Right from the time of delivery, when a child is born and leaves the protected environment of the mother’s womb, the child is exposed to the outside environment. Humoral and other adjustments restrain the temporary slowing of growth. Similarly, illnesses (short or prolonged), altering seasons or nutritional factors influence growth modulation. Whenever the growth of an organism is hindered due to environmental influences, the body tends to respond with an exaggerated growth session when the circumstances become favourable. This phenomenon is called catch-up growth, a concept introduced by A. Prader, J.M. Tanner and G.A. von Harnack in 1963. Hence, catch-up growth occurs following a temporary cessation or reduction of growth consequent to an insult or injury. More accurately, it is defined as the height velocity that exceeds reasonable limits for the child’s age for at least one year after a period of depressed growth. Although the catch-up phenomenon leads to accelerated growth, whether it can adequately compensate for the functional disturbances caused is still being determined. Other factors influencing catch-up growth are chronological age, height, weight, duration and severity of the illness/insult. Catch-up velocity in height can reach at least four times the normal velocity for the chronological age.

Population height charts are obtained by plotting graphically serial measurements of the heights of various subjects of a particular race/community at different time intervals. When an individual is to be evaluated, his/her data can be plotted on a graph and compared with population means. Chart data can be interpreted in the following two ways:

• Distance curve : indicates a point on the graph the subject has reached in height ( Fig. 11.3 A and B). By comparing it with population means, future growth may be forecasted.

  

  (A and B) Percentile height for age charts for girls and boys plotted as a distance curve. (C and D) Distance and velocity curve for Indian population children.

  Source: (A and B) CDC growth charts 2000, http://www.cdc.gov/growthcharts/ . (C and D) Indian Academy of Pediatrics, http://iapindia.org/files/growthchart/IAP%20Girls%20Height%20&%20Weight%20chart%205-18%20years.pdf and http://iapindia.org/files/growthchart/IAP%20Boys%20Height%20&%20Weight%20chart%205-18%20years.pdf .

• Velocity curve : indicates the height gain rate over a period ( Fig. 11.3 C and D). These charts are beneficial for identifying the onset of growth spurts during which rapid increments in height are obtained. The height velocity is expressed in centimetres per year. An idealised velocity curve of human growth for boys is given in Fig. 11.4 .

  • The value thus obtained is then compared with age-specific population norms (means), provided as height-for-age charts, of that state/country. Deviations are measured by reference to population percentiles. WHO recommends cutoff values of ±2 standard deviations, corresponding to the 2.3rd and 97.7th percentiles (modified to 2nd and 98th percentile) to define abnormal growth. Therefore, a child falling out of two standard deviations on either side of the population’s mean is considered unhealthy and would require detailed evaluation. Similar to WHO charts, the Indian Academy of Pediatrics (IAP) created the standard charts for the Indian child population, published in 2007. Later, the growth chart committee of IAP revised growth charts for 5–18-year-old Indian children in 2015. For younger children, IAP recommends the use of WHO 2006 growth standards. The revised growth charts truly represent all zones of India.

  

  Idealised velocity curve of human growth for boys ( Green line ). The purple line is a sixth polynomial curve fit with the velocity data. The polynomial curve does not work well with actual growth curve data due to pulses in the mid-childhood spurt (MCS) and the adolescent spurt (AS). The human velocity curve cannot be fitted adequately by a single continuous mathematical function. Two or more functions are required. A , adolescent; C , childhood; I , infancy; J , juvenile; M , mature adult.

  Source: Reproduced from Ulijaszek SJ, Johnston FE, Preece MA . The Cambridge Encyclopaedia of human growth and development. Cambridge: Cambridge University Press; 1998. p. 464.

• Peak height velocity (PHV) is defined as the maximum rate of gain of height during adolescence. It is considered an excellent indicator of overall somatic and skeletal growth ^, and a good indicator of facial growth ( Fig. 11.5 ). PHV occurs at a mean age of 13.5 years in boys and 11.8 years in girls. On average, girls mature approximately two years earlier than boys. Pubertal growth accounts for about 17% to 18% of final adult height, with an average mean height of 30 to 31 cm in male and 27.5 to 29 cm in female. An average growth spurt lasts 24−36 months.

  

  Graphic representation of average height for age changes from 0 to 18 years in boys ( solid red line ) and girls ( dotted blue line ). (A) Distance curve. (B) Velocity curve. Note that the adolescent growth spurt occurs earlier in females, when the average female is taller than her male counterpart. Also note that the adolescent growth spurt is more prolonged in males and males show a higher peak height velocity (PHV) than females. ( A , adolescent; C , childhood; I , infancy; M , mature adult.)

  Source: Reproduced with permission from Tanner JM, Whitehouse RH, Takaishi M. Standards from birth to maturity for height, weight, height velocity and weight velocity in British children. Arch Dis Child 1966;41:454–71. Available from: https://adc.bmj.com/content/41/219/454 .

When serial height measurement data from a group of individuals are plotted, certain observations become apparent. First, when plotted independently, growth data from individuals show sharp spikes representing the changes in height gain from birth to adulthood. These spikes highlight the variability of growth amongst individuals and at different times. However, when the mean of the growth data from a population is plotted, the spikes are lost and the curves become smooth.

Second, since every individual has their own growth trend, a population growth chart shows wide variation in mean values and large standard deviations. Thus, if the growth of an individual varies considerably from population data, it would not necessarily mean that some underlying disorder is affecting normal growth. Usually, a child is considered to be abnormal if their growth does not fall within two standard deviations of the mean (i.e. 2nd to 98th percentiles).

Children with early-onset pubertal timing have reduced adult height and leg length, and subjects with a low childhood body mass index have reduced adult sitting height. Thus, childhood body composition and pubertal timing have impacts on trunk growth and the growth of long bones.

Generally, the onset of height, facial height, facial size and mandibular length occurs in an orderly fashion. The difference in timing between height and facial size growth spurts is statistically significant. In boys, the onset for height, facial size and mandibular length occurs simultaneously at 11.9, 12.0 and 11.9 years, respectively, while in girls, it occurs at 10.9, 11.5 and 11.5 years. Height peaks significantly earlier than both facial size and mandibular length. In boys, the peak in height occurs slightly (but statistically significant) earlier than the peaks in the face and mandible: 14.0, 14.4 and 14.3 years.

Bones formed in the membrane are characterised by direct deposition of osteoid material by osteoblasts in a fibrous matrix, which then slowly calcifies to form the bone. Most of the skull’s vault bones are produced by intra-membranous ossification. ^,

Endochondral ossification is the process that results in the replacement of the embryonic cartilage. This type of ossification starts in intra-uterine life and continues till early adulthood when growth ceases. Chondrocytes play a central role in this process, contributing to longitudinal growth through a combination of proliferation, extracellular matrix secretion and hypertrophy. Terminally differentiated hypertrophic chondrocytes then die, allowing invasion by a mixture of cells that collectively replace cartilage tissue with bone tissue. Ossification centres develop within the cartilage, which is where calcification starts. Slowly, osteoblasts replace the entire cartilage matrix with osteoid, which calcifies to form mature bone. Most of the bones of the cranial base are formed by endochondral ossification. Common terms used while discussing bone formation are given in Table 11.5 . The differences between intramembranous and endochondral ossification in given in Table 11.6 .

Initial growth of a long bone occurs at the primary ossification centre located in the middle portion of the bone called the diaphysis; later, secondary ossification centres develop on either end of the diaphysis in the epiphysis region. It is at the junction of the diaphysis and epiphysis that major growth in length occurs. This junction is known as the epiphyseal plate and is composed of hyaline cartilage. When growth ceases, the epiphyseal plate loses its cartilaginous nature, calcifies and merges with the diaphysis, forming a continuous long bone. This phenomenon is called epiphyseal plate closure ( Fig. 11.6 ).

A long bone has diaphysis, epiphysis and metaphysis regions. The bone grows along the long axis by growth at the epiphyseal cartilage (plate). Attainment of adulthood is marked by the capping of epiphyses and fusion of the epiphyseal cartilage, which ceases the further growth potential of the bone.

Healthy bone comprises an external periosteal layer and an internal endosteal layer. Endosteal bone contains a mixture of cortical and trabecular bone in varying amounts. The apposition of bone on selective periosteal surfaces and simultaneous resorption at other related surfaces contributes to bone growth. However, periosteal growth is not merely adding bone to the outer surface and resorption from the inner surface. Endosteal resorption and the addition of bone from within the cancellous spaces are also necessary to maintain the appropriate thickness of the cortical layer of bone. The process of balanced apposition and resorption facilitates the growth of the skull vault and helps shape the nasal and oral cavities and the sinuses.

Sutural growth is entirely different from epiphyseal growth. Growth at the sutures does not occur because of the innate potential of sutural tissue to proliferate. Instead, these tissues respond to the tension created by the growth of adjacent soft tissues. A classic example is the growth of the cranial vault. During the early years of life, the cranial vault enlarges in size primarily by growth at the sutures due to the tension created at the suture sites by the rapidly expanding brain. Later, after ossification of the sutures, the cranial cavity expands by growth at the cranial base and surface remodelling of the vault.

It must be remembered that tension causes sutural growth. When there is compression (lack of tension), as in parts of the cranial base and mandibular condyle, endochondral bone formation ensues. The histologic mechanism of sutural response was well described by Koski in 1968 ( Fig. 11.7 ).

Growth at sutures. Essentially two concepts are in vogue. (A) The three-layer theory wherein intermediate connective tissue between the sutures proliferates, which makes the bone grow. (B) According to the five-layer theory, the ends of the bone at sutures have a two-layered periosteal system where primary bone growth takes place. Intermediate connective tissue allows adjustments for bony growth.

Source: Based on the concept of Koski K. Cranial growth centers: facts of fallacies? Am J Orthod 1968;54(8):566–83. doi:10.1016/0002-9416(68)90177-2. PubMed PMID: 4874446.

Remodelling of bone occurs at different sites concurrently with an increase in bone size. Remodelling is a process for progressive adjustment of bones to maintain their shape, proportions and functions. Growth in any area of the bone requires compensatory changes in other parts to maintain functional integrity. Remodelling can be of two types: (1) surface and (2) structural.

• Surface remodelling occurs on the surface of the bone and leads to changes in topography.

• Structural remodelling/Wolff ’ s law causes a change in the inherent architecture of the bone and may lead to a change in the density and mechanical properties of the bone. For example, alignment of the trabeculae along the line of force would be a type of structural bone remodelling (Wolff’s law), while the development of surface elevations/fins for the attachment of muscles and tendons, like the pterygoid plates, are a type of surface remodelling.

Remodelling or bone turnover occurs throughout life and is primarily controlled through paracrine cells signalling to osteoblasts and osteoclasts. Approximately 10% of the skeletal mass of an adult is remodelled each year.

Cortical drift is a remodelling mechanism wherein the bone, or one of its surfaces, moves through space by selective bone deposition and resorption on cortical surfaces. Cortical bone has an inner endosteal surface and an outer periosteal surface. Drift is brought about by deposition on one side and resorption on the opposite side of the same cortical plate. The classic example of cortical drift is provided by the growth of the facial surface of the maxilla. While the entire maxilla is translated downward and forward, the anterior surface of the maxilla shows resorptive patterns and moves in the opposite direction ( Fig. 11.8 A and B). It must be understood that a surface of the cortical plate may be depository at one stage and resorptive at another stage.

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