Signs and symptoms
The signs and symptoms of pericoronitis depend upon the severity, and are variable:

Pain, which gets worse as the condition develops and becomes severe. The pain may be throbbing and radiate to the ear, throat, temporomandibular joint, posterior submandibular region and floor of the mouth. There may also be pain when biting. Sometimes the pain disturbs sleep. Tenderness, erythema (redness) and edema (swelling) of the tissues around the involved tooth, which is usually partially erupted into the mouth. The operculum is characteristically very painful when pressure is applied. Halitosis resulting from the bacteria putrefaction of proteins in this environment releasing malodorous volatile sulfur compounds. Bad taste or sour taste in the mouth from exudation of pus. Intra-oral halitosis. Formation of pus, which can be seen exuding from beneath the operculum (i.e. a pericoronal abscess), especially when pressure is applied to the operculum. Signs of trauma on the operculum, such as indentations of the cusps of the upper teeth, or ulceration. Rarely, the soft tissue around the crown of the involved tooth may show a similar appearance to necrotizing ulcerative gingivitis. Trismus (difficulty opening the mouth). resulting from inflammation/infection of the muscles of mastication. Dysphagia (difficulty swallowing). Cervical lymphadenitis (inflammation and swelling of the lymph nodes in the neck), especially of the submandibular nodes. Facial swelling, and rubor, often of the cheek that overlies the angle of the jaw. Pyrexia (fever). Leukocytosis (increased white blood cell count). Malaise (general feeling of being unwell). Loss of appetite.
Later pediatric endocrinologist Aaron Hanukoglu reported that there are two independent forms of PHA with different inheritance patterns: A renal form with autosomal dominant inheritance exhibiting salt loss mainly from the kidneys, and a multi-system form with autosomal recessive form exhibiting salt loss from kidney, lung, and sweat and salivary glands.The hereditary lack of responsiveness to aldosterone could be due to at least two possibilities: 1. A mutation in the mineralocorticoid receptor that binds aldosterone, or 2. A mutation in a gene that is regulated by aldosterone. Linkage analysis on patients with the severe form of PHA excluded the possibility of linkage of the disease with the mineralocorticoid receptor gene region. Later, the severe form of PHA was discovered to be due to mutations in the genes SCNN1A, SCNN1B, and SCNN1G that code for the epithelial sodium channel subunits, α, β, and γ, respectively.A stop mutation in the SCNN1A gene has been shown to be associated with female infertility. See also
Hyperchloremic acidosis
Pseudohyperaldosteronism

References
External links
GeneReviews/NCBI/NIH/UW entry on Pseudohypoaldosteronism Type II