Antler biology

Cell types

The growing tip of the antler is composed of various types of cells (mesenchymal, pre-chondroblasts and chondroblasts) and is covered by a layer of tissue (comprising epidermis and dermis). The lower (non-growing) regions of the growing antler are composed of further types of cells again (chondroblasts and osteoblasts), as shown in the following diagram.

Antler composition

Mature antler is similar to compact skeletal bone in composition, being 25% calcium and 19% phosphorus. Organic matter contributes 39% to antler weight and water content is 8%.  

Antler has greater tensile strength but less elasticity than the human tibia. Its resistance to impact is greater than ivory. It is able to absorb a considerable amount of energy under impact before breaking.

Blood supply

Blood supply to the pedicles is from internal vascular supply to the frontal bones, from branches of the superficial temporal arteries. Below the pedicle, the superficial temporal arteries give rise to large lateral coronal arteries and smaller medial coronal artiers which ascend the antler in the vascular layer of the velvet to supply blood to the velvet and bone. Deoxygenated venal blood is returned through the antler core. One large vein accompanies the lateral arterial arteries and one smaller vein accompanies the medial arteries, both of which eventually join the superficial temporal vein. Blood supply diminishes as calcification progresses.

Innervation

Innervation to the antler is by the trigeminal nerve by way of supraorbital temporal branches, which are close to the lateral and medial coronal arteries. The posterior border of the pedicle is also supplied by sensory branches of the first cervical nerves. Upon casting, the nerves degenerate back to the pedicle and regenerate upon antler re-generation.

Overview of phases of growth cycle

Each year, antlers drop off and fully regenerate in a growth cycles.  

Each antler growth cycle includes:

• initiation
• rapid growth (velvet phase)
• mineralisation
• velvet shedding
• antler casting

Various factors control the different phases.

Control of antler growth

Being male secondary sexual characters, both pedicle formation and the subsequent antler growth cycle is under the control of testosterone. Testosterone levels at the various stages of the growth cycle are shown in the following table.  

The factor responsible for stimulating antler growth is insulin-like growth factor 1 ('IGF1'). The timing of the peak of IGF1 production is regulated by day length but the key factor influencing the amount of IGF1 production is nutrition. Good nutrition is therefore required to grow big antlers to the animal's full genetic potential. For more on the role of nutrition, see the section on quality >>

Pedicles

Antlers do not grow directly from deer skulls. Instead, they emanate from the top of permanent bumps on the head called pedicles, which begin development in the foetus. The pedicle develops from the periosteum of the frontal bone and has the same structure as that bone. The pedicle increases its diameter throughout the stag's life, by annual deposition of a ring of bone. If the pedicle is removed, antlers can no longer develop. Pedicle development is chemically controlled by steroids.  

Initiation

The pedicles start to grow out of the head when the deer approaches puberty (usually around 5-7 months of age) although growth can be retarded by sub-optimal health and nutrition. Precise timing of initiation is highly correlated with body weight which itself is related to nutrition. When pedicles reach a specific height for the species in question (5-6cm in red deer), a shiny skin develops on the top. This marks the transformation of pedicle to first antler. The tissue at this stage is no longer scalp-like but is in velvet-like form.  

Rapid growth

After transformation from pedicle to antler, the antler enters a rapid growth phase. The first antler usually forms a long, single tapering beam, called a spike, hence a yearling stag is typically referred to as a 'spiker'. However often multi-spikes are observed. The typical pattern of growth of the pedicle and first antler is shown in the figure below.

Mineralisation

The spike becomes fully calcified bone as the rutting season and full puberty approaches. Calcification, or 'mineralisation' completely shuts down the supply of nutrients to the antlers.

Velvet shedding

On account of the lack of mineral supply to the calcified antler, velvet is shedded from the antler, to expose bare, calcified antler bones.

Antler casting

The first hard antlers are cast in the following spring. The clean, hard antler is essentially a dead bone attached to living bone (the pedicle) and so its casting from the stag is not surprising. The main thing that affects the timing of antler casting is changes in day length but nutrition has some effect. After casting of first antlers, development of subsequent antlers enters a well-defined cycle.

Regeneration

When testosterone levels are extremely low, the new antler re-generates out of scar tissue from the previous antler casting, unlike the first antlers which generate from normal skin tissue. Mesodermal cells of the scar tissue over the pedicle differentiate to produce the growing antler tissue. The antler tissue is laid down, and the points of growth duly advance so as to always be present at the tips of the antler. Skin covers the growing antler, from which hairs protrude, giving a velvet-like appearance. Antler during this stage is thus referred to as 'velvet'. Between the skin and the growing cells of the antler is a later of connective tissue. This layer has a blood supply. 

Growth

It is well known that there is a general relationship between antler size and body size in that larger deer have larger antlers. The entire growth phase is 120 days commencing from new antler re-generation. Some growth occurs during the mineralisation phase as, prior to the antler becoming fully calcified, some nutrients continue to be supplied. Growth rates of up to 3cm per day have been recorded at the peak of the rapid growth phase. While the rate of antler growth is affected by nutrition, the actual causative mechanism is not known. However, it seems likely that the influence of nutrition is mediated by hormones.  

Whereas skeletal bones of red deer grow at 34g/day during the first 18 months, their antlers may grow at 100g/day. Minerals obtained from the diet such as calcium and phosphorus are likely to be the key source of antler material, and both feral and farmed deer have been observed chewing shed antler and bones during antler development.

Calcification

Calcification occurs during and after the rapid growth phase. However, it does not usually commence until 55-60 days after growth has commenced. Since the deer antler velvet will not grow any larger without compromise of its full nutrient supply, velvetting for oriental medicinal purposes which seek optimum nutrient levels typically takes place 55-65 days after casting. Calcification is complete by February to March in time for the rut.

The process of calcification involves osteoblasts being converted into osteocytes. Bony 'trabeculae' are formed by the deposition of calcium salts onto a matrix laid down by the osteocytes. These trabeculae become surrounded by more osteocytes and increase in size. The antler structure has a dense trabecular bony centre containing small amounts of non-haemopoietic marrow surrounded by very strong peripheral compact bone. 
Upon completion of calcification, the velvet begins to die and assumes a shrivelled appearance.  It is triggered by rising testosterone levels.

The mature antler is fixed to the pedicle strongly, to allow carriage of the antlers by the pedicle and to withstand the impacts of fighting. The junction of the antler to the pedicle consists of compact bone without a spongy core.  There are few blood vessels in this area.  

Casting

Just before casting, the strong junction between the pedicle and calcified antler is eroded on account of increasing osteoclastic activity and vascularisation. Physical assistance by the stag rubbing against objects, combined with erosion of the junction brings about casting. Blood loss is observed and scar tissue forms at the site.