Infantile obesity is a pathology that is generating greater interest because of its widespread growth in industrialized countries. Since the 1990s, obesity has been regarded as one of the most serious public health and medical problems of our time. The main causes of obesity are large consumption of high-calorie foods and lack of physical activity; however, obesity can also be the result of genetic conditions, hormone dysfunctions, or even mental disorders.

It is possible to distinguish 2 types of obesity: primary and secondary. Primary obesity is caused by an imbalance between food intake and energy expenditure. Secondary obesity is linked to endocrine and genetic pathologies, such as Cushing’s syndrome, hyperthyroidism, insulinoma, Stein-Leventhal syndrome, and endocrine hypothalamic disorders. Clinically, the subject’s stature is an important element differentiating the 2 types of obesity. Subjects suffering from primary obesity usually have tall or normal heights, whereas subjects affected by secondary obesity are usually characterized by shorter heights, delayed growth, and dysmorphisms.

Genetic factors are an etiologic basis for obesity. Certain monogenic forms of obesity are characterized by defective genes that encode molecules involved in the hypothalamic regulation of energetic balance. Also, epigenetic factors play an important role in activating and silencing genes that have their most critical, although not exclusive, expression during the prenatal period and the first few months of a child’s life.

The etiologic theory that tries to explain the onset of obesity from a genetic point of view is based on the adipostat concept. In other words, an organism has an internal set point that can recognize the amount of adipose deposits and consequently regulate calorie consumption to prevent buildup. Control over an organism’s energetic balance is associated with a complex of messenger molecules that connect the hypophysis and the entire endocrine system with the hepatocytes, adipocytes, and muscles. Alterations in this hierarchy can cause a buildup of fat.

The consequences of obesity are numerous and include metabolic complications, such as diabetes mellitus, hypertension, dyslipidemia, liver disorders, tooth disorders, and nonalcoholic steatohepatitis; mechanical dysfunctions, such as obstructive sleep apnea; and psychological problems.

Furthermore, it has been suggested that early-onset obesity can cause increases in vertebral bone density and bone size, and an acceleration of skeletal growth. In particular, obesity has been hypothesized to impact craniofacial growth and lead to more precocious skeletal maturation of the maxilla and the mandible.

The level of body fat can influence the neuroendocrine events that are responsible for the onset of precocious puberty despite low levels of growth hormone. More specifically, leptin, a hormone mainly produced by white adipose tissue to control appetite and the buildup of adipose tissue reserves, might be directly involved in this process. Leptin accelerates the production of gonadotropin-releasing hormone by the hypothalamus and affects the adenohypophysis, promoting accelerated pubertal development. Moreover, leptin has been hypothesized to act directly at the level of skeletal growth centers by inducing chondrocyte differentiation and proliferation. In addition, some effects on bone growth might be mediated by other hormones, such as insulin-like growth factor 1, a hormone similar in structure to insulin that is produced in hepatocytes, fibroblasts, and chondrocytes.

The biologic aspects of facial skeletal growth are fundamentally important to dentofacial orthopedics. Knowledge of the remaining facial growth potential is essential for correct diagnosis and therapy. Treatment timing can influence therapeutic outcomes aimed to produce orthopedic effects in the craniofacial structures. In particular, the optimal treatment timing for Class II skeletal disharmony with functional appliances is during or slightly after the peak in mandibular growth, because the skeletal responses decrease both before and after maximal pubertal growth. For these reasons, the operator should consider alterations in skeletal maturity when performing orthodontic or orthopedic treatments during the deciduous or mixed dentition period to optimize the therapeutic outcomes.

Carpal analysis is a common method used to determine skeletal age. The relationship between chronologic age and skeletal age is called the carpal index. Various methods are used to determine the carpal index. One of the most popular approaches is the Greulich and Pyle method, which consists of a series of standard x-rays (31 for boys, 29 for girls). The x-rays are carried out in chronologic steps that increase gradually from the prenatal stage up to the ages of 19 years in boys and 18 years in girls. These x-rays cover all the phalanx bones of the hand, including the diaphysis and forearm bone. Each x-ray belongs to a subject of a particular age that is characterized by a specific ossification stage. To determine the skeletal age, the x-ray of the carpus must be compared with the corresponding x-ray in the atlas provided by Greulich and Pyle.

Measuring cervical vertebral maturation from lateral cephalometric radiographs is an alternative to the hand-wrist analysis, and it has proven to be an effective way to assess the adolescent growth peak in both body height and mandibular size. One advantage of using the cervical vertebral maturation method is that a lateral radiograph is routinely required for orthodontic treatment planning. Therefore, no additional radiograph is generally required to use this method. Despite this advantage, the cervical vertebral maturation method is not sensitive enough to detect growth maturity outside the growth spurt period.

The objective of this study was to compare skeletal maturation in obese patients and normal-weight subjects. The null hypothesis was that obese and normal-weight subjects show similar degrees of skeletal maturation.