Physiology of the Developing Hip and Pathogenesis of Femoroacetabular Impingement

Fig. 7.1

All the long bones in the body are formed by enchondral ossification, where a bone collar is formed around a hyaline cartilage model and a primary ossification centre forms inside the model (1). The cartilage matrix deteriorates (2) and spongious bone in formed (3). The secondary ossification centre forms in the epiphysis and is invaded by an epiphyseal artery (4). After ossification of the epiphyses, hyaline cartilage only remains in the epiphyseal plates and the articular cartilage. The long bone now consists of an epiphysis, physis, metaphysis and diaphysis (5)

The diaphysis is the primary centre of ossification. It grows circumferentially through appositional growth by the deposition of bone beneath the periosteum, but it does not grow longitudinally. The diaphysis is composed of lamellar bone with a strong cortical exterior.

The metaphysis is composed of spongious, trabecular bone with a thin layer of exterior cortical bone. It connects the diaphysis with the adjacent physis.

The epiphysis is located on top of the physis and forms an articulation with the adjacent bone. Almost all epiphyses contain one or more secondary ossification centres. These ossification centres grow spherically by enchondral ossification and are responsible for less than 5 % of the bone growth in length.

The physis forms a discoid structure between the metaphysis and epiphysis. It is often referred to as the epiphyseal plate/line or growth plate/line. More than 95 % of longitudinal growth of long bones occurs in the physis. When visualised under a microscope, it is a complex structure, with its cellular anatomy defined into different layers or zones (Fig. 7.2). In the resting zone (also called the germinal or reserve zone) on the epiphyseal side, the stem cells accumulate and the storage of nutrients occurs. In the adjacent proliferative zone, the stem cells divide and differentiate into chondrocytes, oriented in columns (sometimes called the columnar zone). The chondrocytes then enlarge in size to form the hypertrophic zone. In the hypertrophic zone, the chondrocytes show increased metabolic activity and go into apoptosis and die. The dead chondrocytes are invaded by vascular channels from the metaphysis and the mineralisation of the intercellular matrix occurs in the calcification zone.

Fig. 7.2

The physis is avascular, but oxygen and nutrients arrive from the epiphyseal and metaphyseal arteries. At the periphery, the blood supply comes from periosteal arteries. Its cellular anatomy is defined into different layers or zones

The physis is avascular, receiving oxygen and nutrients at its periphery from epiphyseal and metaphyseal vessels. Small branches from the epiphyseal arteries pass through the resting zone and terminate at the top of the proliferative zone. On the metaphyseal side, the interosseous artery and metaphyseal arteries combine and form loops that penetrate into the zone of calcification and the hypertrophic zone, bringing nutrition to osteoprogenitor cells producing bone in the cartilage matrix scaffold [5–7, 18, 27, 37, 44, 48, 55].

At the periphery of the physis (the periphysis), the zone of Ranvier is responsible for the horizontal growth of the physis and the perichondrial ring (ring of La Croix) provides mechanical stability to the physis [45]. In the proximal femur, the perichondrial fibrocartilaginous complex replaces the zone of Ranvier and the ring of La Croix [11] (Fig. 7.3). Branches from a periosteal artery supply the zone of Ranvier.

Fig. 7.3

In the proximal femur, the zone of Ranvier and ring of La Croix are replaced by the perichondrial fibrocartilaginous complex

7.2 Acetabular Development

During development the acetabulum is formed from the interposition of the os pubis, os ilium and the os ischium, forming a triradiate cartilage complex. Interstitial bone growth in the triradiate cartilage complex causes the acetabulum to expand during growth. The presence of a spherical femoral head leads to the concavity of the acetabulum. At puberty, three secondary centres of ossification form around the acetabular cavity, one from each epiphyses of the os pubis, os ilium and os ischium. The secondary ossification centre of the os pubis, sometimes referred to as the os acetabuli, forms the anterior wall of the acetabulum. The secondary ossification centre of the os ilium and os ischium form the superior and posterior wall of the acetabulum, respectively. They expand towards the periphery of the acetabulum and thus contribute to its depth. The physes of the triradiate cartilage complex close at around the age of 15–18 years [42, 43].

7.3 Proximal Femoral Bone Growth

The previously described fundamentals of bone growth and physeal anatomy apply to the proximal femur with certain modifications. At birth, the cartilaginous epiphysis forms the femoral head and greater trochanter that have the same shape as in an adult. The epiphysis is supported by a curved physis. With physeal growth, the epiphysis divides into the femoral head epiphysis and the greater trochanter apophysis (Fig. 7.4) [34, 38].

Fig. 7.4

At birth, the cartilaginous epiphysis forms the femoral head and greater trochanter. With physeal growth, the epiphysis divides into the femoral head epiphysis and the greater trochanter apophysis

Blood supply to the proximal femoral physis changes during growth. Arteries in the ligamentum teres supplement the epiphyseal blood supply but only during the first 3–4 years. Between 4 and 7 years of age, the anterior half of the physis receives blood supply from the lateral circumflex artery and the posterior half from the medial circumflex artery. Eventually, after the age of 7 years, the blood supply to the femoral head is received mainly from branches of the medial circumflex artery. The posteroinferior artery supplies the inferior portion of the femoral head, while the posterosuperior artery travels in the intertrochanteric groove and supplies the superior portion of the femoral head. Both arteries traverse the physis superficially, leaving them vulnerable to damage if the femoral neck or physis is fractured (Fig. 7.5). Even though the proximal femoral physis is one of the least injured long-bone physes, the vulnerable blood supply leads to a high complication rate (such as avascular necrosis) when injuries occur [10, 13, 38, 55, 60, 61].

Fig. 7.5

Eventually, the blood supply to the femoral head is received from the posteroinferior (PI) and the posterosuperior (PS) branches of the medial circumflex artery (MCA). Both arteries traverse the physis superficially, leaving them vulnerable to damage if the femoral neck or physis is fractured

Closure of the proximal femoral physis begins superolaterally and continues inferomedially. Complete closure typically occurs in half of 14-year-old females and 17-year-old males [15, 17].

The microscopic anatomy of the proximal femoral physis differs slightly from what is seen in other physes, with the zone of Ranvier and ring of La Croix replaced by the perichondrial fibrocartilaginous complex [11]. The presence of a bony peg on the underside of the epiphysis projecting down into a socket on the metaphysis has also been described. In the literature, it is referred to as the ‘epiphyseal tubercle’ and it is believed to be an important stabiliser of the epiphysis [30, 53, 54] (Fig. 7.6).

Fig. 7.6

The epiphyseal tubercle projects down into a socket on the metaphysis

7.4 Factors Affecting Bone Growth

The mechanisms controlling physeal growth are not well known. Factors known to influence physeal growth can be divided into general factors, which can affect many or all physes, and local factors, affecting only a single physis. Genetics, nutrition, hormones and general health are examples of general factors. Local factors include blood supply, mechanical forces, traumatic injuries and infection. In this section we will focus on how local factors affect bone growth.

7.4.1 Mechanical Forces

A certain physiological load is needed for normal bone growth [33]. The effect of load on bone growth can be summarised in two laws.

Heuter-Volkmann’s Law establishes that physeal growth is retarded by increased load and accelerated by decreased load. This leads to the physis aligning itself perpendicularly to the force applied and usually at a right angle to the longitudinal axis of the bone [23].

Wolff’s Law proposes that the bone in a healthy individual will adapt to the loads under which it is placed. Under increased load, the bone becomes stronger and thicker through appositional growth, while a reduced load leads to weakening of the bone. A fracture of a long bone that heals in an angulated manner therefore has a tendency to straighten when a load is applied because of increased appositional bone growth on the concave side of the fracture [62].

7.4.2 Blood Supply Disturbance

Compromised blood supply disturbs physeal growth, but the way this happens depends on the supply route that is affected.

If the blood supply from the metaphyseal side is compromised, the vascular loops stop invading the hypertrophic zone and the cells in the hypertrophic zone accumulate. The cells in the resting and proliferating zone receive blood supply from the epiphyseal vessels and continue to grow. Longitudinal growth therefore continues and the physis widens in the affected area.

In the event of a diminished blood supply through the epiphyseal vessels, cells in the resting and proliferating zones are deprived of oxygen and nutrients. Longitudinal growth ceases in the affected area, but the vascular loops continue invading the hypertrophic zone and the physis narrows. If only a portion of the physis is affected, the rest of the physis continues to grow and angular deformities occur [25, 56–59] (Fig. 7.7).

Fig. 7.7

A compromised blood supply on the metaphyseal side causes the continued growth and widening of the physis, but growth cessation and narrowing of the physis occurs if the blood supply is compromised on the epiphyseal side

7.4.3 Trauma

Fractures in and around the physis also affect growth, most probably through disruption in blood flow. Hefti et al. [22] described four types of growth disturbance following fractures in children (Table 7.1).

Table 7.1

The four types of growth disturbance seen following fractures in children according to Hefti et al. [22]

Type 1	Increased growth in the whole physis
Type 2	Decreased growth in the whole physis or complete growth arrest
Type 3	Increased growth in part of the physis, creating angular deformation
Type 4	Asymmetrical growth arrest, with the formation of a bone bridge

The exact reason why overgrowth of the physis occurs following a fracture is unclear. One possible explanation is the increase in blood flow following healing of the fracture.

Physiolysis or fracture/physiolysis most often leads to diminished growth or, in the worst case, complete growth cessation. If the injury is confined to the cellular columns or hypertrophic zone of the physis and the epiphyseal blood supply is intact, normal growth usually resumes.

7.4.4 Infection

Growth disturbances due to infections are due either to the direct destruction of the physis or, secondarily, to disturbed blood supply leading to decreased growth in the whole or part of the physis.

7.5 Bone Development and FAI

Knowledge of growth disturbances and chronic physeal damage to the upper and lower extremities and the spine of adolescent elite athletes is well established [4, 8, 16, 31, 32, 50].

The pincer deformity is a local or global overcoverage of the femoral head by the acetabulum leading to linear contact between the acetabular rim and the femoral head-neck junction. Pincer impingement seems to be more common in females [52].

The aetiology of the pincer deformity is unknown. Factors reported as affecting the development of the acetabulum are congenital instability of the hip and epiphyseal fractures of the triradiate cartilage complex. When acetabular development is affected in these cases, acetabular dysplasia usually occurs [12, 29, 40]. There is currently limited knowledge on factors that may predispose individuals to develop pincer-type deformities of the acetabulum.

The cam deformity is a nonspherical shape of the femoral head at the femoral head-neck junction. It usually resides on the antero-superior surface and leads to a reduced offset of the femoral head and neck junction with resultant abutment of the head-neck junction against the acetabular rim, causing FAI (Fig. 7.8).

Fig. 7.8

Horizontal view of a left hip showing the different types of femoroacetabular impingement

The aetiology of the cam deformity is still not completely known. Theories, including evolutionary changes [24], genetic factors [41], abnormal ossification of the proximal femur [35] and growth disorder or childhood condition, like a silent or mild slipped capital epiphysis or Perthes disease [19, 21, 35, 49], have been proposed. The cam deformity seems to be more common and larger in males compared to females [63].

In recent years, evidence has emerged supporting mechanical factors, affecting the proximal femoral physis, as a cause of cam deformity [39]. As early as 1971, Murray showed that the tilt deformity was more prevalent in individuals who were more active in sports during adolescence as compared with their less active peers [36]. The cam deformity has been shown to emerge from the physeal scar of the proximal femoral physis [47] and to develop during adolescence in response to vigorous sporting activity with the period immediately preceding and during physeal closure seeming to be of special susceptibility [1, 2, 9, 46, 51]. In a study on porcine hips, Jónasson et al. concluded that injuries in and around the porcine proximal femoral epiphyseal plate after repeated physiological loading could lead to growth disturbances and consequently to the development of the cam deformity [26] (Fig. 7.9).