Non-inflammatory destructive periodontal disease: a clinical, microbiological, immunological and genetic investigation

Abstract

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.

Plaque‐induced gingivitis: Case definition and diagnostic considerations

“…[8][9][10][11][12][13] In contrast, sites with no or minimal progression of attachment loss over time were characterized by the consistent absence of gingival inflammation over time. 12,[14][15][16][17][18] Overall, these observations suggest that effective long-term control of gingivitis could prevent progressive attachment loss. 13 The established relationship between gingival inflammation and periodontitis calls for the need to establish the clinical criteria that define a gingivitis case (GC).…”

HLA Haplotypes and Genotypes Frequencies in Brazilian Chronic Periodontitis Patients

“…According to previous reports, and in agreement with our results, HLA-DRB1 ∗ 04 was associated with risk to CP [ 38 , 39 ] and aggressive periodontitis [ 9 , 12 , 23 , 30 ], as well as their alleles [ 8 , 30 ]. DRB1 ∗ 04:04 was considered a risk factor for bone loss [ 30 , 40 ]. Contrarily, in a recent investigation, HLA-DRB1 ∗ 04 or HLA-DRB1 ∗ 04/DRB4 ∗ (DR53)/DQB1 ∗ 03:02 haplotype had a decreased colonization risk of Aggregatibacter actinomycetemcomitans [ 9 ].…”

Evidenced‐Based Criteria for Differential Treatment Planning of Implant Restorations for the Partially Edentulous Patient

“…While the level of evidence to link periodontitis to implant failure is not weak, periodontitis is one of a group of multifactorial diseases in which pathogens trigger host chronic inflammatory and immune responses. As genetic typing becomes more mainstream, controlled studies may in fact be able to predict which subset of periodontal patients may be most at risk for implant failure …”