Anatomy, Head and Neck: Levator Labii Superioris Muscle

Structure and Function

Structure

The LLS is a thin, quadrilateral muscle that begins at the infraorbital margin of the maxilla and extends toward the upper lip. LLS muscle fibers are situated between the lateral extension of the levator labii superioris alaeque nasi (LLSAN) and the zygomaticus minor, integrating into the upper lip's muscle mass, the orbicularis oris.[2] Most LLS fibers connect beneath the alar facial crease. Deeper fibers attach to the lower nasal vestibule's skin.

Function

The LLS elevates and everts the upper lip, particularly during smiling. This muscle also broadens the nostril by elevating the nasal ala and upper lip, pulling the alar facial crease and skin outward and upward.

The LLS and surrounding perioral muscles facilitate complex mouth and nose movements for humans' varied facial expressions and speech. The movements of the alar facial crease are predominantly directed by its attached muscles, with the LLSAN, LLS, and nasalis' alar part maneuvering the crease in specific directions to produce facial movements.[3][4][5]

Fat tissue between the posterior nasal opening and nasalis muscle in the alar facial crease's posteromedial area provides mechanical support. Buccal fat pads fill deep facial recesses, ease muscle movement during chewing and facial expressions, and protect vital structures from muscle or external pressures. The fat surrounding the posterior nasal aperture cushions the area, reducing movement stress on the alar facial crease caused by nearby muscle activity.

Embryology

Facial muscles begin to develop between the 3rd and 8th weeks of embryonic development.[6][7] The muscles arise as the 2nd branchial arch's mesodermal thickenings. The infraorbital laminae and occipital platysma are the first laminae to develop. Both infraorbital laminae give rise to the LLS, among many other facial mimetic muscles. Improper development may lead to congenital facial weakness, which often presents with segmental dysfunction corresponding to the affected muscles. The condition contrasts with traumatic or inflammatory facial paralysis, which is most often hemifacial.

Blood Supply and Lymphatics

The LLS receives blood from the angular artery branches inferiorly and the infraorbital artery superiorly. The angular artery is a terminal facial artery branch, while the infraorbital artery diverges from the maxillary artery's 3rd part. Both the facial and maxillary arteries are external carotid artery branches. The infraorbital artery runs through the infraorbital foramen along with the infraorbital nerve, a branch of the maxillary division of the trigeminal nerve (cranial nerve V2). Venous outflow occurs through the facial vein's tributaries corresponding to the arterial inflow. Lymphatic drainage passes through nodes in the nasolabial region.[8]

Nerves

The facial nerve's zygomatic, with contributions from the buccal, branch innervates the LLS and other midfacial muscles between the orbicularis oculi and orbicularis oris. The LLS and LLSAN attach to their nerve branches from their deep surfaces. In contrast, the levator anguli oris, located lateral to the LLS, attaches to its neve branch from its superficial surface.

Physiologic Variants

LLS variants arise from differences in shape and points of attachment. These variants are the rectangular (most common), fan-shaped, and trapezoidal types. The trapezoidal LLS variant attaches to the nasal ala at a significantly higher position than the rectangular form. The fan-shaped LLS variant, which is less commonly attached to the nasal ala, usually extends laterally from the nose, merging with the orbicularis oris muscle. The LLS' medial fibers adhere to the alar facial crease's deep surface, blending with the alar part of the nasalis. Some deeper fibers reach the skin of the nasal vestibule.

Surgical Considerations

The LLSAN, LLS, and nasalis' alar portion are anchored to the alar facial crease and the nasal vestibule's skin. Surgical procedures in this area, such as rhinoplasties, may damage these muscles and alter facial movements.

Excessive gingival display, or "gummy smile," can be corrected in multiple ways, depending on the severity, cause, and amount of jaw protrusion. This cosmetic condition often arises from hyperactivity of the upper lip muscles, such as the LLS. Myotomy and lip repositioning followed by orthodontic treatment can be an effective surgical intervention in such cases.[9][10]

Trauma or cutaneous malignancy surgery may result in soft tissue nasal defects. A pedicled LLSAN flap has been described in the reconstruction of these defects.[11]

Facial reanimation surgeons may replace dysfunctional LLS and zygomaticus major muscles when rehabilitating a patient's smile. Muscles that may be considered include the sternohyoid, omohyoid, serratus anterior, and gracilis.[12][13]

Clinical Significance

Botulinum toxin treatment effectively corrects excessive gingival show arising from overactive upper lip elevators.[14] This newer technique is much less expensive and traumatizing to patients than surgery. However, the toxin's paralytic effect lasts only 3 to 4 months, thus requiring repeat injections. Additionally, botulinum toxin treatment is only helpful if a hyperactive upper lip is the cause of the excessive gingival display.[15] Hyaluronic acid infiltration has also been shown to be a safe, effective, and long-lasting treatment for gummy smiles.[16]

Other Issues

LLS weakness is most often unilateral but can also present bilaterally. The condition's severity ranges from mild paresis to complete paralysis. LLS impairment frequently results from damage to the facial nerve's main trunk or the zygomatic or buccal branch. Common etiologies include trauma and inflammatory conditions like Bell palsy, Ramsay Hunt syndrome, and Lyme disease. Other causes of facial paralysis include multiple sclerosis, poliomyelitis, Guillain-Barré syndrome, and SARS-CoV-2 infection. Iatrogenic facial nerve damage can also paralyze the LLS.[17] Congenital facial paralysis arises when one or more mimetic muscles are atrophic or absent at birth, as in Möbius syndrome.[18] LLS weakness warrants a complete neurological examination to determine the severity and identify accompanying injuries.