Anterior Cruciate Ligament Injuries And Their Treatment

Anterior cruciate ligament (ACL) injuries are usually sustained by a young and active population, often under pressure to continue heavy labor or sports activities at a competitive or recreational level. The natural history of an ACL injury still remains unclear. Conservative (nonsurgical) treatment has been reported to produce unsatisfactory results, such as chronic instability, muscle weakness, and osteoarthritis (OA), but also to render acceptable function for some patients. It is a common algorithm that surgical intervention is recommended if the patient requests a return to high-risk pivoting sports or if symptoms of giving way are persistent after a conservative program. (To our knowledge, however, this has not been scientifically proven in randomized controlled studies.)

ACL surgery and reconstruction with different types of autograft such as patellar or hamstring tendons have been shown to produce favorable and predictable results. The majority of patients can return to heavy labor and sports activities, but normally on a lower level than before the injury. However, the reconstructions are often associated with donor site problems that are well documented in the literature. These problems involve anterior knee pain, patellofemoral tenderness and the development of OA, patellar tendon shortening, loss of sensitivity in the anterior knee region, discomfort during kneeling and knee-walking, and loss of muscular strength.

Another less documented but reported side effect after ACL injury and ACL surgery is the risk of localized or systemic bone loss.

In some respects, the ACL-injured patient is selection biased. The injury usually occurs during sporting activities. The patients are often young, well-trained athletes and have strong bone mass. We know that athletes have higher bone density than the normal population, a combined effect of training and selection, as it is probably more likely that people with good muscle strength choose to play soccer/football compared with smaller individuals.

Peak Bone Mass and Natural Bone Losses

We start adult life with a peak bone mass, 80% of which is determined by genetic factors. This is also the case for fat and muscle tissue, 65%–80% of which are genetically determined. Men have a higher peak bone mass than women ( Fig. 130.1 ). During childhood and adolescence there is a physiological rapid gain of bone mass, and it is an attractive idea that increased activity and sufficient nutrition during this period could enhance bone formation even further. However, the positive effect of training during childhood and adolescence appears to be lost with the cessation of a sporting career.

Schematic bone mass curves showing the peak bone mass and the subsequent loss with age. (Men are represented by the unbroken line and women by the dotted line .)

From the peak bone mass at the age of 20–30 years, there is an annual loss of approximately 0.1%–1%. The loss for women is accelerated in connection with menopause and, during the subsequent 10 years, the annual loss is as much as 2%–4% (see Fig. 130.1 ). The bone metabolism turnover rate is 4–10 times higher in trabecular bone compared with cortical bone. The content of trabecular bone in the calcaneus is 95%; in the lumbar vertebrae, 40%; and in the neck of the femur, 40%. In a period of 8 years, the bone tissue is completely replaced. The potential as an adult to compensate for a low peak bone mass or to significantly increase bone mass by strenuous exercise or an excessive intake of calcium/vitamin D appears to be virtually nonexistent. However, the female athlete triad, a disorder in young females characterized by eating disturbances, amenorrhea, and osteoporosis, could be an exception. For these individuals, there is still the potential for “catch-up” in bone mass in the third decade of life if the condition is reversed. The normal physiological bone loss seen during pregnancy and breastfeeding also appears to be reversible.

Peak Bone Mass and Natural Bone Losses

We start adult life with a peak bone mass, 80% of which is determined by genetic factors. This is also the case for fat and muscle tissue, 65%–80% of which are genetically determined. Men have a higher peak bone mass than women ( Fig. 130.1 ). During childhood and adolescence there is a physiological rapid gain of bone mass, and it is an attractive idea that increased activity and sufficient nutrition during this period could enhance bone formation even further. However, the positive effect of training during childhood and adolescence appears to be lost with the cessation of a sporting career.

Schematic bone mass curves showing the peak bone mass and the subsequent loss with age. (Men are represented by the unbroken line and women by the dotted line .)

From the peak bone mass at the age of 20–30 years, there is an annual loss of approximately 0.1%–1%. The loss for women is accelerated in connection with menopause and, during the subsequent 10 years, the annual loss is as much as 2%–4% (see Fig. 130.1 ). The bone metabolism turnover rate is 4–10 times higher in trabecular bone compared with cortical bone. The content of trabecular bone in the calcaneus is 95%; in the lumbar vertebrae, 40%; and in the neck of the femur, 40%. In a period of 8 years, the bone tissue is completely replaced. The potential as an adult to compensate for a low peak bone mass or to significantly increase bone mass by strenuous exercise or an excessive intake of calcium/vitamin D appears to be virtually nonexistent. However, the female athlete triad, a disorder in young females characterized by eating disturbances, amenorrhea, and osteoporosis, could be an exception. For these individuals, there is still the potential for “catch-up” in bone mass in the third decade of life if the condition is reversed. The normal physiological bone loss seen during pregnancy and breastfeeding also appears to be reversible.