Unit 3 · Hypodermis & cell types
Fat is not one layer, and skin is not one cell type
This unit covers the subcutaneous architecture beneath the dermis, then consolidates the specialised cell populations that run through every layer covered so far. By the end you should be able to explain why filler plane selection follows directly from layered anatomy, and which cell type a given clinical observation — pigmentation, erythema, volume loss, a granuloma — actually implicates.
Learn · The hypodermis
A compartmentalised fat layer, not a uniform cushion
The hypodermis, or subcutis, lies below the reticular dermis and above the deep fascia or periosteum. It consists primarily of lobules of adipose tissue separated by fibrous septa.
In the face, the hypodermis is organised into anatomically distinct fat compartments — both superficial (sub-SMAS) and deep (subperiosteal) — which are critical to facial volumetrics, the understanding of facial ageing, and the safe placement of dermal fillers. Key facial fat compartments include the nasolabial fat, medial and lateral cheek fat, orbital fat (superficial and deep), the temporal fat pad, and the buccal fat pad (Bichat's fat pad).
Facial fat compartments do not age uniformly — some deflate, others descend or herniate. Before reading on, predict which behaviour applies to the medial cheek fat compartment versus the buccal fat pad.
Hold your answer before you open this. The value is in having committed to a prediction first.
The medial cheek and orbital fat compartments tend to deflate preferentially, while the buccal fat pad may descend or herniate rather than simply losing volume.
This distinction is why "facial ageing" is not a single volumetric problem with a single filler answer: a deflating compartment calls for volume replacement in that specific space, while a descending compartment reflects a positional change that volume alone does not correct.
The distinction between superficial (sub-SMAS) and deep (subperiosteal) compartments is what allows practitioners to reason about which structures a given injection depth is actually near. Named compartments are not simply anatomical trivia — they are the basis for predicting which vascular structures sit adjacent to a chosen injection plane in a given facial zone.
The selection of injection plane for dermal filler is a direct application of layered skin anatomy. Superficial dermis injection produces surface-level definition — fine lip lines, tear trough. Mid-dermis injection provides lift and volume for moderate tissue deficiency. Deep dermis to supraperiosteal injection supports skeletal projection — cheekbones, chin, jawline, temples. Injection into or adjacent to a named fat compartment risks compartment disruption, asymmetric volume distribution, or — in the temporal and periorbital zones — vascular occlusion via proximity to named arteries. A thorough working knowledge of both the skin layers and the subcutaneous architecture is inseparable from safe filler practice.
A treatment plan calls for skeletal projection at the chin, using a deep dermis to supraperiosteal injection plane. Per the layered logic of filler placement, this plane is selected because:
Select an option to commit. The reasoning appears afterwards.
Injection plane selection follows directly from layered anatomy: superficial dermis for surface definition, mid-dermis for lift and volume in moderate tissue deficiency, and deep dermis to supraperiosteal for skeletal projection at the cheekbones, chin, jawline and temples.
The corollary is the risk side of the same logic — injecting into or adjacent to a named fat compartment, rather than at the intended plane, risks compartment disruption, asymmetric volume distribution, or vascular occlusion in the temporal and periorbital zones. Plane selection and risk avoidance are the same decision viewed from two directions.
Learn · Key cell types
The cells behind every observation you make in clinic
Each skin layer covered so far contains specialised cells directly relevant to aesthetic medicine — as targets of treatment, as mediators of healing, or as sources of common presentations.
| Cell type | Location | Primary function | Aesthetic relevance |
|---|---|---|---|
| Keratinocyte | All epidermal layers | Barrier formation; structural protein synthesis; cytokine signalling | Re-epithelialisation following resurfacing; target of retinoids and AHAs; source of inflammatory cytokines in wound healing |
| Melanocyte | Stratum basale; hair follicle | Melanin synthesis for UV protection; melanin transfer to keratinocytes | Source of dyspigmentation (melasma, post-inflammatory hyperpigmentation, solar lentigines); target of tyrosinase inhibitors, laser and IPL |
| Langerhans cell | Stratum spinosum | Antigen presentation; immune surveillance; tolerance induction | Reduced in photoaged skin; implicated in contact sensitisation and allergen response to topical treatments |
| Merkel cell | Stratum basale | Mechanoreception (light touch) | Merkel cell carcinoma is a rare but clinically important malignancy to recognise in skin assessment |
| Fibroblast | Papillary and reticular dermis | Collagen I/III, elastin and glycosaminoglycan synthesis; wound healing; matrix remodelling | Primary effector of collagen-stimulating treatments; activity declines with age |
| Mast cell | Papillary dermis; perivascular | Histamine release; IgE-mediated immunity; wound healing | Post-treatment erythema and urticaria; increased density in rosacea — relevant when planning energy-based treatments |
| Macrophage | Dermis; subcutaneous tissue | Phagocytosis; inflammatory regulation; collagen remodelling direction | Key mediator in wound healing; implicated in foreign-body granuloma response to filler |
| Adipocyte | Hypodermis; facial fat compartments | Energy storage; thermal insulation; volumetric support; endocrine function | Facial volume loss (lipoatrophy) is a primary driver of facial ageing; filler replaces deflated compartment volume |
Macrophages direct the inflammatory and proliferative phases of wound healing and are implicated in the foreign-body granuloma response that can follow filler placement — a chronic macrophage-driven reaction to a persisting foreign material, distinct from the acute mast cell-mediated erythema seen immediately after energy-based treatment.
Facial volume loss (lipoatrophy) associated with ageing is primarily driven by changes in which cell type?
Select an option to commit. The reasoning appears afterwards.
Adipocytes, located in the hypodermis and organised into facial fat compartments, provide volumetric support. Facial volume loss — lipoatrophy — is a primary driver of the appearance of facial ageing, and it is this compartment-specific adipocyte volume change that filler placement is replacing.
This is distinct from, and complementary to, dermal collagen loss: an ageing face is typically losing both structural collagen in the dermis and volumetric fat in specific hypodermal compartments at the same time, which is why a single intervention rarely addresses the full clinical picture.
Reduced density of this immune cell type in photoaged skin is implicated in altered contact sensitisation and allergen response to topical treatments:
Select an option to commit. The reasoning appears afterwards.
Langerhans cells sit in the stratum spinosum and perform antigen presentation, immune surveillance and tolerance induction. Their density is reduced in photoaged skin, which is implicated in altered contact sensitisation and allergen response to topical treatments.
This is a practical reason to treat product tolerance differently in significantly photoaged skin: a reduced Langerhans cell population changes how that skin's immune system processes topically applied actives, independent of any change in the stratum corneum barrier itself.
Unit 3 summary
Clinical takeaways
- The hypodermis is not a single fat layer. Distinct named compartments age differently — some deflate, others descend or herniate — directly informing filler strategy.
- Filler plane selection is a direct application of layered anatomy. Superficial, mid and deep planes achieve different clinical outcomes and carry different vascular risk.
- Skin's specialised cells extend well beyond keratinocytes. Melanocyte, Langerhans cell, Merkel cell, fibroblast, mast cell, macrophage and adipocyte each carry distinct clinical relevance — from pigmentation to wound healing to filler complications.
- Lipoatrophy is a primary driver of facial ageing's appearance. Adipocyte volume loss in specific compartments is distinct from, and complementary to, dermal collagen loss.