Macrophage Inflammatory Protein‐1α: A Salivary Biomarker of Bone Loss in a Longitudinal Cohort Study of Children at Risk for Aggressive Periodontal Disease?

Fine, Daniel H.; Markowitz, Kenneth; Furgang, David; Fairlie, Karen; Ferrandiz, Javier; Nasri, Cebile; McKiernan, Marie; Donnelly, Robert; Gunsolley, John C.

doi:10.1902/jop.2009.080296

Cited by 84 publications

(81 citation statements)

References 41 publications

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“…Both assent and consent were received from each student's parent(s) or guardian(s) prior to participation. The initial screening visit was performed in a mobile dental van and consisted of a full oral and dental examination, review of medical and dental histories, and collection of saliva and buccal epithelial cells (BECs) from each subject as described previously (5,22). Subjects were excluded if they required prophylactic antibiotics, had any bleeding disorder, were otherwise medically vulnerable, or if they had extensive dental caries as defined by decayed, missing, or filled surfaces (23).…”

Section: Methodsmentioning

confidence: 99%

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A Consortium of Aggregatibacter actinomycetemcomitans, Streptococcus parasanguinis, and Filifactor alocis Is Present in Sites Prior to Bone Loss in a Longitudinal Study of Localized Aggressive Periodontitis

et al. 2013

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c Aggregatibacter actinomycetemcomitans-induced localized aggressive periodontitis (LAP) in African-American adolescents has been documented but is poorly understood. Two thousand fifty-eight adolescents aged 11 to 17 years were screened for their periodontal status and the presence of A. actinomycetemcomitans in their oral cavity. Seventy-one A. actinomycetemcomitansnegative and 63 A. actinomycetemcomitans-positive periodontally healthy subjects were enrolled, sampled, examined, and radiographed yearly for 3 years. Gingival and periodontal pocket depth and attachment levels were recorded. Disease presentation was characterized by bone loss (BL). Subgingival sites were sampled every 6 months to assess (i) the role of A. actinomycetemcomitans in BL and (ii) the association of A. actinomycetemcomitans and other microbes in their relationships to BL. Sixteen of 63 subjects with A. actinomycetemcomitans developed BL (the other 47 subjects with A. actinomycetemcomitans had no BL). No A. actinomycetemcomitans-negative subjects developed BL. Human oral microbe identification microarray (HOMIM) was used for subgingival microbial assessment. On a subject level, pooled data from A. actinomycetemcomitans-positive subjects who remained healthy had higher prevalences of Streptococcus and Actinomyces species, while A. actinomycetemcomitans-positive subjects with BL had higher prevalences of Parvimonas micra, Filifactor alocis, A. actinomycetemcomitans, and Peptostreptococcus sp. human oral taxon 113 (HOT-113). At vulnerable sites, A. actinomycetemcomitans, Streptococcus parasanguinis, and F. alocis levels were elevated prior to BL. In cases where the three-organism consortium (versus A. actinomycetemcomitans alone) was detected, the specificity for detecting sites of future BL increased from 62% to 99%, with a sensitivity of 89%. We conclude that detecting the presence of A. actinomycetemcomitans, S. parasanguinis, and F. alocis together indicates sites of future BL in LAP. A synergistic interaction of this consortium in LAP causation is possible and is the subject of ongoing research.

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Section: Methodsmentioning

confidence: 99%

“…After collecting buccal cells and saliva, a full periodontal examination was performed, and plaque and crevice fluid were collected from each of the four first molars (5,22). The periodontal examination consisted of soft tissue measurements of pocket depth and attachment-level recordings.…”

Section: Methodsmentioning

confidence: 99%

A Consortium of Aggregatibacter actinomycetemcomitans, Streptococcus parasanguinis, and Filifactor alocis Is Present in Sites Prior to Bone Loss in a Longitudinal Study of Localized Aggressive Periodontitis

et al. 2013

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“…Elevation of salivary macrophage inflammatory protein-1␣, a chemokine that recruits osteoclast progenitors, was suggested as a biomarker of early events in inflammatory-induced periodontal bone loss that precedes radiographic evidence in carriers of Aggregatibacter actinomycetemcomitans, an oral commensal that can cause severe infections in the periodontium (59).…”

Section: Poor Oral Health As a Source Of Inflammationmentioning

confidence: 99%

Systemic Consequences of Poor Oral Health in Chronic Kidney Disease Patients

Akar

Carrero

et al. 2011

Clinical Journal of the American Society of Nephrology

168

136

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SummaryChanges in the oral cavity, such as periodontitis and other manifestations of poor oral health, are common in patients with chronic kidney disease (CKD) and may contribute to increased morbidity and mortality because of systemic consequences such as inflammation, infections, protein-energy wasting, and atherosclerotic complications. Poor oral health in CKD patients may thus represent an important, but often overlooked, problem. Several studies show that uremic patients have higher rates of decayed, missing, and filled teeth, loss of attachment, and periapical and mucosal lesions than the general population. The consequences of poor oral health may be more severe in CKD patients because of advanced age, common comorbidities such as diabetes, concurrent medications, and a state of immune dysfunction that may increase the risk for systemic consequences of periodontitis and other oral and dental pathologic conditions. Poor dentition and other signs of poor oral health should be an alarm clock also at early stages of CKD. However, it remains to be determined whether more successful management of poor oral health and periodontitis will reduce the risk of inflammation, infection, protein-energy wasting, and atherosclerotic complications in CKD patients. This review explores etiological factors and potential systemic consequences of poor oral health in CKD patients as well as possible preventive and therapeutic strategies.

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“…The level of β-glucuronidase, which signals the influx of neutrophils, was confirmed in correlation with the increasing severity of periodontitis (28). Similarly, this correlation was confirmed in IL-1β, an important pro-inflammatory cytokine that is the predominant form of periodontitis (two forms: IL-1 alpha and IL-1 beta) and also in TNF-α (7,8,48). The newly identified anti-inflammatory interleukin IL-35, which is a member of the IL-12 family, is secreted by regulatory T-cells and suppresses the inflammatory response of immune cells.…”

Section: Markers Of Inflammationmentioning

confidence: 57%

“…To date, major gene mutations, which result in the periodontitis phenotype in otherwise systemically healthy 7 individuals, have not been identified and no specific genetic risk factor for the disease has been identified. The aim of the test is to determine several relatively common high-risk polymorphisms, that may mean cumulative high susceptibility genetic profile (47).…”

Section: Gene Polymorphism In Periodontitismentioning

confidence: 99%

Trends in Laboratory Diagnostic Methods in Periodontology

Bolerázska

Mareková

Markovská

2016

Acta Med. (Hradec Kralove, Czech Repub.)

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Summary: This work presents a summary of current knowledge on the laboratory diagnosis of periodontitis. It focuses on the theoretical foundations and is supplemented with new knowledge. It subsequently describes specifically the laboratory diagnosis methods of periodontitis: the protein expression of inflammation, oral microbiology and molecular diagnostics. Periodontitis is a serious disease worldwide and its confirmed association with systemic diseases means its severity is increasing. Its laboratory diagnosis has the potential to rise to the level of clinical and diagnostic imaging. The transfer of diagnostic methods from laboratory to clinical use is increasingly used in the prevention and monitoring of the exacerbation and treatment of periodontal disease, as well as of its impact on systemic disease.

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Macrophage Inflammatory Protein‐1α: A Salivary Biomarker of Bone Loss in a Longitudinal Cohort Study of Children at Risk for Aggressive Periodontal Disease?

Abstract: The superior sensitivity and specificity of MIP-1alpha, which correlated well with probing depths and the onset of bone loss, suggested that it could be used as an early biomarker for LAgP.

Cited by 84 publications

References 41 publications

A Consortium of Aggregatibacter actinomycetemcomitans, Streptococcus parasanguinis, and Filifactor alocis Is Present in Sites Prior to Bone Loss in a Longitudinal Study of Localized Aggressive Periodontitis

A Consortium of Aggregatibacter actinomycetemcomitans, Streptococcus parasanguinis, and Filifactor alocis Is Present in Sites Prior to Bone Loss in a Longitudinal Study of Localized Aggressive Periodontitis

Systemic Consequences of Poor Oral Health in Chronic Kidney Disease Patients

Trends in Laboratory Diagnostic Methods in Periodontology

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