Anterior Cruciate Ligament Injuries and their Treatment

Anterior cruciate ligament (ACL) injuries are usually sustained by a young and active population, often under heavy 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.¹ 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 good 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 all the requirements to have a good 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% to 80% of which are genetically determined. Men have a higher peak bone mass than women (Fig. 73-1). During childhood and adolescence, it is possible to increase bone mass with sufficient nutrition and physical activity. However, the positive effect of training during childhood and adolescence appears to be lost with the cessation of a sporting career.²

Fig. 73-1 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 25 years, there is an annual loss of approximately 0.5% to 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% to 4% (see Fig. 73-1). The bone metabolism turnover rate is 4 to 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 significantly to 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.

Osteoporosis

The World Health Organization (WHO) has proposed a definition for osteoporosis based on bone mineral density measured using the dual-energy X-ray absorptiometry (DXA) technique in the hip, vertebra, or distal radius in postmenopausal women. Osteoporosis is defined as bone mineral density more than 2.5 standard deviations below the mean value for young adults in the same population.

Osteoporosis and its consequences, with an increasing fracture incidence among the aging population in Western countries, have become a challenge to general public health and the welfare system. There are many known risk factors for osteoporosis and/or fractures. They can be divided into (1) nontreatable risk factors such as older age, previous fracture, female gender, menopausal age, heredity, ethnicity, and body height and (2) treatable risk factors such as physical inactivity, low body weight/low body mass index (BMI), cortisone treatment, low bone density, tendency to fall, tobacco smoking, alcohol consumption, low exposure to sunlight, impaired vision, and calcium and vitamin D deficiency.³ Older age and a history of previous fractures are regarded as by far most important risk factors.

Osteoporosis is a silent condition with no symptoms, and the clinical manifestation is usually a low-energy fracture in the vertebra, distal radius, proximal humerus, or hip. The Scandinavian countries of Norway, Iceland, Sweden, and Denmark top the global list for the incidence of hip fractures. The incidence of hip fractures will be an increasing problem worldwide due to an aging population.