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how the core universe forms

WHEN DOES THE CORE DEVELOP?

Fifteen-year old lacrosse players aren’t supposed to worry about their cores. They have more important things on their minds, like whether their hair is long enough to produce a suitably cool “bro flow” out the back of their helmets. But when one visited Dr. Meyers with some hip issues that he couldn’t explain, the focus went from style to substance.

It seems the young laxman had torn some muscles in his core a couple years earlier. Everything seemed all right in that area, but there was that hip problem. Could the 2 issues be related? Hmmm.

The answer, of course, is that nobody knows.

THE BEGINNING (FIGURE 20-1)

No matter the part of the body, human growth and development involves a lot of moving parts. “Moving” in 2 senses: (1) actual bodily movement, transferring from one position to another (ie, the meaning that this book mostly tackles) and (2) in the sense of growing or developing. Both meanings incorporate a timeline as an important element. For the former, time involves very short durations; for the latter, time periods can last way longer. In this chapter, we shall talk more about the latter meaning, rather than the former. Pay particular attention to the fact that, as we grow, our head gets smaller relative to the rest of our body. We go from a head-prevailing physical state of being to a core-dominant existence.

In this chapter, we shall sprinkle out a few facts that have long, seemingly, held true. Most of these facts relate to hip development. We shall proclaim a few “facts” that have probably not been decreed facts before. Notice that we shall not address the all-important elephant-in-the-room question: why. That question is way, way too deep for us country doctors to comprehend.

Here are the nuts and bolts of why that deeper question is way too profound for us. Consider that many regions of our body far away from each other (eg, the feet and hands) grow at the similar rates, while other regions very close to each other (eg, the hip and rest of the bony pelvis) grow at different times and at different rates. The cascades of growth and development occur essentially everywhere with independent clocks. Plus, every individual seems to have a different biologic growth clock and different set of modulators. And also consider the question, once growth or development turns on, what stops it? It’s all way too deep for us to understand.

Think of the bones as the core’s growth lattice. Once bone formation (ossification) occurs, softer structures “fall” into place. Here are some isolated facts. The femur, along with the clavicle, is our first bone to ossify. The femoral head and greater trochanter form separate ossification centers with something called the femoral neck isthmus growth plate that lies between them. The whole complex develops so that the femoral head is offset from the femoral shaft. A somewhat cartilaginous environment allows flexibility at the hip joint. The shape of the femoral neck depends on coordinated growth. It angles 35 degrees forward at birth; this angle reduces to 15 degrees as we become adults. (See Figures 20-2 and 20-3.)

The proximal end of the femur articulates with the os coxa of the acetabulum. As Fares Haddad notes in his brilliant description of hip embryology, the development of a normal hip joint requires well-balanced growth of the multifaceted acetabulum and a centered, spherical femoral head.2 Without the presence of the femoral head, the acetabulum fails to deepen and the cartilage atrophies. Without appropriate acetabular coverage, the femoral head fails to develop spherically. We know that anatomic variations of the hip, regardless of other influences, place individuals at increased risk for hip problems.

The proximal femur develops in concert with the acetabulum, a complex structure that represents the extensions of 3 bones of the pelvis: ilium, ischium, and pubis. The 3 extensions fuse before adulthood. The ilium, an ancient name for Troy, is said to be “war-like”—superior and broad—and extends upward from the acetabulum. The ischium, not so war-like, yet is the lowest and strongest portion of the bone, proceeds downward from the acetabulum, expands into a large tuberosity, and then curves forward and forms, in conjunction with the pubis, a large aperture called the obturator foramen. Our friend the pubis extends medially and downward from the acetabulum and articulates in the middle line with the bone of the opposite side. The articular surface of the acetabulum ends up being made of hyaline cartilage. The fibrocartilaginous “labrum” extends from the margins of the bony acetabulum. In its development, the labrum appears to increase the depth of the acetabulum and perhaps contribute to vacuum-type suction as it becomes continuous with the joint capsule, periosteum, and femoral ligaments.

Ossification of the ball and socket utilizes input from 8 ossification centers and takes 20 years to complete. Just in case you want to know more about these ossification centers, here’s some more information. They are 3 “primaries” (the inferior ileum, ischium, and pubis) and 5 “secondaries” (the iliac crest, anterior inferior spine, ischial tuberosity, pubic symphysis, and the acetabular bottom). And here is the way they form: At birth, the 3 primary centers are quite separate. The crest, bottom of the acetabulum, ischial tuberosity, and inferior rami of the ischium and pubis remain cartilaginous. By the seventh or eighth year, the inferior rami of the pubis and ischium unite with bone. By year 13 or 14, the 3 primary centers have extended their growth into the bottom of the acetabulum. They remain separate but connect via a Y-shaped “tri-radiate” cartilage plate. The os acetabulum, the small piece of bone at the anterior acetabular edge, appears between the ilium and pubis at about 12 years of age and fuses around 18 years; that os forms the “pubic” part of the acetabulum. Then the ilium and ischium join, and lastly the pubis and ischium. Slowly, the tri-radiate “cartilage” is no more. At puberty, ossification begins to replace remaining portions of cartilage, and the whole process does not finish until 20 or 25 years of age.³

The whole process, though, really extends into our 70s and 80s. Think about our ultimate loss of hip articular cartilage, arthritis, etc. Isn’t this just part of a normal development process? Can we affect the progression of arthritis as we get older? You bet we can. Staying in good shape fends off arthritis and its ravages, not only in the hip, but also in the knee and other joints.

If we can prevent the progression, why not begin this progression during adolescence or earlier? That’s one of our main points!

BAD OR BENEFICIAL?

Whether or not you have read each detail of the previous paragraphs, it is now obvious that the complexity of femur and adjacent bone development explains the many variations of hip anatomy. In this book, we talk a lot about femoroacetabular impingement. These particular abnormal hip morphologies develop throughout those years. Commonly, femoroacetabular impingement categorizes into 2 broad groups: femoral head/neck protrusions (cam impingement) and acetabular overcoverage (pincer impingement). Both cause abnormal contact between the femur and the acetabulum. A cam lesion refers to a prominence of the anterosuperior aspect of the junction of the femoral head and neck that can pinch off the labrum and rip underlying articular cartilage. The end product is severe arthritis. The term acetabular under-coverage does not specifically refer to femoroacetabular impingement, but rather a form of dysplasia or lack of development of the hip socket.

But also think about the possible advantages of impingement or dysplasia. With some padding, bone rubbing against bone is not necessarily bad; it gives you more leverage. Think about the tightness of the hips of a power hitter in baseball or a running back in football. Have you ever wondered about those butterfly ice hockey goalies out there? How amazingly deft they appear when they swing around their pads over their heads? How do they do that? Under-coverage of the hips, of course! In fact, that does explain it. Some of these goalies have real hip dysplasia. Others have broken through their nuisance acetabular ossification by years of training. Yes, both sets of goalies are more likely to get hip replacements in the future.

There is also scientific evidence that survival advantages of certain hip morphologies also predispose to injury. Hogervorst et al described 2 stereotypical mammalian hips (ie, coxa recta and coxa rotunda) as likely adaptations in response to the running (coxa recta) and climbing and swimming (coxa rotunda). The manuscript goes on to explain that coxa rotunda represents an evolutionary conflict between upright gait and the birth of a large-brained fetus within the female pelvis; somehow that explains pincer-type impingement.4

Pathologic aspects of these variations have been appreciated since the 1970s. Only recently have we understood that subtle morphologic aberrations and variations in the way we train, and at the ages when we train, likely influence the development of hip problems. For example, intense training in a high-impact sport (such as soccer, ice hockey, and basketball) at the physeal closure development phase likely promotes the cam bump on the femur. The cam enhancement possibly comes from high shear stress applied to the femoral head.^5,6

But not all athletes with cam lesions develop hip problems. In a study of asymptomatic non-athletes undergoing hip imaging for medical conditions unrelated to the hip, 53% of the population had femoroacetabular impingement.⁷ The correlation between the bump on an athlete’s femoral head and intense high-impact training leads to a variety of interesting questions. Are cam lesions already more common among those participating in intensive training? Is that what makes them participate in athletics and play at a higher level in the first place? Are there other variations that predispose the athletes to cam development around puberty? Could cam or associated inflammatory changes in that anatomic region be a marker for overtraining? Some athletes, including some great shot-putters, for example, with cam lesions have dramatically decreased hip range of motion (eg, decreased decline of the pelvis during a squat).⁸ Let’s leave this paragraph with one more question: Might cam development or symptomatic cam also result from variations in flexibility of surrounding core muscles and soft tissue?

WHAT ABOUT THE CORE MUSCLES?

Okay, that’s it for the bones. No one knows much about growth and development of the core musculature, as we have defined this second of the 4 parts of our core. We have some information about certain isolated muscles, but know next to nothing about differences in core muscular function from the embryo to adult. We shall not discuss, in any sort of depth, the growth and development of the other 2 parts of the core—the back and the “other” systems (eg, gastrointestinal, genitourinary, gynecologic). We already know a whole heap about the latter subjects. Let’s walk—pun intended—through what we know about the core muscles, and what likely transpires.

Stability of the active hip joint comes mostly from tension provided by the muscles and the other soft tissues surrounding the joint. That stability works additively to the intrinsic stability within the hip’s immediate environment with its bony and cartilaginous structures. Of course, nobody has studied hip stability within the early developmental stages of life. We don’t know which muscles are initially involved. Hip instability (see Chapter 14) and other hip problems result from, among other things, bad hip morphology, a variability of static hip load types, and the mechanics of the surrounding musculature.⁹ Sporting activities involving repeated axial loading and rotation, such as gymnastics, football, tennis, ballet, martial arts, and golf, influence the development of focal laxity and increase risks. Muscles in the same vertical plane as the hip (eg, gluteus minimus, quadratus femoris, gemelli, obturator internus and externus, iliocapsularis, and iliopsoas¹⁰), as well as other core muscles (rectus abdominis, adductor magnus¹¹), grow at similar rates as the hip, so likely provide an increasingly dynamic stabilization of the femoral head with the acetabulum.

Embryologically, the rectus abdominis muscle forms from the ventral longitudinal column of the ventral hypomere, which, in turn, develops from the lateral plate of the paraxial mesoderm. The ventral longitudinal column divides into the 2 heads of origin for each hemi-abdominal rectus abdominis muscle, attaching at the pubic symphysis and tubercles medially and the upper border of the pubic crest laterally.¹² They run side by side caudo-cranially to broaden out as they reach their superior insertions at the fifth to seventh costal cartilages.

A few additional, perhaps less boring, anatomical tidbits: The attachments of the rectus abdominis onto the fibrocartilaginous plate of the pubis must form after fusion of the pubic symphysis. The pubic rami muscular attachments to the pubic rami likely develop after the central attachments and origins of the thigh adductor muscles.¹³ The adductor longus and rectus abdominis tendons coalesce to form the symphyseal capsule of the pubic symphysis as a non-synovial diarthrodial joint between the pubic bodies.

Each articular surface somehow gets covered by hyaline cartilage, and, presumptively, at about the same time, the symphysis separates from the fibrocartilaginous plate. Probably in early adolescence, the plate joins more tightly to the underlying pubic periosteum via fibrocartilage/bony spicules. Generous potential spaces remain, so that injuries, produced by opposing forces, detach the plate and fluid accumulates within those spaces. Nobody yet knows from where the fluid comes; it makes sense that some of it comes from a disrupted symphyseal joint. That’s what it looks like radiologically.

In both the evolutionary and embryological processes, we progress from 4-legged or crawling creatures and end up as upright adult human beings. The progression process turns out to be similar in the 2 dramatically different scientific worlds. That said, what happens in this process? How does the anatomy change? There must be something to learn here. This process must involve both hips and the muscles. A few paragraphs ago, we speculated about the hips. What about the muscles? (See Figure 20-4.)

Related posts:

Putting It All Together—A Patient’s Perspective on the Core Nerves in the Core—A “Fifth Dimension” The Final Stage of Rehab—Getting All the Way Back The Other Muscles—Hip and Core Stability Biomechanics Presenting…the Core!

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