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A laser based imaging technique that can image up to 2mm beneath skin. Non-invasive, low intensity, 1310nm laser light. Provides real-time video-rate images without any pre-treatment or gels. Image subsurface skin structure and detect changes in the structure caused by skin care products. 2D and 3D visualization
Technology Comparison
OCT
1 m Smallest resolvable feature 10 m
X-ray / CT
100 m 1 mm
PET
10mm
Ultrasound
MRI
Multi-Beam OCT
Ultrasound
Disclaimer
The images below result from research undertaken by MDL and our collaborators. We have included for information our preliminary analysis of features within the images relating to the histologically confirmed diagnosis. This initial analysis should be used as guidance only.
Terminology
Areflective: Areas appearing completely black, objects with no internal scattering Hyporeflective/Hyporeflectivity: Areas with scattering that appear dark or darker relative to another layer/structure Hyperreflective/Hyperreflectivity: Areas with scattering that appear bright or brighter relative to another layer/structure
Reflectivity
Composition
Structures and layers appear differently depending on what they are comprised of Main components: Cells Collagen Keratin Fluid
Composition: Cells
Normal epithelial cells Hyperreflective grain texture Due to cell cytoskeleton Proliferating cells Hyporeflective grain texture Due to nucleus size
Dense proliferating cells Dark hyporeflective grain texture Only seen in basal cell carcinoma periphery
Collagen
Dense collagen fibres Hyperreflective mottled texture Hyporeflective areas due to fluid spaces Seen in the reticular dermis Dense aligned collagen fibres Hyperreflective slight mottled texture Seen mainly in scar tissue
Composition: Keratin
Deposits of loose keratin Hyperreflective appearance Undefined borders Layered keratin deposition Mainly hyporeflective Seen mainly on the surface of SCCs Densely packed keratin Hyperreflective upper region getting more hyporeflective with depth
Composition: Fluid
Water/Tissue fluid Areflective or dark hyporeflective Due to edema or intradermal injection Blood filled spaces Hyporeflective Blood flow can be seen Fluid filled space with cell debris Hyporeflective fluid spaces with hyperreflective cell debris
Optical Effects
Various non-structural optical effects may cause changes in how structures/layers within the skin appear. Optical effects: Shadowing Surface Reflection Degradation of Signal
Shadowing is a result of the signal being absorbed or blocked by a structure obscuring all layers/structures below it Vertical areflective band cast by the structure Dense keratin mainly causes this e.g. hair and keratin cysts
Initial bright hyperreflective band on skin surface Not structural Caused by the large change of refractive index between air and skin.
Progressive loss of signal through a structure or layer Can cause a structure made of a single component, i.e. keratin, to exhibit hyperreflectivity at the surface and increasing hyporeflectivity as depth increases Occurs in all scans causing lower reticular dermis to always appear darker
Layers
Layers of the skin have different characteristics as a consequence of their composition Skin Layers: Epidermis Dermal-Epidermal Junction/Basal Membrane Papillary Dermis Reticular Dermis
Layers
A B C D
C D
Layers: Epidermis
Top layer of follicular skin below the initial bright surface reflection General hyporeflective appearance Heterogeneous fine granular texture due to being comprised mainly of cells, both epithelial and keratinised A thin dark hyporeflective Stratum Corneum layer can sometimes be observed directly below the surface reflection
Layers: Epidermis
Always a distinct textural difference between epidermis and dermis Grain patterned epidermis and mottled dermis Contrast between layers decreases with age and sun damage
Lowest part of the epidermis bordering with the papillary dermis layer Dark hyporeflective line at the change of contrast between the hyporeflective epidermis and hyperreflective papillary dermis The DEJ involves the basal membrane/ Stratum Basale which is a proliferating cell layer and so appears hyporeflective
The dark hyporeflective line may not always be apparent DEJ is the interface of the epidermis and papillary dermis so is identified mainly by the change in contrast between the two layers
Superficial layer of the dermis interfacing with the epidermis Hyperreflective appearance due to collagen and cellular components Hyperreflective cell component main contributor in appearance Mottled texture with horizontal patterning due to hyporeflective vasculature and hyperreflective collagen fibre aggregations
Can be thinner or entirely absent in some cases Usually thinner in more aged skin Can be completely absent in cases of sun damage
Lowest visible layer of the skin Hyporeflective appearance due to dense collagen and frequency of vessel structures Mottled texture with horizontal disposition due to hyperreflective collagen bundle aggregations with areas of tissue fluid and vessel structures
Features: Vessels
Hyporeflective tube structures with tapering ends Internal scatter pattern caused by blood flow Observed in papillary and reticular dermis layers Size and thickness can vary with person, age and lesion type
Appear as a hyporeflective structure spanning the dermal layers and connecting to the epidermis Mostly seen at an incline to the skin surface Evidence of hyperreflective hair protrusion at skin surface
Hyporeflective hair follicle structures within the dermis can have areas of hyperreflectivity within indicating the hair shaft within the hyporeflective hair matrix
Hairs within and external to the skin appear hyperreflective due to their keratin content Hairs external to the skin cast shadows on lower layers caused by the dense keratin
Hyporeflective structure with hazy texture and indistinct more hyporeflective border caused by the keratinised cell boundary Internal scatter caused by hyperreflective cell aggregations with hyporeflective fluid filled secretary spaces Observed in the reticular dermis associated with hair follicles
Loss of layers mainly the papillary dermis Reduced contrast between epidermis and dermis Loss of distinct hyperreflective mottled patterning due to collagen fibre damage Dermal hyporeflectivity due to edema/erythema Areas of localised fluid, edema, pockets
Epidermis visible Loss of layers mainly papillary dermis Dermal pattern change due to collagen breakdown (solar elastosis) Reduction/loss of vasculature Hyporeflectivity of dermis due to erythema and increase in fluid content
Single homogeneous dermis with distinct epidermis Hyperreflective dermis region due to only collagen being the main component Fine vasculature may be present Absence of hair follicles and associated structures
Observed in various sizes in the superficial dermis Hyperreflective surface to the structure and shadow casting due to densely packed keratin Hyporeflective core due to degradation of signal strength Disruptive to surrounding layers
Lesions
Skin lesions present with their own morphological characteristics and often in conjunction with other features: inflammation, sun damage, etc. Skin Lesions: Basal Cell Carcinoma Squamous Cell Carcinoma Seborrheic Keratoses Nevi Scleroderma
A B
A: Superficial Basal Cell Nest B: Nodular Basal Cell Nest C: Basal Cell Nest Aggregation/ Multi-Nodular D: Epidermal Ulceration
Basal cell nests typically appear as ovoid structures Hyporeflective due to proliferating cells Can be associated with the epidermis (superficial) Or observed in the dermis (nodular)
Hyporeflective due to peripheral palisading or densely packed cell proliferation zone Hyporeflectivity of cells due to dense packing of small basaloid cells or cells with high nuclear volumes and low cytoplasm content Size of boundary depends on size and maturity of basal cell nest, most evident on dermis facing side of the nest
Disruption to normal DEJ contours Dermis protruding growth from the basal cell layer DEJ appears more hyporeflective in the area of the basal cell nest due to area of proliferating cells
Hyporeflective ovoid structure within the epidermis Causes severe changes in DEJ contours Peripheral boundary can be less obvious, though normally more evident on dermis facing boundary
Hyporeflective ovoid structure in and protruding in part from the epidermis Causes severe changes in DEJ contours Peripheral boundary can be less obvious, though normally more evident on dermis facing boundary
Hyporeflective ovoid protrusion from the epidermis Dark hyporeflective centre due to necrosis, combination of tissue fluid and cell debris More obvious peripheral boundary on dermis facing
Hyporeflective ovoid structures in the dermis not associated with the epidermis Peripheral boundary more evident encompassing the basaloid nest Usually have visible signs of directed vasculature
Large nodules can cause the entirety of the dermis to be absent Larger basaloid nests are prone to central necrosis Necrosis appears as a change in texture in the nest at the center due to hyporeflective fluid spaces with cell debris
Basal cell nodules can aggregate into larger structures Appearance of a large nodule with internal hyperreflective areas due to collagenous connective tissue trapped between hyporeflective basaloid nests Lower border of the aggregation always most hyporeflective due to proliferating cell band
C
B
Disruption to DEJ contour pattern Hyporeflectivity can occur at border with dermis indicating proliferative area
Increased thickness of epidermis due to squamous cell proliferation Can appear more hyporeflective at the DEJ due to area of proliferation Heterogeneous epidermal thickening area contains bother hyporeflective proliferating cells and hyperreflective intra and extracellular keratin deposits
Loss of contrast between epidermis and dermis Loss of defined DEJ and layer distinction between epidermis and dermis Hyporeflective epidermis invasion into reticular dermis
Superficial keratin layers on skin surface Hyperreflective surface reflection with hyporeflective lower keratin layers Denser deposits in the layers cause shadowing effects Lower hyperreflective surface reflection at the start of skin surface
Only an epidermal component Heterogeneous texture epidermal thickening May have varying amounts of hyperkeratotic layering Protrusion into the dermis but no invasion Distinct divide between epidermis and dermis DEJ can appear altered in contour and more hyporeflective
Regions of epidermal thickening often appear more hyporeflective varying due to proportions of proliferating cells and cells with intracellular keratin deposits Normal structures and layers can usually be observed under the area Papillary dermis may be thinner or absent
Epidermal thickening Loss of distinct divide between epidermis and dermis where invasion has occurred Loss of normal layers and features at site of invasion Epidermal invasion appears as a hyporeflective protrusion with undefined boundaries
Hyperkeratotic can vary in thickness and also be absent in some cases Depth of dermis disruption, epidermal invasion, indicates maturity of lesion Vasculature frequency of appearance and size decreases
Epidermal invasion can appear as tendril-like protrusions into the dermis Hyporeflective protrusions indicate proliferating neoplastic cells Hyperkeratotic layering absent
Localised epidermal thickening causing bulge in the skin surface Only an epidermal component Keratin deposits can occur in the thickened area in varying sizes and frequency The epidermal bulge contains cells and intra and extracellular keratin deposits
Lesions: Nevi
Nevi subtypes: Junctional Pigmented Junctional Characteristic features: Localised Epidermal Thickening Distinct Rete Protrusions Shadow Effect (Pigmented Only)
Localised epidermal thickening Distinct rete protrusions forming an arch-like pattern across the area Hyporeflective rete ridges indicating blood/fluid perfused spaces
Increased size of hyporeflective rete protrusions Heterogeneous presentation of epidermis Increase in vasculature in the area
Prominent increase in rete protrusion size Disruption to the expected DEJ contour Shadowing effect cast from the rete peg apex due to intra and/ or extracellular melanin
Example 1
BCC
Example 2
Example 3
Example 4
VivoSight
The VivoSight OCT imaging system has been developed with the support of clinicians. It is compliant with European CE mark directives and has FDA 510(k) clearance for use in the USA.
For more information please contact: Daniel Woods Michelson Diagnostics Tel. +44 208 144 9836 Email: enquiries@md-ltd.co.uk
For clinical use in the US FDA 510(k) K093520 applies: VivoSight is a Multi-Beam Optical Coherence Tomography (OCT) system indicated for use in the two-dimensional, cross-sectional, real-time imaging of external tissues of the human body. This indicated use allows imaging of tissue microstructure, including skin, to aid trained and competent clinicians in their assessment of a patient's clinical conditions. US Federal law restricts this device to sale by or on the order of a physician.