What are the local and systemic implications of third molar retention?
OBJECTIVE
To establish a relationship between visible third molars (M3s) and increased periodontal probing depths on teeth other than M3s and to examine the hypothesis that the presence of M3s and/or increased probing depths and local inflammation associated with M3s was associated with increased levels of serum inflammatory markers.


METHODS
The data from three previous population studies (Dental Atherosclerosis Risk In Communities [DARIC], Oral Conditions and Pregnancy [OCAP], and National Health and Nutrition Estimates Study [NHANES III]) and the third molar clinical trials of young adults (White et al) are summarized. A secondary analysis determined whether the presence or absence of visible M3s was associated with an increased prevalence of clinical signs of periodontal disease using adjusted logistic regression models. In addition, serum samples collected from the OCAP, DARIC, and White studies were used to measure the markers of systemic inflammation, C-reactive protein, interleukin-6, and soluble intracellular adhesion molecule-1.


RESULTS
In young adults, asymptomatic M3s were associated with an increase in periodontal probing depths of at least 4 mm on second molars and an increase in probing depth of at least 2 mm in 24% of subjects after 2 years. Retention of asymptomatic M3s for 6 years led to a significant increase in the number of subjects with a probing depth of 4 mm or more in non-M3 regions of the mouth. Findings from the DARIC, OCAP, and NHANES III further confirmed the association between the M3 probing depth and periodontal inflammation on non-M3s. Retention of M3s in the presence of periodontal inflammation was associated with significant increases in the serum interleukin-6, soluble intracellular adhesion molecule-1, and C-reactive protein levels.


CONCLUSIONS
Patients deciding to retain M3s should consider the potential long-term effects on their periodontal status and the potential for the retained M3s to serve as a chronic source of inflammation that stresses their systemic health.
Department of Periodontology, University of North Carolina School of Dentistry, Chapel Hill, NC 27599-7450, USA. steve_offenbacher@dentistry.unc.edu
Steven
S
Offenbacher
James D
JD
Beck
Kevin L
KL
Moss
Silvana
S
Barros
Luis
L
Mendoza
Raymond P
RP
White
D000210:Acute-Phase Reaction / Q000097:blood; D000293:Adolescent; D000328:Adult; D000368:Aged; D050197:Atherosclerosis / Q000209:etiology; D002097:C-Reactive Protein / Q000032:analysis; D002908:Chronic Disease; D005260:Female; D006304:Health Status; D006801:Humans; D007249:Inflammation; D018836:Inflammation Mediators / Q000097:blood*; D018799:Intercellular Adhesion Molecule-1 / Q000097:blood; D015850:Interleukin-6 / Q000097:blood; D008875:Middle Aged; D008964:Molar, Third / Q000473:pathology*; D010510:Periodontal Diseases / Q000209:etiology* / Q000382:microbiology; D010512:Periodontal Index; D011247:Pregnancy; D011248:Pregnancy Complications; D014095:Tooth, Impacted / Q000150:complications*; D055815:Young Adult
D018836:Inflammation Mediators; D015850:Interleukin-6; D018799:Intercellular Adhesion Molecule-1; D002097:C-Reactive Protein