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From other websitesContent disclaimerContent on this website is provided for information purposes only. Information about a therapy, service, product or treatment does not in any way endorse or support such therapy, service, product or treatment and is not intended to replace advice from your doctor or other registered health professional. The information and materials contained on this website are not intended to constitute a comprehensive guide concerning all aspects of the therapy, product or treatment described on the website. All users are urged to always seek advice from a registered health care professional for diagnosis and answers to their medical questions and to ascertain whether the particular therapy, service, product or treatment described on the website is suitable in their circumstances. The State of Victoria and the Department of Health shall not bear any liability for reliance by any user on the materials contained on this website. IntroductionPuberty is the process of physical maturation where an adolescent reaches sexual maturity and becomes capable of reproduction. On average, puberty typically begins between 8 and 13 in females and 9 and 14 in males. Puberty is associated with emotional and hormonal changes, as well as physical changes such as breast development in females (thelarche), pubic hair development (pubarche), genital changes in males, voice changes, an increase in height, and the onset of menstruation (menarche). Puberty proceeds through five stages, termed Tanner stages, ranging from prepubertal, to full maturity. Issues of ConcernIn general, puberty follows a predictable pattern of onset and sequence. However, due to differences in each individual, including environment and genetics, puberty may proceed in a less-than-predictable way. Issues of concern related to puberty include, but are not limited to delayed puberty, precocious (early) puberty, contrasexual pubertal development, premature adrenarche (androgens causing early pubertal changes), premature thelarche in girls, and premature or delayed menarche. Of specific concern to adolescent males is the appearance of enlarged breasts during puberty. Gynecomastia of puberty is a benign condition in males, characterized by the proliferation of glandular elements, which results in the enlargement of one or both breasts. During male puberty, there is often a short-lived imbalance between estrogen and testosterone, leading to gynecomastia. If the history and physical examination fall within normal limits, the gynecomastia usually resolves on its own by the age of 18, and only reassurance and monitoring are necessary.[1] Puberty can also bring about emotional changes and stress to individuals as they come to terms with their changing bodies. Voice changes, wet dreams, involuntary erections, and noticeable physical changes such as breast enlargement, acne, widened hips, and growth spurts can cause adolescents to become worried and concerned about being different from their peers. While it is important to recognize the physiologic changes in puberty, it is also important to acknowledge the psychosocial and emotional changes that may occur at this time. CellularGonadotropin-releasing hormone (GnRH) neurons of the hypothalamus control the initiation of puberty. The pulsatile secretion of GnRH by these neurons brings about the physiologic changes associated with puberty. Currently, there are increasing amounts of evidence showing that kisspeptin neurons in the arcuate nucleus release neurokinin B and dynorphin to generate the pulsatile secretion of GnRH.[2] GnRH causes the release of luteinizing hormone (LH) and follicle-stimulating hormone (FSH) from the gonadotropic cells of the anterior pituitary gland. FSH and LH affect the Leydig and Sertoli cells in the testes and the theca and granulosa cells of the ovary. The zona reticularis of the adrenal cortex produces the hormones responsible for adrenarche and function separately from the hypothalamic-pituitary-gonadal axis.[3] DevelopmentTanner staging is a classification system used to assess stages of puberty. A breakdown of each stage can be seen in Tables 1 and 2. Female Development During Puberty [4]
Male development during puberty [5]
Growth Spurt [6] The growth spurt results from interactions between sex steroids (estradiol/testosterone), growth hormone, and IGF-1. The rise in sex steroids leads to an increase in growth hormone levels, which causes an increase in IGF-1. IGF-1 causes somatic growth via its metabolic actions (e.g., increases trabecular bone growth). Following the growth spurt in males, the larynx and vocal cords enlarge, and the boy's voice may 'crack' as it deepens in pitch.[7] Adrenarche Adrenarche refers to the increased secretion of adrenal androgen precursors dehydroepiandrosterone (DHEA), dehydroepiandrosterone sulfate (DHEAS), and androstenedione from the adrenal zona reticularis, which typically occurs prior to puberty in children around the ages of 6-8 years. The eventual phenotypical result of adrenarche is pubarche, as well as apocrine odor, increased oiliness of hair and skin, and acne.[8] Organ Systems InvolvedThe two major systems involved in puberty are the reproductive and endocrine systems. The hypothalamus, pituitary gland, adrenal glands, ovaries, and testes all produce hormones involved in the changes of puberty. However, these hormones produced during puberty affect nearly every system within the body, causing both internal and observable changes. The skeletal system changes, muscles grow, the circulatory and respiratory systems undergo rapid growth and development, and nervous system changes occur. During puberty, increases in estrogen and testosterone bind receptors in the limbic system, which stimulates the sex drive and increases emotional volatility and impulsivity.[9] FunctionThe primary function of puberty is to produce sexually mature adults capable of reproduction. MechanismThe hypothalamus releases GnRH in a pulsatile manner, which then stimulates the release of FSH and LH from the anterior pituitary gland. Prior to puberty, FSH and LH levels in the body are low. Approximately one year before the onset of puberty, CNS inhibition of GnRH subsides, leading to a rise in the release of FSH and LH.[10] FSH and LH act on the gonads (ovaries and testicles) to stimulate the synthesis and release of sex steroid hormones (estrogen/progesterone and testosterone) and support gametogenesis (formation and development of oocytes/sperm). Sex steroids exert negative feedback on the hypothalamus and pituitary gland to ensure circulating levels remain stable. A rise in FSH stimulates an increase in estrogen synthesis and oogenesis in females and the onset of sperm production in males. A rise in LH stimulates an increase in progesterone production in females and an increase in testosterone production in males. Hormonal changes caused by rises in FSH and LH allow for the physical changes of puberty to begin. The first hormonal change showing puberty may be imminent is the appearance of pulsatile LH release during sleep. At the end of puberty, a difference between sleep and wake LH secretory patterns is not seen.[11] Growth hormone (GH) stimulates FSH-induced differentiation of granulosa cells, increases ovarian levels of IGF-1, and amplifies the ovarian response to gonadotropins. The puberty of patients with isolated GH deficiency is frequently delayed, Leydig cell function is diminished, and the response to chorionic gonadotropins decreases. GH administration can restore testicular responsiveness to LH and Leydig cell steroidogenesis. Serum prolactin concentration increases during female puberty but remains relatively stable throughout male puberty. Insulin is essential for normal growth, and levels rise noticeably during puberty, with a strong positive correlation with IGF-1. Related TestingThe first-line assessment for any child experiencing issues with pubertal development is a thorough history and physical exam. The history will allow the healthcare practitioner to gain insight into any possibility of a genetic cause and will provide vital information about the child’s growth pattern and development to date. It may also give clues to other causes of pubertal disorders such as poor nutrition, underlying disease, excessive exercise, or exogenous steroids. The physical exam should include examining the genitalia and the breasts in girls to determine Tanner staging. Tanner staging is a standard system used to categorize the different stages of pubertal development a child has achieved. For boys, Tanner staging includes testicular and penile growth, pubic hair distribution, and linear growth. In girls, Tanner staging includes breast development, pubic hair distribution, and linear growth. In addition to Tanner categorizations, examining the optic fundus and determining if the sense of smell is intact can be helpful. Standardized growth charts tracking the child’s growth over time are also useful in determining if a child is developing appropriately.[12] Skin lesions noted on the physical exam can also point toward specific causes of abnormal puberty, such as McCune-Albright Syndrome. An X-ray of the left wrist is commonly used to determine bone age and whether the child’s bone maturation is more advanced than their age, suggesting they may be going through premature puberty. In addition to an x-ray of the left wrist, central nervous system (CNS) imaging may be performed if there are signs of CNS involvement. Measurement of hormone levels may also be helpful in the presence of abnormal puberty. Levels of estradiol, testosterone, FSH, and LH can be measured by checking for the presence of pubertal or prepubertal levels. A GnRH stimulation test is also helpful to determine a central or peripheral cause. This test involves administering 100 micrograms of GnRH after overnight fasting and observing FSH, LH, estradiol, and testosterone levels at 15, 30, 45, and 60 minutes post-injection. The stimulation test will cause activation of the hypothalamic-pituitary-gonadal axis in central causes resulting in increased levels of the hormones; a peripheral cause will not increase hormone levels.[13] Additional testing may include thyroid hormone levels (TSH, T3, T4), blood glucose levels, a complete blood count, liver enzymes, and an erythrocyte sedimentation rate. A karyotype analysis may also be performed, which will show the patient’s chromosomal pattern and helps determine if there is a genetic cause, such as Turner syndrome or Klinefelter syndrome. Although the clinician may evaluate many other factors after a history and physical, the testing should be tailored individually for each child’s presentation and the most likely cause of their abnormal puberty. PathophysiologyThe pathophysiology of puberty can be broken down into three main categories: premature (precocious) puberty, delayed puberty, and contrasexual development. Precocious Puberty Precocious puberty, or early development of secondary sexual characteristics, is defined as the appearance of secondary sexual characteristics prior to the age of eight in girls or before the age of nine in boys. Precocious puberty can be broken down by pathological location into central or peripheral precocious puberty. Central precocious puberty (CPP) involves activation of the hypothalamic-pituitary-gonadal (HPG) axis, which leads to early but normal pubertal development. CPP is more common in girls, and while most cases are idiopathic, it can be caused by neoplasm, radiation, head trauma, or genetic conditions.[14] Peripheral precocious puberty (PPP) results from an increase in sex steroids that does not come from activation of the HPG axis. Findings in PPP patients typically include a rapid and atypically sequenced pubertal progression. The most notable causes of PPP include McCune-Albright syndrome and testotoxicosis.[15] Many causes of early pubertal development are shared among girls and boys; however, some causes of early puberty are unique to each of the sexes.[16] The causes of precocious puberty shared by either gender include benign premature adrenarche, central nervous system (CNS) and pituitary lesions, constitutional and idiopathic precocious puberty, McCune-Albright syndrome, and exogenous sex hormones.
Causes of premature puberty unique to males include gonadotropin-secreting tumors and testotoxicosis.
Delayed Puberty Delayed puberty is the lack of physical evidence of puberty by 2 to 2.5 standard deviations above the mean age for the initiation of puberty. In boys, this is considered a period longer than four years between the first signs of testicular enlargement and the end of puberty or the absence of testicular growth by 14 years old. Delayed puberty in girls is considered the absence of breast growth by 13 years of age or more than four years between thelarche and menarche. The causes of delayed puberty include hypogonadotropic hypogonadism, hypergonadotropic hypogonadism, hypopituitarism, chromosomal abnormalities, and hypothalamic dysfunction due to secondary causes.[19]
Contrasexual Development Contrasexual development occurs when male or female children develop physical features of the opposite gender. This condition tends to be more common in girls and is commonly caused by polycystic ovaries and increased responses by the adrenal gland. Girls will have a male-like distribution of hair and may develop hirsutism. Girls can also develop clitoromegaly and lose the contour of the breast mass. Possible causes include Cushing syndrome, acromegaly, exogenous androgens, adrenal tumors, ovarian tumors, and hyperprolactinemia. Although contrasexual development is less common in boys, the cause is typically estrogen-secreting tumors when it does occur.[13] Clinical SignificancePuberty is a highly significant process and a part of all children’s development into functional adults. During this time, children begin to gain the capacity for reproduction, which is essential to discuss with children as they progress through puberty. Discussion of safe sexual practices is an important aspect of well-child visits and is pertinent to identifying children with unsafe or high-risk sexual encounters. The discussion of sexuality by pediatricians or other medical caregivers with young teens as they progress into adulthood provides a chance for them to speak to someone under confidentiality and ask specific questions to understand better their sexuality as well as what is considered safe sexual practices.[21] Puberty also coincides with a child’s psychosocial development. Children who may be early or behind in attaining puberty milestones, when compared to their peers, are at a much higher risk of emotional distress and low self-esteem. The ability to monitor the progression of puberty in the pediatric population is vital, as it is essential to their reproductive development and because of the many physical and psychological risks children face during this time in their development. Review QuestionsFiguretanner staging. Created by Logen Breehl utilizing articles referenced in physiology of puberty article References1.Lazala C, Saenger P. Pubertal gynecomastia. J Pediatr Endocrinol Metab. 2002 May;15(5):553-60. [PubMed: 12014513] 2.Skorupskaite K, George JT, Anderson RA. The kisspeptin-GnRH pathway in human reproductive health and disease. Hum Reprod Update. 2014 Jul-Aug;20(4):485-500. [PMC free article: PMC4063702] [PubMed: 24615662] 3.Styne DM. Physiology of puberty. Horm Res. 1994;41 Suppl 2:3-6. [PubMed: 8088700] 4.Rosenfield RL, Lipton RB, Drum ML. Thelarche, pubarche, and menarche attainment in children with normal and elevated body mass index. Pediatrics. 2009 Jan;123(1):84-8. [PubMed: 19117864] 5.Tinggaard J, Mieritz MG, Sørensen K, Mouritsen A, Hagen CP, Aksglaede L, Wohlfahrt-Veje C, Juul A. The physiology and timing of male puberty. Curr Opin Endocrinol Diabetes Obes. 2012 Jun;19(3):197-203. [PubMed: 22499221] 6.Ohta H. [Growth spurts of the bone from infancy to puberty.]. Clin Calcium. 2019;29(1):9-17. [PubMed: 30590354] 7.Busch AS, Hollis B, Day FR, Sørensen K, Aksglaede L, Perry JRB, Ong KK, Juul A, Hagen CP. Voice break in boys-temporal relations with other pubertal milestones and likely causal effects of BMI. Hum Reprod. 2019 Aug 01;34(8):1514-1522. [PMC free article: PMC6688887] [PubMed: 31348498] 8.Auchus RJ, Rainey WE. Adrenarche - physiology, biochemistry and human disease. Clin Endocrinol (Oxf). 2004 Mar;60(3):288-96. [PubMed: 15008992] 9.Arain M, Haque M, Johal L, Mathur P, Nel W, Rais A, Sandhu R, Sharma S. Maturation of the adolescent brain. Neuropsychiatr Dis Treat. 2013;9:449-61. [PMC free article: PMC3621648] [PubMed: 23579318] 10.Whitlock KE, Illing N, Brideau NJ, Smith KM, Twomey S. Development of GnRH cells: Setting the stage for puberty. Mol Cell Endocrinol. 2006 Jul 25;254-255:39-50. [PubMed: 16777316] 11.Wennink JM, Delemarre-van de Waal HA, Schoemaker R, Schoemaker H, Schoemaker J. Luteinizing hormone and follicle stimulating hormone secretion patterns in boys throughout puberty measured using highly sensitive immunoradiometric assays. Clin Endocrinol (Oxf). 1989 Nov;31(5):551-64. [PubMed: 2516786] 12.Klein DA, Emerick JE, Sylvester JE, Vogt KS. Disorders of Puberty: An Approach to Diagnosis and Management. Am Fam Physician. 2017 Nov 01;96(9):590-599. [PubMed: 29094880] 13.Blondell RD, Foster MB, Dave KC. Disorders of puberty. Am Fam Physician. 1999 Jul;60(1):209-18, 223-4. [PubMed: 10414639] 14.Chen M, Eugster EA. Central Precocious Puberty: Update on Diagnosis and Treatment. Paediatr Drugs. 2015 Aug;17(4):273-81. [PMC free article: PMC5870137] [PubMed: 25911294] 15.Soriano Guillén L, Argente J. [Peripheral precocious puberty: clinical, diagnostic and therapeutical principles]. An Pediatr (Barc). 2012 Apr;76(4):229.e1-10. [PubMed: 22119235] 16.Carel JC, Léger J. Clinical practice. Precocious puberty. N Engl J Med. 2008 May 29;358(22):2366-77. [PubMed: 18509122] 17.Dumitrescu CE, Collins MT. McCune-Albright syndrome. Orphanet J Rare Dis. 2008 May 19;3:12. [PMC free article: PMC2459161] [PubMed: 18489744] 18.Daussac A, Barat P, Servant N, Yacoub M, Missonier S, Lavran F, Gaspari L, Sultan C, Paris F. Testotoxicosis without Testicular Mass: Revealed by Peripheral Precocious Puberty and Confirmed by Somatic LHCGR Gene Mutation. Endocr Res. 2020 Feb;45(1):32-40. [PubMed: 31394950] 19.Dye AM, Nelson GB, Diaz-Thomas A. Delayed Puberty. Pediatr Ann. 2018 Jan 01;47(1):e16-e22. [PubMed: 29323692] 20.Soliman AT, De Sanctis V. An approach to constitutional delay of growth and puberty. Indian J Endocrinol Metab. 2012 Sep;16(5):698-705. [PMC free article: PMC3475892] [PubMed: 23087852] 21.Breuner CC, Mattson G., COMMITTEE ON ADOLESCENCE. COMMITTEE ON PSYCHOSOCIAL ASPECTS OF CHILD AND FAMILY HEALTH. Sexuality Education for Children and Adolescents. Pediatrics. 2016 Aug;138(2) [PubMed: 27432844] What are the common changes in both males and females in puberty?Puberty is associated with emotional and hormonal changes, as well as physical changes such as breast development in females (thelarche), pubic hair development (pubarche), genital changes in males, voice changes, an increase in height, and the onset of menstruation (menarche).
What are the common changes that occur in both male and female during puberty class 10?Sudden increase in height.. Change in body shape.. Change in voice. ... . Increased activity of sweat and sebaceous glands.. Reproductive organs begin to mature.. Appearance of secondary sexual characteristics.. |