The foot and ankle of the human body is a complex system of integrated units composed of bones, tendons, muscles, and ligaments. Like a well-oiled machine, each part must move and react in perfect harmony. The joints of the foot and ankle can suffer many trials and tribulations in an otherwise normal human life. The foot and ankle at times must adapt to these instances, from fractures and dislocations to congenital problems. When adaptation leads to a malformation in the unit structure, surgical intervention is required to restore the foot and ankle complex to a working device.

As foot and ankle surgeons, our responsibility lies in restoring the foot and ankle to a relatively pain-free structure. Primary indications for regarding any joint fusion in the human body include deformity, instability and, more importantly, pain. Fusions involving single and multiple joints are indicated for a myriad of conditions including primary osteoarthritis, posttraumatic arthritis, neoplasms, malunion, nonunion, congenital anomalies, and neurotraumatic injury.

This article gives an overview of the indications for performing joint fusions at the foot and ankle.

To begin the discussion of indications of foot and ankle arthrodesis, a review of what constitutes a joint is needed. A joint or articulation is the union of 2 or more bones, allowing transmission of forces (shear, compressive, and torsion), differential growth, and movement. Two classification schemes designed to describe joints have been developed. The amount of movement between the bones and the type of connection between the joints has been described. The traditional classification scheme describing movement between joints is divided into synarthrosis, amphiarthrosis, and diarthrosis. Synarthrosis joints in the foot and ankle include the tibiofibular joint, joints that provide very little movement. Amphiarthrosis joints are those such as the calcaneocuboid joint or the metatarsal cuneiform joints, which allow greater flexibility but are connected by fibrocartilage. Joints that permit free movement between bones are classified as a diarthrosis or synovial joint.¹

A modification of the aforementioned joint classification scheme is based on the type of connection between bones rather than the amount of movement involved. In the foot and ankle there are several examples of such joints. The interphalangeal joints are described as hinge or ginglymus joints. The bones that provide this motion have trochlear articular shapes at the facets, are reinforced with collateral ligaments on each side, and provide one axis of motion, mainly flexion and extension. The ankle joint is a modified hinge joint in that the majority of its motion lies in the sagittal plane with slight motion of the transverse plane occurring as well.² The metatarsophalangeal joints are described as ellipsoid or condyloid joints. The bones that provide this motion have facets that are concave that rotate on an oval head that is much greater in length than width. Metatarsophalangeal joints have 2 axes of motion, adduction and abduction on the short axis and flexion and extension on the long axis. The calcaneocuboid joint is described as a saddle or sellar joint in which the facets have a saddle shape and one side of the facet is turned down. The calcaneocuboid joint has 2 axes of motion; however, motion at this joint is very limited, due to the strong ligaments surrounding this joint. The talonavicular joint is described as a ball and socket or enarthrodial joint, which allows circumduction as well as allowing 3 axes of motion.

The joints of the foot and ankle are surrounded by a great synovial lining called the great tarsal cavity. Each joint surface is covered by varying thickness of articular cartilage. Joint contact is limited between these cartilaginous surfaces, resulting in a low coefficient of friction. Synovial fluid bathes these surfaces and acts like a lubricant. The synovial fluid is also involved in maintenance of living cells in the articular cartilage. Articular cartilage has a slightly compressible and elastic surface. This configuration allows it to be able to absorb the large compressive forces generated by movement across these surfaces. Thickness of articular cartilage ranges from 1 to 2 mm. There is an age difference in the appearance of articular cartilage; in youth it tends to be compressible whereas in aged individuals it tends to be brittle with an irregular surface. Articular cartilage is molded to the joint surfaces and varies in thickness depending on the surface. Concave articular cartilages are thinnest centrally and thicker peripherally, and convex articular cartilages are thickest centrally while thinning peripherally. The peripheral vascular plexus in the synovial membrane is said to provide nutrition to the articular cartilages. Also, articular cartilage has no blood vessels or nerve supply. With increasing age, the articular cartilage will develop wear and tear in the form of jagged edges and small debris within the synovial joint.³

Synovial membrane secretes synovial fluid. Synovial membrane is derived from embryonic mesenchyme and covers all nonarticular areas where movement occurs between surfaces. Specifically in joints, it lines the intracapsular ligaments, tendon sheaths, and fibrous capsules. It does not line the articular cartilage; there is a structural transition zone between the articular cartilage and the synovial membrane.

Articular fat pads are accumulations of adipose tissue that occur in synovial membranes in joints. Articular fat pads occupy the irregularities and potential spaces in joints and when the joint undergoes motion to accommodate to the changing shape and volume of the irregularities. The fat pads allow the distribution of synovial fluid over articular surfaces. Synovial villi line the internal synovial membrane. These villi rest near articular margins and increase with age, which can become a factor in the majority of pathologic joint dysfunction.

Understanding the biology of bone healing is paramount to the understanding of correct arthrodesis techniques for the foot and ankle surgeon. As part of the surgeon’s armamentarium of understanding, knowing the basic biology of bone can be to the surgeon’s advantage and can prove beneficial in the surgical theater.

A mineralized version of connective tissue, bone, is unique in that it allows for scarless tissue regeneration provided the bone is reapproximated in an anatomic fashion. Bone is formed by cells called osteoblasts. These osteoblasts deposit a type-I collagen matrix that releases magnesium, calcium, and phosphate ions, which form a matrix in the form of hydroxyapatite. The composition of bone is twofold, being composed of a hard mineral and a flexible collagen matrix, which makes it stronger and harder than cartilage. These two properties prevent the structure of bone from being brittle, unlike cartilage, which can become quite brittle over time.⁴

The functional unit of bone is the osteon, which consists of a Haversian canal system containing blood and nerve supply. The osteon contains concentric layers of mineralized matrix called concentric lamellae. Two types of osseous tissue are spongy and compact. Spongy bone encompasses the hollow interior while compact bone consists of the hard exterior.

Of importance is that bone tissue and bone are two different entities. Bone tissue is a type of connective tissue that is specifically made of the mineral matrix whereas bones are structures made up of bone tissue, marrow, nerves, blood vessels, and epithelium. Cortical bone studies have shown that bone has poor tensile strength of approximately 133 MPa in the longitudinal plane and 51.0 MPa in the transverse plane, and a low shear stress strength of 51.6 MPa.⁵ However, bone has a relatively high compressive strength of 193 MPa in the longitudinal plane and 133 MPa in the transverse plane.⁶ These results clearly show that the compressive strength of bone is much greater than the tension and shear strength.

An understanding of the basics of fracture healing is paramount to the fundamental principles of arthrodesis. Fracture healing is divided into two types, direct and indirect healing. Direct fracture healing or primary fracture healing is performed by internal remodeling and occurs only with absolute stability, and is the process of osteonal bone remodeling.⁴ Indirect or secondary healing occurs with relative stability and is performed by callus formation. Arthrodesis principles require that the patient undergo primary healing of bone. Because of the high incidence of nonunion in arthrodesis procedures, secondary bone healing must and should be prevented.

Regardless of the type of bone healing involved, both primary and secondary healing undergo 4 basic stages: inflammation, soft callus formation, hard callus formation, and remodeling.⁷ The inflammatory stage begins rapidly and continues until formation of cartilage, fibrous tissue, or bone begins. This phase takes place from 1 to 7 days after the initial fracture has occurred. At first there is inflammatory exudation from damaged blood vessels and hematoma formation. At the ends of the fracture bone necrosis occurs. Embedded in this hematoma is a dense network of reticulin fibrils, fibrin, collagen, and cytokines that produces vasodilatation to the surrounding tissues. The formation of fracture hematoma gradually is replaced by granulation tissue. The bone fragment ends, although minimal in primary healing, begin to become resorbed by osteoclasts that remove the necrotic ends of bone.

The next stage, soft callus formation, brings a decrease in pain and swelling and corresponds to the immovable free ends of the bone fracture. This stage takes place approximately 2 to 3 weeks postfracture. Unfortunately, while the stability of the soft callus stage is adequate to prevent shortening, angulation at the site of fracture may still occur, leading to a malalignment of the fracture ends. The characteristic property of the soft callus stage is growth of callus. Osteoblasts are created from the cells in the periosteum and endosteum. The fracture ends slowly bridge and link together to form a soft callus with a combination of chondrocytes and fibroblasts.

The hard callus formation stage begins when the soft callus links the two bone ends together. The soft callus within the gap undergoes endochondral bone formation, and the callus is transformed into a rigid calcified tissue called woven bone. This bone callus forms at the periphery of the fracture site where the strain on the bone is lowest.

The remodeling stage starts when the fracture has united with the woven bone. Lamellar bone slowly replaces the woven bone the osteonal remodeling. This stage is the longest in that it can last several months to years.

Each phase has distinct characteristics; however, they have a seamless transition from one phase to the other.^8–10 Primary fracture healing and secondary fracture healing undergo different lengths of phases of bone healing as well, in that hard and soft callus formation is minimal in primary fracture healing.

As already mentioned, primary healing is achieved by absolute stability by means of interfragmentary compression. In an arthrodesis, 2 or more joint surfaces are denuded of cartilage, and the opposing subchondral bone ends are stabilized and compacted so the remaining bone can be maintained in permanent apposition. Histologically, the healing of bone undergoing primary healing requires no movement across the bone ends so the initial hematoma, formed during the stages of bone healing, is resorbed rather quickly and transformed into repair tissue. Next the Haversian system begins to repair the intricate network of systems that were once in the bone. The Haversian system is reformed by the use of an osteon, which carries at its tip a cluster of osteoclasts acting as drills that tunnel into the dead bone. After the dead bone has been resorbed, osteoblasts from behind the tip create new bone and a connection to the capillaries within the canal.