Periodontitis comprises a group of multifactorial diseases in which
periodontopathogens accumulate in dental plaque and trigger host chronic inflammatory
and immune responses against periodontal structures, which are determinant to the
disease outcome. Although unusual cases of non-inflammatory destructive periodontal
disease (NIDPD) are described, their pathogenesis remains unknown. A unique NIDPD
case was investigated by clinical, microbiological, immunological and genetic tools.
The patient, a non-smoking dental surgeon with excessive oral hygiene practice,
presented a generalized bone resorption and tooth mobility, but not gingival
inflammation or occlusion problems. No hematological, immunological or endocrine
alterations were found. No periodontopathogens (A. actinomycetemcomitans, P.
gingivalis, F. nucleatum and T. denticola) or viruses
(HCMV, EBV-1 and HSV-1) were detected, along with levels of IL-1β and TNF-α in GCF
compatible with healthy tissues. Conversely ALP, ACP and RANKL GCF levels were
similar to diseased periodontal sites. Genetic investigation demonstrated that the
patient carried some SNPs, as well HLA-DR4 (*0404) and HLA-B27 alleles, considered
risk factors for bone loss. Then, a less vigorous and diminished frequency of
toothbrushing was recommended to the patient, resulting in the arrest of alveolar
bone loss, associated with the return of ALP, ACP and RANKL in GCF to normality
levels. In conclusion, the unusual case presented here is compatible with the
previous description of NIDPD, and the results that a possible combination of
excessive force and frequency of mechanical stimulation with a potentially bone loss
prone genotype could result in the alveolar bone loss seen in NIDPD.