Carbidopa acts as a peripheral DDC inhibitor, as carbidopa, itself, cannot cross the blood–brain barrier. In other words, carbidopa has no effect on brain DDC conversion of levodopa/L-DOPA to dopamine. Ultimately, a greater proportion of the exogenously provided levodopa/L-DOPA reaches the brain. Commercially, carbidopa/levodopa combinations are available in the treatment of central dopamine deficiencies. Along with carbidopa, other DDC inhibitors are benserazide (Ro-4-4602), difluromethyldopa, and α-methyldopa. pharmacology 2
Carbidopa, an inhibitor of aromatic amino acid decarboxylation, is a white, crystalline compound, slightly soluble in water, with a molecular weight of 244.3. It is designated chemically as N-amino-α-methyl-3-hydroxy-L-tyrosine monohydrate. Its empirical formula is C10H14N2O4•H2O. Used in tandem with L-DOPA (also known as levodopa, a dopamine precursor converted in the body to dopamine), it increases the plasma half-life of levodopa from 50 minutes to 1½ hours. CarbiDOPA cannot cross the blood–brain barrier, so it inhibits only peripheral DDC. It thus prevents the conversion of L-DOPA to dopamine peripherally. This reduces the side effects caused by dopamine on the periphery, as well as increasing the concentration of L-DOPA and dopamine in the brain. The combination of carbidopa/levodopa carries the brand names of Kinson, Sinemet, Pharmacopa and Atamet; while Stalevo is a combination with entacapone, which enhances the bioavailability of carbidopa and levodopa. Carbidopa is most commonly used as a method to inhibit the activity of dopamine decarboxylase. This is an enzyme that breaks down L-Dopa in the periphery and converts it to dopamine.
Gingivitis associated with plaque only
Gingival diseases modified by systemic factors
Gingival diseases modified by medications
Gingival diseases modified by malnutrition
Non-plaque-induced gingival lesions
Gingival diseases of specific bacterial origin
Gingival diseases of viral origin
Gingival diseases of fungal origin
Gingival diseases of genetic origin
Gingival manifestations of systemic conditions
Traumatic lesions
Foreign body reactions
Not otherwise specified

2017 Classification
As defined by the 2017 World Workshop, periodontal health, gingival diseases/ conditions have been categorised into the following:
Periodontal health and gingival health
Clinical gingival health on an intact periodontium
Clinical gingival health on a reduced periodontium
Stable periodontitis patient
Non-periodontitis patient
Gingivitis – dental biofilm-induced
Associated with dental biofilm alone
Mediated by systemic or local risk factors
Drug-influenced gingival enlargement
Gingival diseases – non-dental biofilm induced
Genetic/ developmental disorders
Specific infections
Inflammatory and immune conditions
Reactive processes
Neoplasms
Endocrine, nutritional & metabolic diseases
Traumatic lesions
Gingival pigmentation

Prevention
Gingivitis can be prevented through regular oral hygiene that includes daily brushing and flossing. Hydrogen peroxide, saline, alcohol or chlorhexidine mouth washes may also be employed. In a 2004 clinical study, the beneficial effect of hydrogen peroxide on gingivitis has been highlighted. The use of oscillation type brushes might reduce the risk of gingivitis compared to manual brushing.Rigorous plaque control programs along with periodontal scaling and curettage also have proved to be helpful, although according to the American Dental Association, periodontal scaling and root planing are considered as a treatment for periodontal disease, not as a preventive treatment for periodontal disease. In a 1997 review of effectiveness data, the U.S. Food and Drug Administration (FDA) found clear evidence showing that toothpaste containing triclosan was effective in preventing gingivitis.