Periodontal Pathogenesis and Host Response Flashcards

Which cytokines are the principal mediators of osteoclast-driven bone resorption in periodontal disease?

Answer: IL-1β and TNF-α

IL-1β and TNF-α are the dominant pro-inflammatory cytokines that upregulate RANKL expression and directly stimulate osteoclastogenesis, driving alveolar bone loss in periodontitis.

As the periodontal lesion progresses from gingivitis to chronic periodontitis, the predominant infiltrating immune cell transitions through which sequence?

Answer: Neutrophils → T lymphocytes → B cells and plasma cells

Per Page and Schroeder's staging, the initial/early lesions are dominated by neutrophils and T lymphocytes, while the established/advanced lesion is characterized by B cells and plasma cells as the primary infiltrate.

RANKL contributes to alveolar bone destruction in periodontitis primarily by:

Answer: Activating osteoclast precursor differentiation and osteoclast resorptive activity

RANKL binds to RANK on osteoclast precursors, triggering their differentiation into mature osteoclasts and activating their bone-resorbing capacity, a process blocked by the decoy receptor osteoprotegerin (OPG).

In active periodontal disease sites, the RANKL-to-OPG ratio is:

Answer: Increased, tipping the balance toward net bone resorption

Periodontitis sites show elevated RANKL and suppressed OPG production from PDL fibroblasts and osteoblasts, resulting in a high RANKL:OPG ratio that favors osteoclastogenesis and bone loss.

Matrix metalloproteinases (MMPs) contribute to periodontal tissue destruction primarily by:

Answer: Degrading extracellular matrix components including type I and III collagen

MMPs, particularly MMP-1, -2, -8, and -13, cleave fibrillar collagens and other ECM proteins in the periodontal ligament and connective tissue, irreversibly destroying the structural attachment apparatus.

Which complement activation pathway is primarily triggered by bacterial lipopolysaccharide (LPS) present in the periodontal pocket?

Answer: Alternative pathway via spontaneous C3 hydrolysis amplified by LPS

LPS from gram-negative periodontal pathogens preferentially activates the alternative complement pathway through C3 tickover, and P. gingivalis gingipains further dysregulate complement to evade its effector functions.

Prostaglandin E2 (PGE2) contributes to periodontal bone destruction primarily through:

Answer: Enhancement of RANKL expression and osteoclast activation

PGE2, produced in large quantities at inflamed periodontal sites, upregulates RANKL on stromal cells and osteoblasts while suppressing OPG, creating an environment that strongly favors osteoclastogenesis and bone loss.