The epidermis is the most superficial layer of the skin and provides the first barrier or protection against the invasion of foreign substances in the body. The main cell of the epidermis is called a keratinocyte. The epidermis is subdivided into five layers or strata, the stratum germinativum (SG), the stratum spinosum (SS), the stratum granulosum (SGR), the stratum lucidum (not seen in this photomicrograph), and the stratum corneum (SC) at the that a keratinocia gradually migrates to the surface and sloughs off in a process called desquamation.

The condition of the epidermis determines how “fresh” your skin looks and also how well your skin absorbs and retains moisture. Stains, pores, uniformity, porphyrins and UV stains are manifested in our epidermis.

Wrinkles, however, form from changes in the dermis.

The dermis assumes the important functions of thermoregulation and supports the vascular network to supply nutrients to the avascular epidermis. The dermis is typically subdivided into two zones, a papillary layer and a reticular layer. The dermis contains mainly fibroblasts that are responsible for secreting collagen, elastin, and ground substance that give the skin support and elasticity. Immune cells that are involved in defense against foreign invaders that penetrate the epidermis are also present.

The papillary dermis (PD) contains vascular networks that have two important functions. The first is to support the avascular epidermis with vital nutrients, and second, to provide a network for thermoregulation. The vasculature is organized so that by increasing or decreasing blood flow, heat can be conserved or dissipated. The vasculature interdigitates in areas called dermal papillae (DP). The papillary dermis also contains free sensory nerve endings and structures called Meissner’s corpuscles in highly sensitive areas.

The reticular layer of the dermis (RD) consists of dense irregular connective tissue, this differs from the papillary layer, which is composed mainly of loose connective tissue (note the difference in cell number). The reticular layer of the dermis is important in giving the skin its overall strength and elasticity, as well as housing other important epithelial-derived structures such as glands and hair follicles. This reticular layer is our target for collagen production.


Collagen is a member of connective tissues: cartilage, bone, tendons, fascia, ligaments, and blood vessels. The character of any connective tissue is determined by the function of the specific cells that comprise that tissue. The main fibrous proteins are collagen and elastin. The predominant non-fibrous components are mainly complex carbohydrates: hyaluronic acid, proteoglycans and glycoproteins. Collagens are a class of proteins, members of which have chemical and structural characteristics in common, but each is the product of a specific gene (hence, specific connective tissue disorders). A property of all collagen molecules is the unique triple helix, a particular conformation of three-component polypeptide (alpha) chains, each containing approximately 1,000 amino acids. The conformation of the chains is determined by the amino acid content, with glycine constituting one-third of the total and occurring at every third position in the amino acid sequence. There are two main classes of collagen: interstitial and pericellular. Interstitial collagens are the main collagen of the skin and essentially exclusive to the type of bone (type I); articular cartilage and nucleus pulposus (type II); and the collagen present in the skin, the walls of the blood vessels and the matrix of the parenchymal organs (type III). Pericellular collagens are types IV and V and predominate in the basement membranes.


The biosynthesis of collagen chains is a multistep process in which a precursor form (procollagen) is first synthesized, with peptide extensions at each end. During synthesis, several amino acids are modified only post-translationally (after incorporation into polypeptide chains). These post-translational modifications include the hydrozylation of praline residues (hydroxyproline) and lysine residues (hydroxylysine) and the addition of sugars (glucose and galactose) to hydroxylysines, and the formation of hydroxylized aldehydes and lysine. Specific proteases act to separate the extensions from the procollagens to produce the processed collagen molecules, which can then polymerize to form fibrils and fibers. Our lasers target the cellular mediators that stimulate the production of procollagen I and III.


Cutaneous (skin) aging is a complex biological phenomenon. Disorders in aged skin are more the result of photoaging (UVR) than chronological aging. There is a gradual atrophy of the dermis and epidermis and a massive accumulation of abnormal elastic tissue with its associated microfibrils and proteoglycans. These elements replace the normal collagen-rich dermal base, leading to a thinner and weakened dermal layer. UVR consists of UVA (320-400nm) + UVB (280-320nm) and UVC which currently does not penetrate our atmosphere. UVA light is the main offending agent of collagen loss and subsequent wrinkles. The shorter wavelength of UVB only affects the epidermis. As the dermal layer “sinks in”, it also follows the epidermis and wrinkles appear. This decrease in collagen is due more to further deterioration (UVA) than to a significant decrease in production (age). The term solar elastosis is used to describe photodamaged skin.

Skin thickness changes with age: young skin gradually thickens up to the age of about 20, after which there is gradual atrophy of the dermis. At the level of the papillary dermis, a relatively non-echoic band appears that develops with age. The exact reasons for the appearance of this shadow are unknown, but it corresponds to a homogenization of the papillary dermis, the local disappearance of elastic and collagen fibers, and their replacement by an undifferentiated matrix of hydrated glycosaminoglycans (elastotic tissue). The extent of this shade increases steadily with age and is a reliable marker of skin aging (loss of collagen density).

This shade is found on both types of aged skin: photo and chronological. An increase in dermal thickness from laser therapy is found in the upper dermis and is due to an increase in collagen fibers and not the other components of the matrix.

The heat of the laser causes a partial denaturation of the old collagen and accelerates the process of synthesis of new collagen by fibroblasts and the deposition of new glycosaminoglycans and leads to a resorption of elastic material. An increase in the echogenic band in the upper dermis is easily visualized with ultrasound and is directly attributable to an increase in collagen. Two possible benefits occur with laser collagen remodeling therapy. The thickness of the dermis increases and/or the density of collagen increases.


Anti-aging modalities are classified by type:

Type I therapy is directed at the epidermis (microdermabrasion/chemical peel/laser)

Type II therapy targets the dermis (laser/chemical peel/ultrasound)

Type III therapy is surgical or injectable (facelift, botox, fillers).