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Local anesthetic injections are given in specific areas of the mouth, rather than the whole body. Although several different medications are available, the most commonly used local anesthetic to prevent pain in the area around a tooth is lidocaine (also called xylocaine or lignocaine). Lidocaine's half-life in the body is about 1.5–2 hours. [2]
In short, when used properly, lidocaine spray can produce a significant improvement in performance, helping you to avoid early climax and last for as much as six or seven times as long in bed.
Lidocaine, also known as lignocaine and sold under the brand name Xylocaine among others, is a local anesthetic of the amino amide type. [10] It is also used to treat ventricular tachycardia and ventricular fibrillation .
Many local anesthetics fall into two general chemical classes, amino esters (top) and amino amides (bottom). A local anesthetic (LA) is a medication that causes absence of all sensation (including pain) in a specific body part without loss of consciousness, [1] providing local anesthesia, as opposed to a general anesthetic, which eliminates all sensation in the entire body and causes ...
Dental abscess; Other names: Dentoalveolar abscess, Periapical abscess, tooth abscess, root abscess: A decayed, broken down tooth, which has undergone pulpal necrosis.A periapical abscess (i.e. around the apex of the tooth root) has then formed and pus is draining into the mouth via an intraoral sinus ().
Benzalkonium chloride/lidocaine (trade name Bactine among others) is an antiseptic, first-aid treatment distributed by Wellspring Pharmaceutical Corporation.Bactine was developed in 1947 and first marketed in 1950 by Miles Laboratories.
Periapical periodontitis may develop into a periapical abscess, where a collection of pus forms at the end of the root, the consequence of spread of infection from the tooth pulp (odontogenic infection), or into a periapical cyst, where an epithelial lined, fluid-filled structure forms.
In 1890, W.D. Miller, considered the father of oral microbiology, was the first to associate pulpal disease with the presence of bacteria. [11] This was confirmed by Kakehashi, who, in 1965, proved that bacteria were the cause of pulpal and periradicular disease in studies using animal models; pulpal exposures were initiated in both normal and germ-free rats, and while no pathologic changes ...