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Antler Growth and Physiology

Murray  Woodbury DVM, MSc.

Specialized Livestock Research and Development Program
Department of Large Animal Clinical Sciences
Western College of Veterinary Medicine
University of Saskatchewn
Saskatoon, Saskatchewan    S7N 5B4

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Prior to a discussion on the development and physiology of antlers it is useful to make a few distinctions and provide some definitions that may clarify the subject.

This presentation and discussion is largely concerned with antler growth in wapiti, red deer and white-tailed deer. There are sometimes differences in physiology, form, and function in other species and this article will not be all inclusive.

Strictly speaking, the term "velvet" refers to the skin covering a growing antler. It describes the fuzzy texture provided by many fine hairs growing on the surface. "Velvet antler" refers to the entire antler when it is in the growth phase. At this stage it is soft and lacks the mineralized characteristics of "hard antler" which is nothing less than bone. Frequently "velvet" and "velvet antler" are used interchangeably to refer to the antler in its growth phase. It is at this stage that the entire antler is harvested for drying and use in pharmaceutical preparations. The finished antler product is therefore often referred to as "velvet antler".

The antler pedicle is an area on the frontal bone that generates antler. It is a permanent feature of the skull and remains after the antler is cast off. It is the perennial source of the regenerating antler. In the following discussion one must make the distinction between the pedicle and the antler. They have some differences in physiology and anatomy.

Somewhat artificial distinctions can be drawn between the control mechanisms for the growth of the antler tissue and the mechanisms responsible for timing the annual cycle of antler development and loss. Hormonal control of these events can become confusing unless it is clear what specific process is influenced; a growth process vs a cycle event.


Pedicle Development

Antler pedicles develop in the fetus from osteogenic centres on the frontal bone area. They were once thought to be derived from the periosteum of the frontal bone but research shows the existence of a separate center that fuses with the frontal bone in the developing fetus, becoming structurally identical to the frontal bone. The pedicles may or may not be palpable at birth, but become evident at approximately 6 months of age.

Removal of the pedicle from the frontal bone results in the absence of antler formation. Damage to the pedicle causes abnormal antler growth and depending on the extent of damage this effect may be permanent, producing an abnormal antler in all subsequent antler cycles. Transplanting the antlerogenic area to another region of the body results in growth of antler tissue in the transplanted area. For example, experimental relocation of pedicle tissue to the tibia of an animal resulted in muted, abnormal antler tissue growth on, or from the tibia.

Testosterone stimulation is required for pedicle initiation and growth. Early post natal castration prevents pedicle initiation and growth. Testosterone supplementation to these early castrates recommences growth and stimulates pedicle development in both sexes. It is thought that testosterone is needed to initiate and maintain the changes in ossification occurring in late pedicle growth. In general, the pedicle grows by intramembranous ossification and the antler grows by the process of endochondral ossification. Intramembranous ossification occurs when new bone is directly laid down by bone forming cells. Endochondral ossification occurs when existing cartilage is remodeled and mineralized into bone. Internally, the inexact point where the ossification type changes becomes the antler-pedicle junction. Externally, there is a change in skin and hair type to that of the typical "velvet" of the antler.

In the first year of growth the antlers differentiate from the pedicle to form "spike" antlers (hence the name "spikers" given to yearling males). These first antlers mature, clean, and are shed according to the annual antler cycle and a new pair of antlers is regenerated from the pedicles every year thereafter.

Antler Growth and Calcification

After casting of the old antlers, the skin of the pedicle grows over and heals the wound left by the discarded antler. The mesodermal cells, derived from the skin or the pedicle or both, multiply and differentiate to make antler tissue. Hyperplastic fibroblasts deposit collagen at the point of growth of the antler, forming a well vascularized and innervated mass on the pedicle. This growth continues in the outermost layers of the tip and differentiation of cells into chondroblasts and chondrocytes associated with the formation of cartilage begins in the portions closest to the antler base. Growth is very rapid; a wapiti antler is capable of growing more than 2 cm in a 24 hour period. Subsequently the antler continues to enlarge by the differentiation process at the tip and by elaboration of fibrocartilage underneath those portions.

The process of ossification occurs through modified endochondral ossification. It is endochondral ossification because bone formation will be accomplished through the changing of cartilage into bone rather than the de novo creation of bone by osteocytes. It is termed "modified" for 2 reasons. Firstly, unlike other cartilage, antler cartilage is heavily vascularized. There is a very extensive capillary network throughout the growing antler. Farther from the tips of the antler this network becomes sinusoidal, draining the antler through the middle rather than at the periphery. Secondly, cartilage becomes bone not by osteoclastic resorption and subsequent bone formation, but by becoming directly converted to bony tissue by the deposition of mineralized material within the cartilaginous matrix. The chondrocytes at this point become hypertrophic and exhibit alkaline phosphatase activity leading to the formation of trabeculae and the spongy reticulum characteristic of the interior of antler.

The reticulum is then strengthened by osteoblastic activity laying down bone on the surfaces of the trabeculae. (intramembranous ossification) This activity eventually leads to the hardening of the entire mature antler. The calcification and ossification process proceeds up the antler from the base to the tip. The thickening of the trabeculae and narrowing of the sinusoidal blood channels eventually result in the death of the bone and the typical hard antler.

Mineral Requirements

Mineral requirements for antler growth exceeds those for skeletal growth. Wapiti antlers grow at approximately 100gm/day, while skeletal growth occurs at about 34 gm/day. Mineral for antler calcification is partly satisfied by bone resorption. At times of peak demand skeletal bone is less dense. The ribs likely contribute the most mineral and the loss from these bones has been termed "physiological osteoporosis". There is little doubt that the diet provides the greater portion of calcium and phosphorous for antler growth and mineralization. However, supplementation of these elements beyond optimal levels does not increase antler growth beyond genetic potential in farmed wapiti or deer.

Velvet Shedding

Coincidental to advanced antler calcification the skin covering the antler begins to die. The exact mechanism of velvet shedding is poorly understood but there is no doubt that vascular changes initiate the process. Velvet shedding occurs at the same time as testosterone levels are rising and administration of exogenous testosterone will cause premature shedding of antler velvet. Testosterone may cause constriction of antler arteries which have a thick muscular layer, or there may be interference in tissue metabolism by testosterone, resulting in tissue necrosis and the biochemical events leading to arterial constriction.

Antler Casting

The base of the antler consists of compact bone that appears to be continuous with pedicle bone. The union is certainly secure enough to withstand the forces of gravity and impact from fighting. Microscopically, the junction is characterized by irregularly interwoven Haversian canals and bone spicules (typical bone architecture). The line of future separation called the abscission line is indicated by a narrow transverse band of minute blood vessels. Osteoclastic activity across this abscission line between the dead bone of the antler and the living bone of the pedicle is responsible for the separation of antler from the pedicle.

Osteoclasts and associated lacunae (cavities containing an osteoclast) begin to appear first at the circumference of the antler-pedicle junction. With time these are found at progressively deeper locations and within 2 weeks have spread centripetally into the center of the junction. At the same time, the Haversian canals have become wider and are lined with osteoclasts. These widening vascular channels are filled with connective tissue, which in the precasting stage forms a mesodermal pad approximately 1mm thick. Later, a circumferential cleft is formed under the antler burr, and connective tissue from the surrounding pedicle skin invades the space between the antler and pedicle. Eventually enough bone is removed from the junction that the antler separates from the pedicle. There are some behavioural indications that pain is associated with this separation. After casting the ingrowing skin-derived tissue fuses with the mesodermal tissue from the vascular channels of the pedicle to give rise to a developing antler bud under the scab covering the pedicle.

Blood Supply and Innervation

Knowledge of the vascular and nervous anatomy of the antler is important to the procedures for regional anesthesia needed for antler removal. Delivery of the local anesthetic to the correct blocking site is desirable for humane reasons. Injection of anesthetic solution into the vascular system is to be avoided.

Blood supply to the pedicles is from internal vascular supply to the frontal bones. The velvet antler is supplied by branches of the superficial temporal artery. Below the pedicle the superficial temporal artery branches into the lateral and medial coronal arteries whose branches then ascend the antler in the vascular layer of the velvet. A large vein accompanies the lateral and a smaller vein accompanies the medial arterial supply and these eventuate into the superficial temporal vein.

The nerve supply to the antlers is supplied mainly by the infratrochlear and zygomaticotemporal branches of the ophthalmic division of the trigeminal nerve. In approximately 25% of red deer, wapiti and fallow deer the small dorsal branch of the auriculopalpebral branch of the facial nerve reaches far enough dorsally to supply sensation to the pedicle and antler. It is this nerve that is frequently responsible for the failure of total regional block when the specific nerve block method is used for local anesthesia.

Historically, there was a general assumption that hard antler lacked innervation and that polished antlers were in fact dead tissue. Recent microscopic studies showed that there are living cells within the calcified antler which are nourished though an elaborate system of canals transporting fluids through the antler. The same studies demonstrated the existence of microscopic nerves inside hard antler.


Because of the economic worth of antlers, there has been much speculation and study on the subject of antler growth and methods for improving the amount of antler available for harvest. The influence of genetics and of diet have received attention in past research. In general terms, it has been shown that antler size is a heritable trait and that stag selection for animals with large antlers is important in breeding programs to improve herd performance for antler yield.

The effect of diet on antler size continues to be a controversial subject with commercial producers. The role of metabolic energy content and protein content in diets fed to stags, and the timing of their supplementation is often debated. The addition of calcium and phosphorous with other trace elements is included in the argument. Most deer scientists now agree that addition of nutrients beyond the optimum needed for growth cannot offer results that are beyond the genetic potential of the individual stag. It remains important to supply the animal with those nutritional factors that will allow expression of this genetic potential.

Recently, research has focused more closely on the precise mechanisms of growth regulation and physiological control of antler formation. Early observational studies indicated that neuroendocrine pathways could be major control factors in antler growth. It was hypothesized that the central nervous system had "antler growth centers" that are responsible for the regulation of size, shape, and rate of antler growth. The peripheral innervation of the pedicle and antler would then be the mediator for central nervous system control of the growing antler. By sectioning the peripheral nerves serving the pedicle and antler and achieving nearly normal growth, researchers demonstrated that innervation is not necessary for antler growth. It was established that although growth was stunted somewhat by denervation, rather normal antler was formed. Mechanisms other than CNS control are responsible for initiating pedicle growth in neonates and for regulating the growth of mature antlers.

Hormonal control seems to be a more likely mechanism for growth control. Early studies on hormone levels were able to correlate the rise and fall of serum levels of various hormones with stages in the growth cycle. It seems reasonable that at least a few of these were implicated in the regulation of antler growth.

Prolactin, Thyroid hormone, and Testosterone

At various times a variety of hormones including prolactin, LH, and growth hormone have been considered as antler stimulating hormones. However, none of these have direct cartilage growth promoting activity and in view of the fact that the developing antler is composed of cartilage, it is unlikely that they are primary antler stimulating hormones.

The innovations of receptor site physiology have given researchers the ability to differentiate hormonal activity directed at the antlers from that which influences mainly other organs. For example, the absence of receptor sites for some hormones like prolactin and the abundance of sites for others such as IGF1 is evidence for the relative importance of individual hormones to antler growth.

The fact that plasma levels of testosterone are low during velvet antler growth indicates that testosterone exerts no direct velvet antler growth stimulation. In addition, receptor site research has found few receptors for testosterone in the growing antler. There are however testosterone receptors in the pedicle which leaves room for this hormone to exert some influence over the events of the antler cycle. Receptor sites for testosterone have been demonstrated in the fetal and neonatal pedicle which supports the idea that testosterone is needed to initiate pedicle growth, but not for antler growth.

Insulin-like Growth Factor (IGF1) and Growth Hormone

Growth hormone and insulin-like growth factor one (IGF1) appear to be two factors involved in antler growth. Plasma growth hormone fluctuates seasonally with the greatest amplitude in spring at the time of antler growth. IGF1 plasma levels are also seasonal with highest levels in mid spring and early summer.

Growth hormone from the pituitary is known to cause the release of IGF1 from peripheral tissues such as the liver. Studies of receptor binding in antler have shown the cartilage at the growing tip to be high in receptor sites for IGF1 but not to growth hormone. Since the serum levels for both of these hormones is increased at the time of antler growth it can be hypothesized that the increase in growth hormone during this period causes the production of IGF1 and that the IGF1 exerts influence on the antler tissue after being bound to specific binding sites. Thus current knowledge would suggest that antler growth is under the indirect control of growth hormone through IGF1.

To definitively state that IGF1 stimulates growth, investigators needed to demonstrate this effect on antler tissue. Tissue culture techniques allowed New Zealand researchers to show that there was a dose related increase in growth of antler cells due to the presence of IGF1.

There is much more to be learned about the control of antler growth in general and more specifically about those local factors influencing the differentiation and growth of cellular components of antler. Nerve growth factor, and epidermal growth factor are two examples of as yet uncharacterized compounds that influence the development of specific antler components. Their role in determining overall antler growth is not understood.


Antler growth cycles are closely related to sexual cycles in stags and are directly attributable to variations in seasonal photoperiod influencing gonadal stereogenic activity. The seasonal onset of reproductive activity (rut) in stags is associated with rising circulating levels of gonadotrophins and consequently testosterone secretion.

Photoperiod and Melatonin

Experimental evidence points to the pineal gland and its response to light as being the modulator of those mechanisms responsible for gonadotrophic control and hormonal control of the antler cycle and the male and female reproductive cycle. When the duration of daylight reaches a peak and the length of darkness is least the pineal gland responds by elaborating very little melatonin. As day length decreases and the period of darkness increases the pineal gland responds by secreting increasing levels of melatonin. Melatonin production is greatest when day length is decreasing to the lowest annual levels.


Rising levels of melatonin act on the pulse generator of the hypothalamus causing the pulsatile production and release of gonadotrophin releasing hormone (GnRH). The appropriate frequency and amplitude of the GnRH pulses causes the pituitary to produce and secrete gonadotrophins. ie. luteinizing hormone(LH) and follicle stimulating hormone(FSH) These hormones regulate the testicular output of testosterone which is thought to ultimately control the timing of the antler cycle along with the male reproductive cycle.


As day length decreases, testosterone secretion increases in response to rising LH levels and reaches a peak immediately prior to the rut. Thereafter, levels begin to decline until spring when a rapid decline in circulating testosterone is associated with antler casting. While testosterone levels remain low new antlers begin to grow. When antler growth nears completion the testosterone levels are once more rising. High levels of testosterone are associated with hardening and cleaning of the antler, coinciding nicely with the behavioral need for antlers during the rut.

The immediate effects of castration depend on the stage of the antler cycle. Castration while in velvet results in the permanent retention of the velvet. Castration while in hard antler results in immediate casting and replacement of the antler by velvet antler which will remain soft the following cycle. In some species of deer castration can result in "peruke antlers" which are almost neoplastic abnormal antler tissue, resembling the peruke wigs of old English aristocracy. Therefore, the lack of testosterone prevents hardening and cleaning of immature antler and prevents retention of hard antler.

In an entire male, testosterone administration during the velvet phase results in calcification and cleaning of the antler. Administration during the hard antler phase results in retention of the antler. Therefore high concentrations of testosterone promote calcification and velvet shedding as well as prevent casting of hard antler. Sustained high concentrations of testosterone also prevent the growth of new antlers.


The composition of hard antler is similar to bone. It contains approx. 25% calcium and 19% phosphorous by weight. Organic matter makes up 39% of the antler by weight and water content is 8%.

As one might expect, the composition of velvet antler depends on the stage of growth. Growing antler contains a complex variety of hormones, growth factors, minerals and compounds. To complicate things further, the relative amounts of the constituents also vary according to what part of the antler is analyzed. For example, the selenium levels in the growing tip of the antler are 5 to 10 times that which are found elsewhere in the antler.

In general, those portions closer to the tip of the antler have a higher relative content of lipid fraction. Those portions farther from the tip have higher ash content. The converse relationships are also true. Further, as the antler matures and the antler weight increases the relative amount of ash increases and the relative amount of lipid decreases. The relative content of calcium and phosphorous increases over time and the relative amounts of selenium, sodium, potassium, and sulphur decrease.

New Zealand research into the characteristics of antler quality have led to the identification of gangliosides and free amino acid content as being indicators of biological activity and therefore quality. Gangliosides are animal glycosphingolipids occurring mainly in the central nervous system but also distributed in other tissues. The gangliosides referred to by Korean researchers have turned out to be sphingomyelins (Sm), which are phospholipids. These sphingomyelins are believed to be biologically active and therefore important for antler quality. Free amino acids (FAA) are the basic building blocks from which proteins are made. They are essential nutrients for cell growth and because they are found in high concentrations in rapidly growing tissue, are in abundance in velvet antler. A number of amino acids are "essential" amino acids in the sense that they cannot be synthesized from other dietary material in the diet and must be provided as is for optimal growth of animals. Velvet antler, as a dietary supplement, might be expected to provide high levels of essential amino acids.

Studies have shown that there is a significant decrease in sphingomyelin content from the tip of the antler to the base. The distribution of free amino acids in the antler has a similar pattern when expressed as total FAA, but individual amino acids did not necessarily follow this gradient from tip to base. There is a strong linear relationship between total Sm level and total FAA level within the antler regardless of the distribution of these compounds in the antler.

New Zealand research has also examined the biological effectiveness of various antler extracts. Researchers have developed both aqueous and organic extractions of velvet antler, and not surprisingly have shown that the yield of extractable substances is higher in the tips compared with the bases.

Organic extracts from antlers have been tested in an antitumour assay. Samples of extract were incubated for 72 hours with P388 murine leukemia cells. The concentration of sample needed to reduce the P388 cell growth by 50% as compared with controls is determined. The result is expressed as an IC50 in µg of extract/ml of solvent. The demonstration of various levels of antineoplastic activity in various extract sources is less important to our discussion than the fact that there is indeed antineoplastic active substances in velvet antler.

The aqueous extracts have been evaluated for biological effectiveness by measuring their effects on growth of antler cells in tissue culture. The results show that there are potent stimulators of cell division in aqueous antler extracts. It was also shown that there is considerable variation in mitogenicity of extract from antler to antler and also the portion of antler sampled.

In the future, determination of antler quality and economic value, will place more reliance on the content of the antler expressed in terms of biologically active substances than on the traditional assessment of weight, size, shape and color.


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