in the upright or standing position and during gait [3,4].

In the upright or standing posture, the knee joint is practically locked due to an automatic rotation. This allows the flow of weight-bearing forces from the hip, through the knee, to the ankle-foot unit. From a biomechanical standpoint, the foot represents the ultimate endpoint in the lower kinetic chain, namely, the hip, knee, ankle, and foot. The foot serves to transmit force between the lower limb and the ground. In addition, the fundamental task of the ankle-foot unit is to provide adaptability, stability, and adequate interface between the whole body and the ground, both in standing posture and during locomotion. A proper functioning of the ankle-foot unit influences the ability of the lower extremity to absorb the forces of weight-bearing. It is essential for the lower extremity to distribute and dissipate evenly compressive, tensile, shearing, and rotatory forces in standing posture as well as during gait [3,4].

The pelvis rotates approximately 20 degrees forward during gait. The lower leg simultaneously rotates inwardly in relation to the thigh. The ankle axis also rotates inwardly as the foot maintains a straight position. The foot acts as a flexible shock absorber. It can momentarily deform in contact with uneven surfaces. However, at the end of the gait cycle, after undergoing a series of responsive biomechanical changes, the foot now functions as a rigid lever necessary to exert force [5]. The different phases of the gait are described later in this chapter.

The ankle-foot unit, with all its anatomical components, represents the main joint for locomotion. The well-coordinated functioning of bones, joints, muscles, ligaments, and tendons provides for the biomechanical function of the foot-ankle unit. This requires ankle and foot to be sufficiently pliable to absorb and translate the weight-bearing forces while assuring the whole-body stability. Understandably, the inadequate absorption and distribution of these forces may lead to abnormal mechanical stress and eventual breakdown and degeneration of connective tissue, muscles, and ligaments, resulting in gradual and irreversible deformity of the ankle-foot unit, as seen in advances stages of the diabetic foot.

According to Donatelli [4] and others [5–7], the normal biomechanical function of the ankle-foot unit depends on static and dynamic components:

1. The static components consist of structures that include bones, ligaments, joint surface congruity, tendons, and the plantar fascia or plantar aponeurosis.

2. The dynamic components include the arthrokinematics or range of motion of the midfoot bones and the function of all muscles that attach to and support the ankle-foot unit.

1.1.2.1 Static components

Hicks [8] was the first to study the role of the beam action of the metatarsal bones and the tensile strength of the plantar aponeurosis. He emphasized the importance of these structures in the normal biomechanics of the ankle-foot unit during gait (Fig. 1.2).

Figure 1.2 (A) MR T1W sagittal image of the medial aspect of the ankle-foot unit. Note the normal talo–navicular–cuneiform–metatarsal–phalangeal alignment. (Ti=tibia, Ta=talus, Na=navicular, Cu=cuneiform, M=metatarsal, Ph=phalanx). The PF, The AT. (B) MR T1W coronal image showing the plantar fascia (arrows), plantar muscles (*), TTL, TFL. (C) MR proton density (PD) Fat sat axial image showing the flexor tendons [TP, DT, hallucis tendon (HT), PL&B, and the AT]. AT, Achilles tendon; DT, digitorum; PF, plantar fascia; PL&B, peroneus longus and brevis; TFL, talofibular ligament; TP, tibialis posterior; TTL, tibiotalar ligament.

The metatarsal bones, with their beam action, play a supportive role in the biomechanical function of the ankle-foot unit. Since the metatarsals are the major stabilizers of the foot, they absorb a considerable amount of stress. In the normal ankle-foot unit, in standing posture, the body weight is transmitted from the ankle joint through the talus. The ankle joint has a relatively large load-bearing surface area of 11 to 13 cm², resulting in reduced stresses across the joint. The load transmitted to the dome of the talus is distributed in equal measure posteriorly (to the calcaneus) and anteriorly to the medial and lateral segment of the midfoot and forefoot. The calcaneus absorbs 50% of the weight. The central and medial compartments of the foot absorb 33% of the weight, while the lateral segment receives only 17% [9]. The bony trabecular patterns reflect the direction of force transmission into the foot. Kapandji [10] found that the orientation of the trabecular bone follows the alignment of the medial and lateral arch of the foot (Fig. 1.3).

Figure 1.3 (A and B) Plain radiographs of the right foot: frontal (A) and lateral (B) views of the ankle-foot unit showing the biomechanical load distribution through the hindfoot, midfoot, and forefoot. The (CA) receives 50% of the load. The remaining 50% are distributed through the medial and sentral columns (33%) and the lateral column (17%). CA, calcaneus.

Another stabilizing factor of the foot is joint congruity. Root et al. [11] and Warwick et al. [12] studied the biomechanical function of the foot. They found the congruity of the articulating surfaces of the tarsal and metatarsal bones to have a definite influence in the stability of the synovial joints of the ankle-foot unit.

The plantar aponeurosis (or plantar fascia) is indispensable for maintaining the shape and stability of the foot. In the upright posture, the plantar aponeurosis receives up to 60% of the stress of weight-bearing. The ability of the plantar aponeurosis to absorb stress enhances with toe extension. This mechanism is described as the windlass effect. At maximum extension of the toes, the aponeurosis winds around the metatarsophalangeal (MTP) joints. This twisting effect increases the tension of the tissue fibers and allows the plantar aponeurosis to absorb greater amounts of stress. The tension within the plantar aponeurosis also facilitates the supination of the subtalar joint, in addition to absorbing more stress (Fig. 1.4).

Figure 1.4 (A and B) The windlass effect. (A) The plantar fascia originates from the CA and extends distally to the phalanges. It maintains the medial longitudinal arch. (B) Dorsiflexion shortens the distance between the calcaneus and metatarsals and elevates the medial longitudinal arch (arrow). CA, calcaneus.

The calcaneonavicular ligament, or spring ligament, with its three components (superoplantar, medioplantar, and inferoplantar) assists in the stability of the ankle-foot unit. The long and short plantar ligaments also contribute to a lesser degree in stabilizing the unit [4,13–17] (Fig. 1.5).

Figure 1.5 Illustration of the calcaneonavicular spring ligament. The three components of the spring ligament, SP, MP, and IP, are displayed. IP, inferoplantar; MP, medioplantar; SP, superoplantar.

1.1.2.2 Dynamic components

The ankle-foot unit is a critical anatomical element of the human body. Its three main functions include weight transmission to the ground, postural balance, and support for ambulation. The viability of the ankle-foot unit depends greatly on the dynamic components which include the arthrokinematics or range of motion of the midfoot, and the muscles attached to the ankle and foot. Anatomically, the ankle-foot unit consists of several bones, joints, ligaments, and extrinsic and intrinsic muscles. These muscles are described with greater details in Chapter 13. The unit is subdivided into the rearfoot (or hindfoot), midfoot, and forefoot [18].

The movement of the ankle and foot is a complex action involving several joints of the three subdivisions of the unit. Functionally, Steindler [19] defined the ankle and foot similar to a closed kinetic chain. This is defined as a combination of several joints successively constituting a complex motor unit, where the terminal joint of the chain meets with significant resistance. The motion of one joint influences the motion of the remaining joints within the chain. The complex array of motion within the ankle-foot unit reflects the interdependence of pronation and supination of its joints.

Pronation and supination are described as triplane motions [11,20]. Pronation comprises the body plane movements of abduction, dorsiflexion, and eversion with the three movements occurring simultaneously. Supination is the triplane motion that includes adduction, plantar flexion, and inversion. During gait, pronation and supination occur at different points in the stance phase. They facilitate the movements of the joints, assist in joint stabilization, and especially aid in force distribution within the lower limb and foot (Fig. 1.6).

Figure 1.6 Illustration of supination (A) and pronation (B) of the foot. Illustration of inversion (C) and eversion (D) of the foot.

Root et al. [11] describes five triplane joints within the ankle-foot unit that provide for pronation and supination. These five triplane joints include

1. talocrural joint

2. subtalar joint

3. midtarsal joint

4. first ray or first metatarsal–cuneiform joint

5. fifth ray or fifth metatarsal

Stauffer et al. [21] studied the forces that influence the dynamics of the normal ankle-foot unit during walking and running. They found the main compressive force across the ankle during gait is produced by the contraction of the gastrocnemius and soleus muscles. The pretibial musculature engenders mild compressive forces, in early stance, of less than 20% body weight. In later stance, a compressive force of 5 times body weight is produced by the contraction of the posterior calf musculature. During running, the localized forces at the ankle may reach values as high as 13 times body weight [21,22].

Manter [23] analyzed the magnitude of loads generated in the foot during walking and running. The peak vertical forces reach 120% body weight during walking. They increase to nearly 275% body weight during running. Under static loading, in standing posture, Manter [23] found that the talonavicular and the cuneonavicular joints bear most of the load through the tarsal joints. The medial column of the foot which comprised the talus, navicular, cuneiforms, and the first, second, and third metatarsals receives most of the load. However, the lateral column of the foot, consisting of the calcaneocuboid joint, and the lateral two metatarsals bear the lesser load (Fig. 1.7).

Figure 1.7 Illustration of the forefoot and midfoot with the three columns (medial, sentral, and lateral). Please see the online version to view the color image of the figure.

The studies conducted by Cavanaugh et al. [24] revealed more specific details about the distribution of load through the ankle-foot unit of subjects during barefoot standing. They stated that the heel received 60% of the load, the midfoot 8%, the forefoot 28%, and the toes 4%. They found the peak pressures under the heel to be 2.6 times greater than the forefoot pressures. The forefoot peak pressures occurred under the second metatarsal head. According to Brukner et al. [25], the second metatarsal suffers stress fracture or fatigue fracture more commonly than the other metatarsal because it is recessed within the distal tarsal bones, resulting in limited mobility. (Fig. 1.8).

Figure 1.8 Radiograph (A) and MRI (B) of the right foot. The second metatarsal base (stars) is recessed between the MC and the LC. LC, lateral cuneiform; MC, medial cuneiform; MRI, magnetic resonance imaging.

It is also believed that athletes with pes cavus are more likely to suffer stress fractures of the tibia due to the limited capacity of the rigid foot (pes cavus) to absorb impact forces. Barnes et al. [26] affirmed that individuals with extremes of foot types—very low arched and very high arched footwear—are more susceptible to stress fractures of the tibia due to associated foot rigidity and failure to absorb impact forces.

1.1.2.3 Plantar pressure in the normal foot, effects on the foot sole during walking

Force attenuation within the ankle-foot unit occurs due to a series of static mechanisms, including the windlass effect of the plantar aponeurosis and the tensile strength of all plantar ligaments and muscles. The studies from Cavanagh et al. [27] and Hutton et al. [28] proved that during walking the dynamics of gait have a significant influence on plantar pressure. More importantly, they found that the center of pressure progressed across the sole of the foot during walking. During barefoot walking, the center of pressure is first situated in the central part of the heel. It moves rapidly through the midfoot to reach the forefoot where the velocity decreases. The peak forefoot pressures are centered under the second metatarsal, during stance phase of the gait. The metatarsal heads are in contact with the ground during at least one-half of the stance phase. At toe-off (TO), or the beginning of the swing phase of gait, the center of pressure is located under the hallux (see illustration of gait phases later in this chapter). This constant increased pressure at the heel, the hallux, and the metatarsal heads during gait may explain the frequent occurrence of soft tissue wounds in these locations in the diabetic foot. In addition, as a consequence of migration of infection from the infected wound to the adjacent bones, osteomyelitis occurs more frequently in these locations (Fig. 1.9).

Figure 1.9 MR T1W (A) and prton density (PD) fat-suppressed (B) sagittal images of the left ankle of a 52-year-old diabetic patient showing acute osteomyelitis of the calcaneus. Note the wound (arrows) adjacent to the posterior aspect of the calcaneus.

The distribution of plantar pressures varies with footwear. Peak heel pressure is reduced by footwear. Footwear induces a more even distribution of pressure under the heel. However, with shoes, the forefoot load distribution shifts medially with maximum pressure under the first and second metatarsal heads. As footwear increases the pressures under the toes, the foot suffers more structural damage in individuals who wear smaller shoes with a narrow toe box and high heels. A narrow toe box compresses the forefoot laterally and medially inducing the development of hammer toes, hallux valgus, and bunions [29–31]. Shoes with elevated heels increase the forefoot pressure significantly compared with barefoot. According to Snow et al. [32], a 1.9 cm heel elevates forefoot pressure by 22%. A 5.0 cm heel increases the peak pressure by 57%. An 8.3 cm heel elevates the peak pressure by 76%. The elevated heel also causes discomfort and localized pain under the metatarsal heads. In addition, it may contribute to the formation of interdigital neuromas. A study by Murray et al. [33] demonstrated that the elevated heel may result in Achilles tendon contracture with limited dorsiflexion of the ankle joint, resulting in joint instability in the ankle-foot unit. The consequence may be irreversible structural damage and associated alteration of the normal gait. As heel height increases, the range of motion of the ankle joint decreases, producing severe biomechanical derangement of all joints in the ankle-foot unit [34]. In patients with diabetes, attention should be given to footwear, as the inadequate shoe may enhance the occurrence of damage to the skin and subcutaneous fat tissues where foot pressures are abnormally increased. In education programs for diabetic patients at high risk of skin ulceration, adequate footwear is recognized as a vitally important preventive measure.

During running, the distribution of plantar pressures is uniquely altered. Two types of runners have been identified based on their first point of contact with the ground: (1) the rearfoot striker and (2) the midfoot striker. The rearfoot striker makes initial ground contact with the posterior third of the shoe, involving mainly the calcaneus, subtalar, and ankle joint. The presence of instability in one or any of these joints may necessarily affect the performance of the runner. For the midfoot striker, the initial ground contact takes place in the middle third of the shoe from the Chopart joints to the tarsometatarsal (TMT) joints. This involves the two components of the Chopart joints, namely, the calcaneocuboid joint and the talocalcaneonavicular joint, and all remaining midfoot or intertarsal joints. In both types of runners, the first contact occurs along the lateral border of the foot, involving the lateral foot compartment. The peak pressure does not differ between runners [34–46].

During running and walking, several forces have been detected between the foot and the ground. These forces are (1) vertical force, (2) medial and lateral shear, and (3) rotational torque. The peaks of these forces vary in intensity and location during the phases of gait. As the center of pressure is in the distal 30% of the shoe during walking and running, most time is spent on the forefoot in both types of runners. This explains the high frequency of stress or fatigue fracture at the metatarsals, especially, the second metatarsal where the forefoot peak pressure constantly occurs under the second metatarsal head, as mentioned earlier [24,26,30,35,47].

1.2 The ankle-foot unit: anatomy and structural organization

The goal of this section is not to review the whole anatomy but rather to illustrate the different structures related to the ankle-foot unit. We will emphasize on the biomechanical and functional interactions of bones, joints, and soft tissues within the ankle-foot unit.

There are 31 bones in the unit (tibia, fibula, trigonum, talus, calcaneus, navicular, cuboid, 3 cuneiforms, 5 metatarsals, 14 phalanges, and 2 sesamoids). There are several articulations: ankle mortise, subtalar, midtarsal (Chopart), intertarsal, TMT (Lisfranc), MTP, and interphalangeal (ITP) joints. There are also joints formed between the medial and lateral sesamoid with the first metatarsal. The muscles of the ankle-foot unit, the ligaments and the tendons of the ankle-foot unit are described separately in other chapters with the relevant anatomy and pathology.

From a biomechanical standpoint, the talus is considered by many anatomists as component of both the ankle and the foot. This is due to its anatomical location and close contact with the midfoot structures, namely, the navicular and the cuboid with which it articulates. Anatomically and biomechanically, the ankle-foot unit has three functional entities:

1. rearfoot or hindfoot

2. midfoot

3. forefoot

1.2.1 The rearfoot

The rearfoot, also called hindfoot, ankle joint or talocrural joint, is composed of the articulations of the tibia, fibula, and talus. The subtalar joint is functionally an integral component of the rearfoot. The ankle joint per se is a single hinge joint that comprises the tibial plafond (or plateau), the tibial medial malleolus, the fibular lateral malleolus, and the talus. The horizontal axis of the ankle joint is oriented at a mildly oblique angle where the lateral portion (or lateral malleolus) is located posterior to the medial portion (or medial malleolus). This axis forms an approximately 10-degree angle with the straight horizontal medial-lateral axis in the coronal plane and an approximately 6-degree angle with the horizontal medial-lateral axis in the transverse plane. The horizontal axis of the ankle joint is considered as reference during different motions of the joint in pronation, supination, plantar flexion, and dorsiflexion. During foot pronation, the sole of the foot faces laterally. During foot supination, the sole faces medially [48] (Figs. 1.10 and 1.11).

Figure 1.10 MR GRE T2 W coronal (A) and proton density (PD) fat-suppressed sagittal (B) images of the ankle joint. The coronal image displays the distal tibiofibular joint and the talofibular joint. The sagittal image shows the tibiotalar joint. The subtalar joint (arrows) is displayed in both planes. Note the accessory os subfibulare (curved arrow) on the coronal image.

Figure 1.11 (A and B) MR proton density (PD) fat-suppressed sagittal images of the subtalar joint. (A) The calcaneotalar cervical ligament (arrow) is seeing in the anterior aspect of the joint. (B) The interosseous ligament (arrow) lies in the posterior portion of the joint.

1.2.1.1 Ankle joint stability, anatomy, and kinematics

The ankle joint is very stable. The joints stability depends on the bony congruency and the ligamentous support. The bony congruency provided by the tibial plafond and the two malleoli form a so-called mortise joint with the dome of the talus. Morphologically, the talus looks like a truncated cone, or frustum. Its apex is directed medially when observed in coronal and axial plane. The talus is approximately 4.2 mm wider anteriorly than posteriorly. The anterior increase in size is crucial for the biomechanical function of the joint. During ankle dorsiflexion, the anterior portion of the talus is compressed between the tibia and fibula, spreading the mortise slightly. The ankle joint becomes close packed in a position of maximal stability [48–50]. Given the direction of the axis, and the shape of the mortise joint, the talus is relatively free to move into dorsiflexion and plantar flexion. But, the talus is highly constrained along the vertical and anterior–posterior axes, which severely limits the transverse and coronal plane motion at the ankle joint.

Ankle joint stability also depends on the functional and structural integrity of its ligaments. On the lateral aspect of the joint, the lateral ankle ligaments are responsible for resistance to inversion and internal rotation. These ligaments are the anterior talofibular ligament, the posterior talofibular ligament, and the calcaneofibular ligament. On the medial side of the joint, the superficial and deep deltoid ligaments (or the deltoid complex) are responsible for resistance to eversion and external rotation stress. These ligaments are the tibiotalar ligament, tibionavicular ligament, tibiocalcanear ligament, tibio-spring ligament, and the calcaneonavicular ligaments or spring ligament complex. The spring ligament complex consists of three components: the superomedial, medioplantar oblique, and inferoplantar longitudinal ligaments [50,51] (Fig. 1.12).

Figure 1.12 (A) Illustration of the lateral ligaments of the ankle joint. (B) Illustration of the medial ligaments of the ankle joint.

The stability between the distal tibia and fibula is maintained by the syndesmotic ligaments. These ligaments include the anterior inferior tibiofibular ligament, posterior inferior tibiofibular ligament, inferior transverse tibiofibular ligament, the inferior interosseous ligament, and the interosseous membrane [52] (Fig. 1.13).

Figure 1.13 (A) Illustration of the anterior view of the distal tibiofibular joint with the interosseous membrane, the anterior tibiofibular ligament, and the interosseus ligament. (B) Illustration of the posterior view of the distal tibiofibular joint with the posterior tibiofibular ligament, the inferior transverse tibiofibular ligament, and the interosseus membrane.

It is worth emphasizing that a syndesmotic ligament injury, also called high ankle sprain, may be isolated or associated with injury of the other ligament groups. The latter can be caused by trauma, inflammatory conditions, and neuroarthropathy. In patients with diabetes and Charcot neuroarthropathy, it is still unclear to what extent the deformity of the foot, especially the midfoot, results entirely or partially from ligament damage. Neither is it clear which group of ligaments is primarily or secondarily affected. Because of the resulting instability of the whole ankle-foot unit in the deformed diabetic foot, hypothetically, there may be a global involvement impacting all ligament groups, including the syndesmotic ligaments.

The kinematics of the ankle joint has been subject to several studies [53–55]. The normal range of motion can be evaluated either radiographically or by goniometer. The goniometric measurements revealed a normal motion of 40- to 55-degree plantar flexion, and 10- to 20-degree dorsiflexion (Fig. 1.14).

Figure 1.14 Illustrations of the plantar flexion (A) and dorsiflexion (B) of the foot. Goniometric measurements reveal a normal motion of 40- to 55-degree plantar flexion and 10- to 20-degree dorsiflexion of the foot.

The analysis of the instant centers of rotation as well as the surface velocities in asymptomatic ankle joints and in diseased ankle joints (by arthritis and neuroarthropathy) demonstrated striking differences. In the normal ankle, the axis of rotation barely varies during dorsiflexion/plantar flexion. The surface motion shows minimal distraction as dorsiflexion begins. This is followed by a posterior talar gliding, until full dorsiflexion is reached as compression of the talus within the tibia/fibula occurs. Contrarily, in the arthritic and neuropathic ankles, the instant centers and the surface velocity vary considerably. Joint compression occurs earlier in dorsiflexion motion compared with the normal ankle. Distraction of the joint also takes place earlier during dorsiflexion. This is a reliable sign of ankle joint instability as seen in moderate and advanced stages of arthritis and diabetic neuroarthropathy where there is no consistent pattern in the direction of displacement of the contact points between talus, tibia plafond, and fibula [55].

1.2.2 The subtalar joint: anatomy and biomechanics

The subtalar joint plays an important role in the stability and motion of the ankle-foot unit. Anatomically, the subtalar joint comprises two separate joint cavities. However, there is an anterior, middle, and posterior facet connecting the talus to the calcaneus. Anteriorly, the articulation is formed by the talar head, anterior-superior facet, the sustentaculum tali, and the concave surface of the navicular bone. The talocalcaneonavicular joint is a well-integrated joint; it functions as a ball and socket. Posteriorly, the joint is formed between the infero-posterior talar facet and the supero-posterior facet of the calcaneus. The posterior facet makes up to 70% of the articulating surface of the subtalar joint. [17,56] (See Fig. 1.10). These joints are separated by the sinus tarsi. The posterior and combined anterior and middle facets have separate joint capsules, although they share a similar axis of rotation.

Occasionally, an accessory anterolateral talar facet can be identified. It has been reported as an anatomical variant of the subtalar joint [57]. This extra talar facet can be found in symptomatic or asymptomatic populations. It was first described by Sewell in 1904 as facies externa accessoria corporis tali [58]. It has been found in up to 25%–34% of cadaveric specimens in several studies [59–62]. The accessory talar facet can be visualized with computed tomography (CT) and magnetic resonance imaging (MRI). It has been considered as an etiologic factor in painful talocalcaneal impingement in individuals with rigid flatfoot during adolescence and adulthood. Focal subjacent bone marrow edema changes are detected on MR images of patients with painful subtalar joint and accessory talar facet. The eventuality of an accessory talar facet should be kept in mind in the presence of bone marrow edema around the subtalar joint in symptomatic patients [63–65].

There are three groups of structures that provide support and stability to the subtalar joint: the deep ligaments, peripheral ligaments, and retinaculae.

The deep ligaments are the interosseous ligament and cervical ligament. The interosseous ligament is located posteriorly in the joint and runs superiorly and medially. The cervical ligament lies anterior to the interosseous. It runs from the cervical tubercle of the calcaneus to the talar neck.

The peripheral ligaments stabilize the subtalar joint. They are the calcaneofibular ligament, lateral talocalcaneal ligament, and fibulotalocalcaneal ligament.

The lateral support is provided in part by the inferior extensor retinaculum. The retinaculum has three roots: lateral, intermediate, and medial. Also contributing to the subtalar joint stability are the deltoid ligament and the lateral ligaments of the ankle joint.

Biomechanically, the range of motion of the subtalar joint is set at an oblique angle that is oriented upward at an angle of 42 degrees from the horizontal baseline in sagittal plane (or lateral view). On a frontal view, the subtalar joint has a motion that is oriented 16 degrees medially from the midline (Fig. 1.15).

Figure 1.15 (A and B) Illustration of the subtalar joint axis in two planes. In sagittal plane (A), the axis rises up to 42 degrees from the plantar surface. In transverse plane (B), the axis is oriented about 16 degrees medial to the midline of the foot.

The subtalar joint has almost equal range of motion in abduction/adduction and in inversion/eversion. Its reduced amount of freedom in the medial-lateral axis suggests that the subtalar joint has very little motion in plantar flexion/dorsiflexion, which is considered clinically negligible compared with the talocrural joint that moves freely in plantar flexion and dorsiflexion. But the talocrural joint has reduced amounts of inversion/eversion and abduction/adduction motions.

The motions of the subtalar joint are identical in weight-bearing and in nonweight-bearing. Considering the position of the talus relative to the calcaneus, in nonweight-bearing, the talus is typically stationary, but the calcaneus moves. In weight-bearing, the calcaneus is stationary, and the talus moves on the calcaneus. The relative motion between the talus and calcaneus is about the same although the stationary versus the active role of each bone can be different. Since the primary motions of the subtalar joint are inversion/eversion and abduction/adduction, the combination of the talocrural and subtalar joints allows freedom of motion in all three planes. The talocrural joint provides primarily for forward progression during locomotion, while the subtalar joint provides freedom for the lower leg to rotate in the transverse plane or rock side to side in the coronal plane without requiring the foot to move on the ground. Practically, the ankle-foot unit offers a stable and fixed platform on the ground with the possibility to move forward, balance, change direction, or operate on uneven surfaces as the talus moves around a relatively fixed calcaneus [23,66].

1.2.2.1 The Chopart joints or (transverse tarsal joint) and relationship with the subtalar joint

The Chopart joints (talonavicular and calcaneocuboid) are at the boundary between hindfoot and midfoot. These joints are occasionally included in the definition of the midfoot, their degree of freedom and coupled motion with the ankle joint make them more appropriately incorporated into the hindfoot, as the ankle joint, the subtalar joint, and the Chopart joints form a working unit. From a biomechanical standpoint, the Chopart joints can be considered as a functioning link between the hindfoot, the midfoot, and particularly the subtalar joint. The Chopart joints also play a definite biomechanical role during gait, as these joints are essential in facilitating movements between flexibility and rigidity of the midfoot in different gait phases allowing a rotational motion of the forefoot. This motion is possible due to the interaction of the other joints with the Chopart joints. The latter has two axes of motion: the oblique axis and the longitudinal axis. The action along the two axes results in considerable motion in all three planes. The oblique axis is oriented 57 degrees anteromedially, and 52 degrees dorsal from the horizontal. Extension and flexion occur essentially about the oblique axis. The longitudinal axis is oriented 9 degrees medially from the longitudinal axis of the foot, and 15 degrees upward from the horizontal. The motion of eversion and inversion occur primarily about the longitudinal axis [66,67] (Fig. 1.16).

Figure 1.16 (A and B) Illustration of the longitudinal axis of the Chopart joint. The longitudinal axis is oriented 15 degrees upward from the horizontal (A) and 9 degrees medially from the longitudinal axis of the foot (B). Eversion and inversion occur primarily about the longitudinal axis.

Other studies investigating the mobility of the Chopart joints confirmed that the talonavicular joint had a larger range of motion than the calcaneocuboid joint. However, when the mobility of the Chopart joints is compared with the subtalar joint, both joints (Chopart and subtalar) have similar amounts of supination and pronation. This similarity in motion has been demonstrated by various biomechanical studies of the normal foot [67–69]. Obviously, in the diabetic foot, a difference in the range of motion of both joints may be observed because in most cases the Chopart joint, in particular the talonavicular joint, is deranged while the subtalar joint is less affected or normal.

Huson [70] found a close biomechanical relationship between the subtalar joint and the Chopart joints (transverse tarsal joint) and described it as the tarsal mechanism. The subtalar joint facilitates supination and pronation. The supination/pronation flexibility at the subtalar joint provides motion from the hindfoot to the midtarsal joints (or midfoot) in a consistent pattern. In this model of subtalar joint–tarsal joint relationship, the four bones: talus, calcaneus, navicular, and cuboid form an interlocking chain of motion. The navicular and cuboid are almost immobile relative to each other. During supination, the inversion and adduction forces generated by the calcaneus and applied to the cuboid are directly transmitted to the navicular bone. As the cuboid adducts, it inverts underneath the foot; it tends to elevate and abduct the navicular. Then, the navicular force is transmitted to the talus to further facilitate supination. The same mechanism works in reverse during subtalar joint pronation [70,71].

This close biomechanical relationship between the subtalar, talonavicular, and calcaneocuboid joints has also been demonstrated by Astion et al. [72] utilizing experimental selective fusion of these joints. They found that subtalar joint arthrodesis can reduce talonavicular motion to 26% of its normal range. It reduces calcaneocuboid motion to 56% of normal. Furthermore, the calcaneocuboid arthrodesis can diminish subtalar motion to 92% of its normal range. In addition, they found that the selective fusion of the talonavicular joint had the most significant effect on the remaining joints of ankle-foot unit. In patients with diabetes and neuroarthropathy, there is a high frequency of derangement of the talonavicular joint ranging from talonavicular subluxation to complete collapse of the navicular bone and subsequent deformity and dysfunction of the foot. Of notable significance, a reduction in size of the navicular in the diabetic foot, compared to the nondiabetic, has been reported [73,74] (Fig. 1.17).

Figure 1.17 MR T1W sagittal image of the right foot of a 47-year-old diabetic patient. There is midfoot dislocation with complete destruction of the navicular (*). Courtesy of Dr. Tanya Tivorsak.

Likewise, derangements of the calcaneocuboid joint frequently occur in patients with diabetic neuroarthropathy accompanied by a high prevalence of cuboid plantar subluxation, probably secondary to acquired damage of the calcaneocuboid ligament. In a comparative study between diabetics and nondiabetics a higher prevalence of occult cuboid fractures has been reported in the former [75]. Damage to the two bones (navicular and cuboid) in the diabetes neuroarthropathy may have an underlying biomechanical mechanism. Hypothetically, the flattening of the navicular and the fractures of the cuboid may originate from the higher inversion and adduction forces applied to the cuboid and transmitted to the navicular during supination; and from the navicular to the cuboid during pronation of the subtalar joint (Fig. 1.18).

Figure 1.18 MR T1W (A) and short tau inversion recovery (STIR) (B) sagittal images of the right foot of a 35-year-old diabetic patient showing a nondisplaced fracture