Clinical AV Bone Flashcards
(15 cards)
What is alveolar bone homeostasis, and why is it critical for maintaining periodontal health?
Alveolar bone homeostasis refers to the balance between bone formation and resorption. It is essential for maintaining the integrity of the periodontium, supporting teeth, and preventing bone loss associated with periodontal disease.
What are the primary cellular components involved in alveolar bone remodeling?
Osteoblasts (bone formation), Osteoclasts (bone resorption), Osteocytes (mechanosensory and regulatory functions), Progenitor cells (precursors for osteoblasts and osteoclasts).
Describe the role of RANK, RANKL, and OPG in the regulation of bone resorption in the alveolar bone.
RANK: Receptor on osteoclast precursors, activated by RANKL to promote osteoclast differentiation. RANKL: Ligand expressed by osteoblasts and stromal cells, stimulates osteoclast activity. OPG: Decoy receptor produced by osteoblasts, binds RANKL to inhibit osteoclast formation.
How does inflammation influence alveolar bone resorption in periodontal disease?
Inflammatory cytokines (e.g., IL-1, TNF-α) upregulate RANKL expression. Increased RANKL binding to RANK enhances osteoclastogenesis, leading to bone resorption.
What systemic conditions can impact alveolar bone homeostasis, and how do they affect bone metabolism?
Diabetes: Impairs bone healing and increases inflammation, promoting bone loss. Osteoporosis: Decreases bone density and accelerates alveolar bone resorption. Hormonal imbalances: Estrogen deficiency increases RANKL expression, leading to greater resorption.
What is the significance of mechanical loading in the maintenance of alveolar bone density?
Mechanical loading stimulates osteoblast activity and bone formation. Lack of mechanical loading (e.g., tooth loss) leads to bone resorption due to decreased mechanical stress.
How do bisphosphonates work in preventing alveolar bone loss, and what are potential risks?
Bisphosphonates inhibit osteoclast activity and bone resorption. Risks: Osteonecrosis of the jaw (ONJ), particularly after invasive dental procedures.
Explain how PTH (Parathyroid Hormone) affects alveolar bone remodeling.
PTH at low, intermittent doses promotes bone formation by stimulating osteoblasts. Chronic elevation of PTH enhances RANKL expression, increasing bone resorption.
What are common clinical signs of alveolar bone loss associated with periodontal disease?
Increased probing depth, Tooth mobility, Radiographic evidence of bone loss, Gingival recession and attachment loss.
How does smoking impact alveolar bone homeostasis and periodontal health?
Smoking reduces blood flow and impairs immune function. Increases oxidative stress, leading to greater bone resorption and delayed healing.
Describe the process of osteoclast differentiation and activation in the context of alveolar bone resorption.
RANKL binds to RANK on osteoclast precursors. NF-κB pathway activation promotes osteoclastogenesis. Osteoclasts adhere to the bone surface and form a ruffled border to secrete resorptive enzymes.
What are the implications of implant placement on alveolar bone homeostasis?
Implants distribute mechanical forces to surrounding bone. Proper osseointegration prevents bone resorption; however, peri-implantitis can lead to bone loss.
How do cytokines IL-1 and TNF-α specifically contribute to alveolar bone resorption in periodontitis?
Both cytokines increase RANKL expression and suppress OPG production. Promote osteoclast differentiation and bone matrix degradation.
What diagnostic tools are used to assess alveolar bone loss in clinical practice?
Probing depth measurements, Radiographs (e.g., periapical, panoramic), Cone beam computed tomography (CBCT) for 3D imaging, Biomarker analysis (e.g., RANKL/OPG ratio in gingival crevicular fluid).
How does the alveolar bone respond to tooth extraction, and what preventive measures can be taken to minimize bone loss?
Alveolar bone undergoes rapid resorption post-extraction due to loss of mechanical loading. Preventive measures: Socket preservation grafts, immediate implant placement, and guided bone regeneration.
