Early plaque in health consists of a relatively simple bacterial community dominated by Gram-positive cocci and rods. As plaque matures and gingivitis develops, the communities become increasingly complex with higher proportions of Gram-negative rods, fusiforms, filaments, spirilla and spirochetes. Later experimental gingivitis studies, using culture, provided more information regarding the specific bacterial species present in plaque. Taxa associated with gingivitis included Fusobacterium nucleatum subspecies polymorphum, Lachnospiraceae [G-2] species HOT100, Lautropia species HOTA94, and Prevotella oulorum (a species of Prevotella bacterium), whilst Rothia dentocariosa was associated with periodontal health. Further study of these taxa is warranted and may lead to new therapeutic approaches to prevent periodontal disease. Risk factors
Risk factors associated with gingivitis include the following:

age
osteoporosis
low dental care utilization
poor oral hygiene
overly aggressive oral hygiene such as brushing with stiff bristles
mouth breathing during sleep
Orthodontic braces
medications and conditions that dry the mouth
cigarette smoking
genetic factors
stress
mental health issues such as depression
pre-existing conditions such as diabetes

Diagnosis
Gingivitis is a category of periodontal disease in which there is no loss of bone but inflammation and bleeding are present. Each tooth is divided into four gingival units (mesial, distal, buccal, and lingual) and given a score from 0–3 based on the gingival index. The four scores are then averaged to give each tooth a single score. The diagnosis of the periodontal disease gingivitis is done by a dentist. The diagnosis is based on clinical assessment data acquired during a comprehensive periodontal exam.
Isolated neutropenia in infants can occur in viral infections, autoimmune neutropenia of infancy, bone marrow suppression from a drug or toxin, hypersplenism, and passive placental transfer of maternal IgG.A bone marrow test can assist in diagnosis. The bone marrow usually shows early granulocyte precursors, but myelopoietic development stops ("arrests") at the promyelocyte and/or myelocyte stage, so that few maturing forms are seen. Neutrophil survival is normal. Treatment
Regular administration of exogenous granulocyte colony-stimulating factor (filgrastim) clinically improves neutrophil counts and immune function and is the mainstay of therapy, although this may increase risk for myelofibrosis and acute myeloid leukemia in the long term.Over 90% of SCN responds to treatment with granulocyte colony-stimulating factor (filgrastim), which has significantly improved survival. See also
Neutropenia
Cyclic neutropenia
GATA2 deficiency

References
Klein, Christoph (2011). "Genetic Defects in Severe Congenital Neutropenia: Emerging Insights into Life and Death of Human Neutrophil Granulocytes". Annual Review of Immunology. 29: 399–413. doi:10.1146/annurev-immunol-030409-101259. PMID 21219176. Further reading
Deotare UR, Patel PD, Parikh RP, Bhagat EA (January 2012). "Uncommon cause of recurrent infections". Indian J Med Paediatr Oncol. 33 (1): 51–3. doi:10.4103/0971-5851.96971. PMC 3385280. PMID 22754210. External links
Search for Neutropenia to see on-going projects at Orphanet
Severe Congenital Neutropenia (SCN) of Inherited Bone Marrow Failure Syndromes (IBMFS)
Severe congenital neutropenia at NIHs Office of Rare Diseases