Salivary proteins and cytokines in drug-induced gingival overgrowth.

نویسندگان

  • S Ruhl
  • S Hamberger
  • R Betz
  • T Sukkar
  • G Schmalz
  • R A Seymour
  • K-A Hiller
  • J M Thomason
چکیده

Little is known about the involvement of saliva in gingival overgrowth (GO). It was hypothesized that, in this situation, the composition of saliva is altered. Thus, proteins, albumin, cytokines, and growth factors in whole and glandular saliva were investigated. Differences between glandular and gingival contributions to the composition of saliva were explored in patients medicated with cyclosporin who exhibited GO (responders), those without GO (non-responders), and non-medicated subjects (controls). In whole saliva, interleukin-1alpha (IL-1alpha), IL-6, IL-8, epidermal growth factor (EGF), nerve growth factor (NGF), and albumin were detected, but in glandular saliva only EGF and NGF were identified. Albumin and IL-6 differed significantly between responders and controls, although the overall profile of salivary proteins remained unchanged. Thus, inflammatory cytokines and albumin are confined to whole saliva and are associated with GO, whereas its content of EGF and NGF appears unaffected by cyclosporin.

برای دانلود متن کامل این مقاله و بیش از 32 میلیون مقاله دیگر ابتدا ثبت نام کنید

ثبت نام

اگر عضو سایت هستید لطفا وارد حساب کاربری خود شوید

منابع مشابه

Using Salivary Nitrite and Nitrate Levels as a Biomarker for Drug-Induced Gingival Overgrowth

AIM Drug-induced gingival overgrowth has a multifactorial nature and the pathogenesis is still uncertain. It has been suggested that Nitric Oxide (NO) might play a role in the pathogenesis of drug-induced gingival overgrowth due to the contribution of NO to immune response and matrix degradation. NO levels in biological fluids have been used as a diagnostic biomarker in many diseases. The aim o...

متن کامل

On the Cellular and Molecular Mechanisms of Drug-Induced Gingival Overgrowth

INTRODUCTION Gingival overgrowth has been linked to multiple factors such as adverse drug effects, inflammation, neoplastic processes, and hereditary gingival fibromatosis. Drug-induced gingival overgrowth is a well-established adverse event. In early stages, this gingival enlargement is usually located in the area of the interdental papilla. Histologically, there is an increase in the differen...

متن کامل

The Possible Potential Therapeutic Targets for Drug Induced Gingival Overgrowth

Gingival overgrowth is a side effect of certain medications. The most fibrotic drug-induced lesions develop in response to therapy with phenytoin, the least fibrotic lesions are caused by cyclosporin A, and the intermediate fibrosis occurs in nifedipine-induced gingival overgrowth. Fibrosis is one of the largest groups of diseases for which there is no therapy but is believed to occur because o...

متن کامل

مروری بر افزایش حجم لثه مرتبط با دارو در بیماران کودک و نوجوان

Gingival overgrowth is a drug-associated side effect occurs in pediatric patients. Phenytoin, cyclosporine, calcium channel blockers, and amphetamine are primary drugs that can cause gingival enlargement in children. Pediatric patients are more prone to drug-associated gingival overgrowth rather than adults. Gingival overgrowth may cause functional, phonetic, and nutritional difficulties, and m...

متن کامل

Drug-induced Gingival Overgrowth

Many terms have been used to describe gingival overgrowth. The expression gingival hyperplasia (“abnormal increase in the number of normal cells in a normal arrangement in an organ or tissue, which increase in volume”) and gingival hypertrophy (“enlargement or overgrowth of an organ or part due to an increase in size of its constituent cells”) have been also used, although gingival overgrowth i...

متن کامل

ذخیره در منابع من


  با ذخیره ی این منبع در منابع من، دسترسی به آن را برای استفاده های بعدی آسان تر کنید

برای دانلود متن کامل این مقاله و بیش از 32 میلیون مقاله دیگر ابتدا ثبت نام کنید

ثبت نام

اگر عضو سایت هستید لطفا وارد حساب کاربری خود شوید

عنوان ژورنال:
  • Journal of dental research

دوره 83 4  شماره 

صفحات  -

تاریخ انتشار 2004