Group 6
Members: Jasmine, Amanda, Nathan
e-Facilitator: Cathy


Learning Outcomes
  • Identify and locate the endocrine gland which secretes the Growth Hormone (GH)
  • Discuss normal GH physiology over the lifespan
  • Describe homeostatic imbalances that are caused by hyper or hyposecretion of GH
  • Highlight the effects seen in your elderly dental patients with the cessation of GH production and secretion


ENDOCRINE GLAND - GROWTH HORMONE (GH)
INTRODUCTION:
As part of the endocrine system the pituitary gland helps store, produce and secrete different types of hormones to various targets, when required by the body. Transportation occurs via the bloodstream to targets such as organs, tissues or cells. One of these hormones is Growth Hormone (GH) which is important in humans and animals, in stimulating cells, reproduction and the growth process (Hormone Foundation 2009).

What is Growth Hormone (GH)?
Growth Hormone (GH) is a 191 single chain - amino acid peptide. Hormones are classified as either amino acid or steroid based, with the majority of hormones, amino acids. Growth hormone's main function is to promote linear growth including height, bone length and muscle growth (Marieb & Hoehn 2007).

Where is it found?
The endocrine gland which secretes Growth Hormones (GH) is the pituitary gland (see Figure 1 showing the location within the head). The Pituitary gland is situated in the ‘Sella Turcica’ of the Sphenoid bone and releases a number of different hormones (at least 8) (See Table 1 & Figure 2) through its posterior and anterior lobes (Marieb & Hoehn 2007).

sella_turcica_position.jpg
Figure 2: Shows the sella turcica just below the pituitary http://www.pituitarysociety.org/public/overview
Pituitary_gland.gif
Figure 1: Location of the Pituitary gland where the Growth Hormone is secreted. http://www.pituitarysociety.org/public/overview





Table 1: Below showing the hormones secreted by both the anterior and posterior pituitary lobes of the pituitary gland.

Anterior Pituitary hormones
Posterior Pituitary hormones
Growth Hormone (GH)
Oxytocin
Thyroid-stimulating hormone (TSH)
Antidiuretic hormone (ADH) or vasopressin
Adrenocorticotropic hormone (ACTH)

Follicle-stimulating hormone (FSH)

Luteinizing hormone (LH)

Prolactin (PRL)

Source: (Hormone Foundation 2009 and Marieb & Hoehn 2007).


The ‘Posterior Pituitary Lobe’ is chiefly composed of ‘Pituicytes’ (supporting cells) and nerve fibres and releases nuerohormones, which are received from the hypothalamus. Therefore, the posterior lobe is not a true endocrine gland as it is essentially a hormone storage area. In contrast, the ‘Anterior Pituitary Lobe,’ also known as the Adenohypophysis (See Figure 3), which creates and secretes a number of hormones, via cells known as Somatotrophs and, is consequently responsible for the production of GH (Marieb & Hoehn 2007).


Pituitary_gland_ant_&_post.gif
Figure 3: Showing the hormones produced by the anterior and posterior lobes of the Pituitary gland. http://www.pituitarysociety.org/public/overview


Although GH stimulates most cells in the body to increase in size and propagate, its primary structures of interest are the bones and skeletal muscles (Marieb & Hoehn 2007). Stimulation of the Epiphyseal plate results in the growth of long bones, while stimulation of skeletal muscles promotes an increase in muscle mass. Essentially, according to Marieb and Hoehn (2007), GH promotes protein synthesis and encourages the use of fats, rather than glucose, for energy. See Figure 4 for the stimulation through GH.

Effects of GH:
Growth hormone effects the tissues by causing an increase in protein synthesis, free fatty acid release and amino acid uptake (Greenspan & Gardner 2004). Most growth-promoting effects of GH are controlled by Somatomedins (insulin-like growth factors) which are proteins that are produced by the liver, skeletal muscle, bone and other tissues (Marieb & Hoehn 2007). In addition, these Somatomedins not only stimulate the uptake of amino acids from the blood stream to be integrated into cellular proteins throughout the body, but also stimulate the uptake of sulfur into the cartilage matrix (specifically through IGF-1). The absorbed sulfur acts to synthesise chondroitin sulfate, which consequently, provides an important structral component for cartilage as it allows for compression. Dietary supplements of this glycosaminoglycan are used to treat osteoarthritis (Arthritis Foundation, 2007). Acting directly, Growth Hormone also mobilises fats for transport to cells, which consequently increases the levels of fatty acids within the blood. GH also encourages the breakdown of glycogen in the liver, therefore also releasing glucose into the blood. Essentially, glucose uptake and metabolism is decreased, and as a result, the levels of glucose in the blood is dramatically increased. This elevation of the blood glucose level is called the 'diabetogenic effect' as it imitates the high blood glucose levels of diabetes mellitus. It also decreases the use of carbohydrate as its anti-insulin effects occur (Arthritis Foundation, 2007).

Figure 4: Stimulation through GH http://www.drugs.com/enc/images/images/en/15176.jpg
Figure 4: Stimulation through GH http://www.drugs.com/enc/images/images/en/15176.jpg

How is it regulated?
The secretion of GH is chiefly regulated by two antagonistic, hypothalmic hormones; Growth Hormone-Releasing Hormone (GHRH) which stimulates the release of GH, and Growth Hormone-Inhibiting Hormone (GHIH) (also known as somatostatin) which inhibits its production. GHIH is released because it wants to bring the body back to homeostasis. Therefore, its release is triggered by the feedback of GH and IGF levels. In addition, it should be noted that besides the inhibition of GH secretion, GHIH also blocks the release of thyroid stimulating hormones, and gastrointesinal and pancreatic secretions (Marieb & Hoehn, 2007).

Normal Growth Hormone physiology over the lifespan:
The secretion of growth hormone (GH) is influenced by sleep, exercise, stress (both physical and emotional), the ingestion of certain foods and light, with its rapid metabolism only allowing a short plasma half-life usually less than 60 minutes, with some variation (Kettyle & Arky, 1998). The GH secretions are released in a daily cycle at low levels, occurring throughout most of the day and peaking at short intervals. Secretions can also rise in states of starvation and can decrease considerably in obesity (Greenspan & Gardner, 2004) . GH levels are low in newborns and neonates and progressively rise during infancy and the pre-pubertal period (Harvey, Scanes & Daughaday,1995). Furthermore, these levels then peak during adolescence, but decline with age, being at their lowest in the elderly. Effectively, Growth Hormone levels rise in childhood as to enable normal growth and development during these years, and then peak during adolescence (Emedicine Health 2009). Finally, due to the increase in Somatostatin (GH inhibiting hormone), GH levels decline with age (Bowen 2003). It should also be noted that GH levels also rise in females during pregnancy (Emedicine Health 2009).

Homeostatic imbalances that are caused by hyper or hyposecretion of GH

Homeostatic imbalances of Growth Hormone (GH) can cause structural abnormalities including hyposecretion and hypersecretion. Hyposecretion is caused by non-secretory pituitary gland tumor which causes a deficiency in GH secreted and can result in pituitary dwarfism in children only, which is a slowed and long bone growth (Marieb & Hoehn 2007 and Hormone Foundation 2009). Their average maximum height is around 1.2 metres, but otherwise other body segments are within normal proportions. See Figure 5 for an image of dwarfism. Hyposecretion can also occur with radiation of a pituitary gland tumor or surgery.

dwarfism
Figure 5: Dwarfism, http://www.encyclopedia.com/topic/dwarfism.aspx
giantism
Figure 6: Gigantism, http://www.encyclopedia.com/topic/gigantism.aspx





Hypersecretion is caused by a secretory pituitary gland tumor, which produces growth hormone. It can result in gigantism in children because the GH produces excess and targets the epiphyseal plates prior to fusing, which results in rapid growth rate (Marieb & Hoehn 2007). Therefore the individual has increased linear growth that can often reach an abnormally tall height of 2.4 metres and once again like dwarfism the rest of the body proportions are usually normal (see Figure 5). These tumors can also make excess GH of the hormone that stimulates the thyroid gland, leading to an overproduction of thyroid hormones. In adults an excess can lead to 'acromegaly' which results after the epiphyseal plates have closed. Treatment to remove excess amounts of the GH tumor is surgical removal (Marieb & Hoehn, 2007).

See this link for more information on and an example of gigantism:
http://www.youtube.com/watch?v=Ebhf1qKVA9A&feature=related


4.) Effects with the cessation of GH production and secretion in elderly patients
With increasing age, growth hormone production and secretion tends to decrease. Thus in elderly dental patients some effects of the cessation of GH production and secretion include increased risks of;

- carbohydrate metabolism (producing hyperinsulinemia, glucose intolerance and diabetes mellitus)
- the cardiovascular system (producing hypertension, edema and congestive heart failure)
- the musculoskeletal system (producing arthritis and arthralgia) (Vance 1990).

For example a patient with diabetes would need to monitor blood sugar levels as there is great variability in changes in insulin sensitivity because of differences in body composition, age, and genetic predisposition. Patients with type II diabetes need special attention because growth hormone therapy hinders control of that disease until the patient looses excess abdominal fat (Vance 1990).

Affects on dental care for the elderly patients:
The impacts of cessation of GH can affect the dental care given to the elderly patient such as having increased medical conditions that would need to be considered, especially with cardiovascular medications that may have a direct effect on local anaesthetics that would be used (eg. anaesthetics containing adrenalin that has vasoconstricting actions which could cause strain on the heart) (Bird & Robinson 2002). For diabetic patients to cease GH, the considerations for dental care include; dehydration of soft tissues due to xerostoma including swollen, red and painful gingiva, alveolar bone loss, delayed healing, tooth aches and acetone breath (Bird & Robinson 2002). Operators must instruct diabetics to continue with maintaining a normal healthy diet before appointments. Also the musculoskeletal system (such as the condition arthritis) can have risks of periodontal disease including decreasing the bone remodeling process, therefore the alveolar bone healing processes would be affected aswell as the strength of the alveolar bone to keep the teeth stable, otherwise mobility can occur (Drake et al., 2003). Eventually may lead to loss of teeth due to the disease process. These factors can affect the dental care needed, to ensure the visit is care free for both the patient and the operator.

REFERENCES
Arthritis Foundation 2007, 'Glucosamine and Chondroitin Sulfate,' The Arthritis Foundation, viewed 28/09/09,
<http://ww2.arthritis.org/conditions/alttherapies/glucosamine.asp.>

Bird, DL & Robinson, DS 2002, Torres and Ehrlich modern dental assisting, 7th edn, Saunders, Elsevier, USA.

Bowen, R 2003, 'Growth hormone and ageing', viewed 14/10/09
<http://www.vivo.colostate.edu/hbooks/pathphys/endocrine/hypopit/ghaging.html>.

Drake, WM, Carroll, PV, Maher, KT, Metcalfe, KA, Camacho-Hubner, C, Shaw, NJ, Dunger, DB, Cheetham, TD, Savage, MO & Monson JP 2003, 'The effect of cessation of growth hormone (GH) therapy on bone mineral accretion in GH-deficient adolescents at the completion of linear growth', The Journal of Clinical Endocrinology & Metabolism, vol 88, no 4, pp. 1658-1663.

Drugs information online 2009, viewed 28/09/09
<http://www.drugs.com/enc/images/images/en/15176.jpg>


Emedicine Health 2009, 'Growth hormone deficiency in children', viewed 14/10/09,
<http://www.emedicinehealth.com/growth_hormone_deficiency_in_children/article_em.htm>.

Greenspan, F & Gardner, D 2004, Basic & clinical endocrinology, 7th edn, McGraw-Hill, USA.

Harvey, S, Scanes, C, Daughaday, W 1995, 'Growth hormone', viewed 14/10/09,
<http://books.google.com.au/books?id=qzl6CGYvrsUC&pg=PP273&lpg=PP273&dq

Hormone Foundation 2009, 'Pituitary disorders overview', The Hormone Foundation, Chevy Chase, MD, viewed 29/8/2009
<http://www.pituitarysociety.org/public/overview>

Kettyle, W & Arky, R 1998, Endocrine Pathophysi​ology, Lippincott-Raven, Philadelphia, PA.

Marieb, E & Hoehn, K 2007, Human anatomy & physiology, 7th edn, Pearson Education, San Francisco, CA.

Neal, JM 2000, Basic endocrinology, Blackwell Science, Muncie, Indiana.

Vance, ML 1990, 'Growth hormone for the elderly?', The New England Journal of Medicine, vol 323, pp.52-54.