Skin Laxity



Skin Laxity


Macrene Alexiades



BACKGROUND

Skin laxity is a primary finding in skin aging and manifests as sagging of the skin. The survey by the American Society for Dermatologic Surgery reported that 67% of the population seeks treatment to sagging skin on jawline and neck.1 From 1900 to 1990, plastic surgery, including rhytidectomy or the surgical face lift, was the primary cosmetic treatment option for skin laxity. In the 1990s, ablative resurfacing lasers were introduced and applied to achieve facial skin tightening.2 Despite high efficacy for rhytid reduction, ablative devices required significant recovery time, prolonged wound healing, and an increased risk of side effects and complications. Nonablative and minimally invasive technologies with little to no recovery time and a more favorable risk-reward profile without epidermal vaporization were subsequently developed. In the early 2000s, skin tightening energy-based technologies were developed, including radiofrequency (RF) and infrared wavelengths. Although the gold standard of skin tightening remains surgical rhytidectomy or redraping, patients continue to demand for treatment alternatives in light of the anesthesia risks, morbidity, and the potential for unwanted cosmetic outcomes associated with plastic surgery. Nonsurgical skin tightening technologies are not yet a replacement for those with advanced to severe skin laxity but provide alternative for mild to moderate skin laxity candidates willing to accept less efficacy in exchange for facile recovery and rare risk of side effects or complications (see Table 4.5.1).


PRESENTATION

Patients with skin laxity present with a complaint of sagging or lax skin. They describe the skin in the undereyes and cheeks as sunken, complain of folds in the perioral regions, note the worsening of jowls, and/or report looseness to the skin. Similar complaints regarding body skin laxity refer to folding in the abdominal skin, linear undulations, and crepiness or irregularity to the skin of the thighs or arms.









TABLE 4.5.1 Quantitative Comprehensive Grading Scale of Rhytids, Laxity, and Photoaginga

































































































Grade


Descriptive Parameter


Alexiades Classification and Grading Scale of Skin Aging


Rhytids


Laxity


Elastosis


Dyschromia


Erythema-Telangiectasia (E-T)


Keratoses


Texture


0


None


None


None


None


None


None


None


None


1


Mild


Wrinkles in motion, few, superficial


Localized to nasolabial (nL) folds


Early, minimal yellow hue


Few (1-3) discrete small (<5 mm) lentigines


Pink E or few T, localized to single site


Few


Subtle irregularity


1.5


Mild


Wrinkles in motion, multiple, superficial


Localized, nL and early melolabial (mL) folds


Yellow hue or early, localized periorbital (po) elastotic beads (eb)


Several (3-6), discrete small lentigines


Pink E or several T localized 2 sites


Several


Mild irregularity in few areas


2


Moderate


Wrinkles at rest, few, localized, superficial


Localized, nL/mL folds, early jowls, early submental/submandibular (sm)


Yellow hue, localized po eb


Multiple (7-10), small lentigines


Red E or multiple T localized to 2 sites


Multiple, small


Rough in few, localized sites


2.5


Moderate


Wrinkles at rest, multiple, localized, superficial


Localized, prominent nL/mL folds, jowls, and sm


Yellow hue, po and malar eb


Multiple small and few large lentigines


Red E or multiple T, localized to 3 sites


Multiple, large


Rough in several, localized areas


3


Advanced


Wrinkles at rest, multiple, forehead, periorbital and perioral sites, superficial


Prominent nL/mL folds, jowls and sm, early neck strands


Yellow hue, eb involving po, malar and other sites


Many (10-20) small and large lentigines


Violaceous E or many T, multiple sites


Many


Rough in multiple, localized sites


3.5


Advanced


Wrinkles at rest, multiple, generalized, superficial; few, deep


Deep nL/mL folds, prominent jowls and sm, prominent neck strands


Deep yellow hue, extensive eb with little uninvolved skin


Numerous (>20) or multiple large with little uninvolved skin


Violaceous E, numerous T little uninvolved skin


Little uninvolved skin


Mostly rough, little uninvolved skin


4


Severe


Wrinkles throughout, numerous, extensively distributed, deep


Marked nL/mL folds, jowls and sm, neck redundancy and strands


Deep yellow hue, eb throughout, comedones


Numerous, extensive, no uninvolved skin


Deep, violaceous E, numerous T throughout


No uninvolved skin


Rough throughout


aThis 4-point grading scale has been extensively tested and employed for evaluating laser and energy-based cosmetic treatments.1,2,3






PATHOGENESIS

The properties of elasticity and resilience of the skin are conferred by the elastic fiber system in the connective tissue. These major insoluble extracellular matrix assemblies allow for the deformability and passive recoil of tissue. The elastic fibers complement the collagen fibers, which confer tensile strength. The elastic fiber system comprises roughly 2% to 4% of the dermis (dry weight) in sun-protected adult skin. Each elastic fiber is formed from an amorphous elastin core and a surrounding mantle of elastic microfibrils, comprising fibrillin, fibulin, microfibrillar-associated glycoproteins, and elastin receptors.8 In diseases characterized by alterations in elastic fibers, the skin is loose and sagging with a loss of recoil, elasticity, and resilience9,10 (Table 4.5.2). Elastic fiber mutations, deficiency, degradation, or alteration result in reduced skin elasticity and increased skin laxity, which may be reversed through stimulation of neoelastogenesis.11









TABLE 4.5.2 Elastic Fiber System Genes, Functions in Skin Elasticity, and Associated Skin Laxity Syndromes

















































Protein


Gene


Function


Syndrome


Elastin


ELN


Structural core of elastin fiber complex



Fibrillins


FBN1


Structural proteins of microfibrils, extracellular matrix; components and structural support of elastin fibers


Marfan


FBN2


Congenital contractural arachnodactyly


FBN3


Marfan


Fibulins


FBLN1


Endothelial development




FBLN2


FBLN3


FBLN4


FBLN5


Elastin-microfibril interface


Binds tissue inhibitor of metalloproteases 3 (TIMP3)


(EFEMP2) Binds LOX and FBN1


Binds ELN, FBN1, LTBP2, LOXL1, and integrins


Autosomal recessive cutis laxa, type 1


ATP7a


ATP7a


Transmembrane Cu2+ transport protein; required for function of Cu containing enzymes such as lysyl oxidase


Meinke’s


ATP-binding cassette subfamily C member 6


ABCC6


Transmembrane transporter protein


Pseudoxanthoma elasticum


LEMD3


LEMD3


Inner nuclear membrane protein


Buschke-Ollendorf


Jun 29, 2020 | Posted by in Dermatology | Comments Off on Skin Laxity
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