The muscles found in the nasopharynx include the levator palatini and the pharyngeal constrictors. The superior pharyngeal constrictor muscle forms the superior aspect of the lateral walls of the nasopharynx.

Adenoids decrease in size with age, typically atrophying completely by the teenage years. Persistence of adenoid tissue into adulthood is an uncommon clinical finding. Nonetheless, a disease process of the adenoids requires investigation in those presenting with symptoms of nasal obstruction. Immunocompromised patients, such as those diagnosed with human immunodeficiency virus (HIV) and organ transplant recipients, can exhibit adenoid hypertrophy. The thinking is that this finding is thought to be caused by regressed adenoid tissue reproliferating in response to infections.[3][5]

Adenoid tissue may separate into two parts in some individuals. This variant can occur through two means: by a fissure extending from the pharyngeal bursa or by a median fold passing towards the nasal septum from the pharyngeal bursa. 

Adenoidectomy: An adenoidectomy is the surgical excision of adenoid tissue. Primary indications for adenoidectomy include otitis media with effusion of at least 3 months duration, chronic adenoiditis, obstructive sleep apnea lasting 3 months or greater, and recurrent upper respiratory infections. Patients post-adenoidectomy require special consideration for hemorrhage as a potential (though rare) complication. The basisphenoid artery supplies a portion of the nasopharyngeal tonsil and can be a potential source of bleeding post-operatively.[6]

Adenoid hypertrophy (AH): Impaired mucociliary clearance has been implicated as playing a role in adenoid hypertrophy, a condition typically seen in children. An enlarged adenoid may block breathing and be a cause of snoring or obstructive sleep apnea. Adenoid hypertrophy can also lead to comorbid conditions such as serous otitis and sinusitis. AH is higher in frequency in children with allergic diseases, with the most common allergen being house dust. Other risk factors noted for developing AH include cigarette smoke exposure and allergic rhinitis. In a child with these risk factors, AH should be a consideration during a routine examination. Assessing adrenal size can be achieved through flexible nasal endoscopy, where adenoid size grading is on a scale of I to IV. This scale represents the percentage of the posterior choana blocked by the adenoid tissue, with grade IV representing the highest level of obstruction. While adenoidectomy remains a common surgical treatment for adenoid hypertrophy, intra-nasal steroids are an option as a non-surgical treatment regimen.[7][8][6]

Adenoiditis: Adenoiditis refers to inflammation of adenoid tissue secondary to an infection. Those affected with adenoiditis may present with nasal obstruction, rhinorrhea, mouth breathing, and cold-like symptoms. Adenoiditis may occur on its own or in combination with acute or chronic rhinosinusitis. Common pathogens leading to adenoiditis are often the same as those implicated in rhinosinusitis and include Streptococcus pneumoniae, Hemophilus influenza, and Moraxella catharrhalis. Nasal endoscopy showing purulent secretion of the adenoids can be useful to confirm adenoiditis.[1]

Adenoid faces: Adenoid faces describes the differences in physical characteristics seen in children with adenoid hypertrophy. The belief is that adrenal hypertrophy results in obstruction in proper nasal breathing, leading to mouth breathing and issues with dental and maxillofacial development. Adenoid faces characteristically demonstrate narrowed maxillary and dental arches, upper lip incompetence, retropositioning of mandibular incisors and hyoid bone,  and a posterior-rotated mandible. There is also a downward tongue displacement and a lower position of the mandible. Removal of excessive adenoid tissue allows for the recovery of proper craniofacial growth.[9]