骨組織是一種活組織，在一生中的任何時候都不斷在新陳代謝。舊的骨頭不斷被破骨細胞吸收，造骨細胞也不斷工作形成新的骨頭。這個過程就是骨轉換。在兒童期、青春期的時候，身體生成新骨頭的速度會比分解舊骨更快，因此骨骼在大小和密度上會不斷增加。以女性為例，最快速的骨骼生長發生在青春期到18 歲左右。大多數人在30 至35 歲左右達到巔峰骨量(peak bone mass) ，之後因為正常的老化過程開始慢慢下滑。如果巔峰骨量不高，隨著時間的推移，有可能失去足夠的骨質，最終可能會導致骨質疏鬆症。反之，巔峰骨量越高，維持骨骼健康的骨骼就越多。青春期的發育依賴於Kisspeptin (KiSS 1) 和荷爾蒙(GnRH) 神經元的發展變化，青春期成熟可能也包括KiSS 1 和GnRH神經元偶合通路的發育，下丘腦的KiSS1-KiSS1 R-GnRH訊號系統與青春期的開始有密切關係。de Vires 等研究發現中樞性性早熟女孩的血清KiSS 1 水平高於正常女孩。因此，血清KiSS 1 水平也許可以作為中樞性性早熟的診斷標準之一。KiSS 1-KiSS1 R系統在促性腺軸的激活、青春期發育以及生殖功能的調控等方面有扮演關鍵角色。換句話說，KiSS 1 是生殖系統的重要調控因子，而下丘腦的KiSS 1 細胞是傳遞性激素對GnRH神經元反饋的中樞環節。但是KiSS 1 的表達與KiSS 1 神經細胞在青春期的對應關係還需要進一步研究。雖然已有大量證據表明KiSS 1-KiSS1 R系統激發了青春期的開始，但GnRH神經元的激發是一個複雜的過程，KiSS 1 與其他影響因子的關係還有待研究。事實上，人類巔峰骨量(peak bone mass)是一生中骨質密度最高時期。全身骨量的一半都是在青春期生長而成。若在兒童時期沒有發育完成最強壯骨骼，可能會造成人們到晚年時，罹患骨質疏鬆以及骨折。在影響顛峰骨質量的因素中，男性的骨質量與骨密度通常比女性高。在青春期之前，男孩與女孩的骨質量生長速度相似。但青春期後男孩的骨質量增長量通常比女孩多。性荷爾蒙( 包括雌激素及睪丸酮) 對於骨質量的增長至關重要。月經較早開始的女孩通常具有較高的骨密度，經常無月經的女孩會有較低的骨密度。因為KiSS 1 似乎是調控青春期發動時間的最重要因素，所以KiSS 1 的生理性異常或其相關的基因異常，均可能導致年老後的骨鬆症，而這也提供了一些診斷預測骨鬆症和治療上的新可能性。

Bone tissue is a living tissue that is constantly being metabolized at any time of life. Old bone is constantly absorbed by osteoclasts, and thereafter osteoblasts continue to work to form new bones. This process is bone turnover. During childhood and adolescence, the body produces new bones faster than it breaks down old bones. Therefore, bones will continue to increase in bony structure and density. Taking women as an example, the fastest bone growth occurs in Adolescence to about 18 years old. Most people reach peak bone mass around the age of 30 to 35. Then the process begins to slowly decline due to the normal aging process. If the peak bone mass is insufficient, as time goes by, it is possible to lose enough bone mass, which may eventually lead to osteoporosis. On the contrary, the higher the bone mass, the quality of bone can be maintained healthy. The development of puberty depends on the development and changes of KISS 1 and GnRH neurons. Adolescent maturity may also include the development of the coupling pathway of KISS 1 and GnRH neurons. The kisspeptin-KISS1 R-GnRH signaling system of the hypothalamus is closely related to the onset of puberty. The serum Kisspeptin level of girls with central precocious puberty is higher than that of normal girls. Therefore, serum kisspeptin level may be used as one of the diagnostic criteria for central precocious puberty. The Kisspeptin-KISS1 R system plays a key role in the activation of the gonadotropin axis, puberty development and the regulation of reproductive function. In other words, Kisspeptin is an important regulator of the reproductive system, and Kisspeptin cells in the hypothalamus are the central link that transmits sex hormones to GnRH neurons. However, the relationship between the expression of KISS 1 and Kisspeptin nerve cells in puberty needs further study. Peak bone mass is the period of highest bone density in a lifetime. Half of the body’s bone mass is grown during puberty. If the strongest bones are not developed during childhood, very bad results may be produced decades later. This may increase the risk of osteoporosis and fractures in old age. Among the factors that affect the quality of peak bone mass, the quality and density of men are usually higher than those of women. Before puberty, the growth rate of bone mass in boys and girls is similar. However, after puberty, the bone mass of boys usually increases more than that of girls. Estrogen and testosterone are essential for the growth of bone mass. Girls with early menstruation usually have higher bone density, and girls with frequent amenorrhea have lower bone density. Because KISS 1 appears to be the most important factor regulating the timing of puberty. Therefore, the physiological abnormality of KISS 1 or related genetic abnormality, may lead to osteoporosis in old age. It also offers new possibilities for diagnosis, prediction and treatment of osteoporosis.