The amount of tinnitus is not necessarily related to the degree or type of hearing impairment. Tinnitus develops due to irritation of the delicate nerve endings in the inner ear. Since the nerve carries sound, this irritation is manifested as ringing, roaring or buzzing. It is usually worse when the patient is fatigued, nervous or in a quiet environment. Causes
Otosclerosis can be caused by both genetic and environmental factors, such as a viral infection (like measles). Ribonucleic acid of the measles virus has been found in stapes footplate in most patients with otosclerosis. Populations that have been vaccinated against measles had a significant reduction in otosclerosis. While the disease is considered to be hereditary, its penetrance and the degree of expression is so highly variable that it may be difficult to detect an inheritance pattern. Most of the implicated genes are transmitted in an autosomal dominant fashion. One genome-wide analysis associates otosclerosis with variation in RELN gene.Loci include:

Pathophysiology
The pathophysiology of otosclerosis is complex. The key lesions of otosclerosis are multifocal areas of sclerosis within the endochondral temporal bone. These lesions share some characteristics with Pagets Disease, but they are not thought to be otherwise related. Histopathological studies have all been done on cadaveric temporal bones, so only inferences can be made about progression of the disease histologically. It seems that the lesions go through an active "spongiotic" or hypervascular phase before developing into "sclerotic" phase lesions. There have been many genes and proteins identified that, when mutated, may lead to these lesions.
Presence of systemic health problemsILI utilization is expected to increase because dental patients prefer fewer soft tissue anesthesia and dentists aim to reduce administration of traditional inferior alveolar nerve block (INAB) for routine restorative procedures.Injection methodology: The periodontal ligament space provides an accessible route to the cancellous alveolar bone, and the anesthetic reaches the pulpal nerve via natural perforation of intraoral bone tissue.Advantages of ILI over INAB: rapid onset (within 30 seconds), small dosage required (0.2-1.0 mL), limited area of numbness, lower intrinsic risks such as neuropathy, hematoma, trismus/jaw sprain and self-inflicted periodontal tissue injury, as well as decreased cardiovascular disturbances. Its usage as a secondary or supplementary anesthesia on the mandible has reported a high success rate of above 90%.Disadvantages: Risk of temporary periodontal tissue damage, likelihood of bacteriemia and endocarditis for at-risk populations, appropriate pressure and correct needle placement are imperative for anesthetic success, short duration of pulpal anesthesia limits the use of ILIs for several restorative procedures that require longer duration, postoperative discomfort, and injury on unerupted teeth such as enamel hypoplasia and defects. Technique description:

All plaque and calculus to be eradicated, optimally before the operative visit to assist gingival tissue healing. Before injection, disinfect gingival sulcus with 0.2% chlorhexidine solution. Administration of soft tissue anesthesia is recommended prior to ILI administration. This helps to enhance patient comfort. Needle gauges of sizes 27-gauge short or 30-gauge ultra-short needle are usually utilized.