Bone Disease, Osteoarthritis, Rheumatoid Arthritis Flashcards
Describe the key components of bone extracellular matrix (ECM) and their functions.
- Collagen: Provides flexibility and tensile strength
- Calcium compounds (hydroxyapatite): Provides rigidity and compression strength
- Phosphate compounds: Works with calcium to form mineral crystals
Explain the roles of the three main types of bone cells and their relationships to each other.
- Osteoblasts: Build bone by producing ECM
- Osteocytes: Mature osteoblasts that become entrapped within the ECM; they regulate bone mass through mechanosensing and signaling
- Osteoclasts: Responsible for bone resorption, breaking down bone tissue as part of the remodeling process. These cells work in concert to maintain healthy bone turnover.
Describe the complete hormonal regulation of bone metabolism, including the actions and sources of each hormone.
1.Parathyroid hormone (PTH)
- Source: Parathyroid gland
- Action: Increases blood calcium by stimulating osteoclasts to release calcium from bone
2.Calcitonin
- Source: Thyroid gland
- Action: Decreases blood calcium by inhibiting osteoclast activity
3.Vitamin D
- Source: Either ingested or synthesized from UV radiation + cholesterol
- Action: Increases blood calcium by enhancing calcium absorption in intestines and kidneys
Explain the pathophysiology of osteoporosis and its relationship to bone remodeling.
Osteoporosis develops through:
- An imbalance between osteoclast and osteoblast activity, where resorption exceeds formation
- Progressive reduction in bone density
- Deterioration of structural integrity
- Results in increased risk of fragility fractures (fractures from low-level trauma)
- Peak bone mass occurs around age 30, followed by gradual loss
- Post-menopausal women experience faster decline due to loss of protective effects of estrogen
What are fragility fractures?
a fracture which results from low level trauma (fall from standing height or less)
*Vertebral
*Wrist
*Hip
*Pelvis
What are risk factors of osteoporosis?
- Older age
- Female
- Post-menopause
- Vitamin D deficiency
- Poor dietary calcium intake
- Long-term corticosteroid use
- Lack of physical activity
- Smoking and alcohol
- Family history of osteoporosis
- Low body mass index (BMI)
Describe the complete diagnostic approach for osteoporosis and explain how each component works.
two components
Assessment Tools:
QFracture tool or FRAX tool
Predicts 10-year risk of osteoporotic fracture
Takes into account multiple risk factors
DEXA Scan:
Uses dual-energy X-ray absorptiometry
Calculates bone mineral density
Compares results to healthy young person’s bone density
Provides objective measurement of bone loss
Explain the comprehensive management approach for osteoporosis, including both pharmacological and non-pharmacological interventions.
Lifestyle Measures:
- Smoking cessation and alcohol reduction
- Weight-bearing physical activity
- Optimizing dietary intake
- Vitamin D and calcium supplementation
Medical Interventions:
- Hormone replacement therapy (HRT) in appropriate cases
- Bisphosphonates (1st line)
- Denosumab (2nd line)
Compare and contrast bisphosphonates and denosumab in terms of their mechanisms, administration, and considerations.
Bisphosphonates:
- Mechanism: Inhibit osteoclast formation and activity
- Administration: Daily/weekly tablet or annual IV infusion
- Half-life: Up to 10 years
- Examples: Alendronic acid, risedronate sodium, zoledronic acid
Denosumab:
- Mechanism: Monoclonal antibody targeting RANKL, preventing osteoclast activation
- Administration: Subcutaneous injection every 6 months
- Different mechanism but similar end result of reducing bone resorption
What can osteoporosis medication cause?
What should dentists do regarding this
impaired bone healing after injury
*E.g. dental extraction, dental implant placement
Medication-related osteonecrosis of the jaw (MRONJ)
- Complete any treatment before starting medication
- Preventative advice
- Consider treatment which avoids extraction (e.g. retaining roots
Compare the pathophysiology and characteristics of osteoarthritis to normal joint function.
In osteoarthritis:
Affects synovial joints (inflammation of joint)
Usually unilateral
Involves imbalance between cartilage damage and repair
Results in:
Loss of cartilage
Remodeling of bone
Structural changes within joint
Typically affects weight-bearing joints
Pain characteristics: Worse with activity, improves with rest, worse in evening
Explain the comprehensive clinical presentation and diagnostic approach for osteoarthritis.
Clinical Presentation:
- Pain pattern: Worsens with activity, improves with rest, worse in evening
- Joint stiffness
- Crepitus
- Functional loss
- Mild joint swelling
- Potential deformity
Diagnosis based on:
- History and physical examination
- Radiographic findings
- Risk factors include:
- Advanced age
- Sports injuries
- Previous Trauma
- Family history
How is osteoarthritis managed?
- Lifestyle – weight loss, therapeutic exercise, physiotherapy (aim to strengthen muscles around joint)
- Adjuncts – walking aids
- Topical NSAIDs
- Oral NSAIDs (plus proton pump inhibitor to protect stomach)
- Intra-articular steroid injections
- Surgical – joint replacement
What are the dental implications of osteoarthritis?
- Impaired oral hygiene - if affecting hands/upper limbs
- NSAIDs use - antiplatelet effect (COX inhibition)
- Access to care
- TMJ involvement
Describe the complex pathogenesis of rheumatoid arthritis and its systemic manifestations.
- Unknown initial trigger
- Inflammatory cell infiltration of synovium (T cells, macrophages, B cells, neutrophils)
- Production of rheumatoid factor (RF) and anti-CCP antibodies
- Formation of pannus
- Bone and cartilage erosion
Extra-articular manifestations (~40% of cases):
- Fever and fatigue
- Rheumatoid nodules
- Pulmonary fibrosis
- Sjögren’s syndrome
- Increased cardiovascular disease risk
- Anemia of chronic disease
What is rheumatoid arthritis and what joints does it affect?
chronic inflammation of synovial lining
small joints symmetrically (MCP, PIP joints)
What are risk factors for rheumatoid arthritis?
- Female
- Middle age (younger than OA)
- Smoking
- Family history
What are the symptoms of rheumatoid arthritis?
- Pain – improves with activity, worse in morning
- Swelling – more prominent than in OA
- Symmetrical, small joints (e.g. hands, wrists and feet)
- Heat
- Stiffness in morning
- Deformity
- Fatigue
How is RA diagnosed?
- Imaging – radiograph, ultrasound, MRI
- Blood test – RF and/or anti-CCP antibodies
Explain the comprehensive treatment approach for RA, including mechanisms and side effects of major drug classes.
NSAIDs:
For symptom relief
Side effect: Antiplatelet effect
Prednisolone:
Mechanism: Potent anti-inflammatory/immunosuppressant
Effects: Reduces vasodilation, capillary permeability, inflammatory cytokines, WBC migration
Side effects: Adrenal suppression, osteoporosis, hyperglycemia, hypertension, delayed wound healing
DMARDs:
Hydroxychloroquine:
Mechanism: Inhibits antigen presenting cells
Side effects: Retinopathy, oral pigmentation
Methotrexate:
Mechanism: Inhibits folate pathway
Side effects: Oral ulcers, bone marrow suppression
Biologics:
Specific targeting of inflammatory cascade elements
Examples: Infliximab, Adalimumab (TNF inhibitors), Rituximab (CD20 inhibitor)
Side effects: Immunosuppression, infection risk, skin cancer risk
What is adrenal suppression?
- Prolonged / large doses of corticosteroids
- Lead to suppression of natural HPA axis
- Therefore need to carefully wean off steroids
What are the dental implications of RA?
Disability from disease
* Oral hygiene, impaired dexterity
* Access to care
Extra-articular manifestations
* (Secondary) Sjögren’s syndrome
Medications
* NSAIDs – antiplatelet effect
* Hydroxychloroquine – oral pigmentation
* Methotrexate – oral ulceration
* Biologics – immunosuppression, skin cancer
* Bisphosphonates if also on corticosteroids - MRONJ
Periodontal disease
* Bidirectional link
* Porphymonas gingivalis
Create a detailed comparison between osteoarthritis and rheumatoid arthritis across all major clinical parameters.
Age of Onset:
OA: >50 years
RA: 30-50 years
Onset Speed:
OA: Gradual
RA: Rapid
Pathogenesis:
OA: Cartilage damage/repair imbalance
RA: Autoimmune inflammatory mechanism
Pain Pattern:
OA: Worse during/after activity
RA: Worse in morning, improves with activity
Joint Involvement:
OA: 1-2 weight-bearing joints, unilateral
RA: Multiple small joints, symmetrical
Swelling:
OA: Mild, hard, bony
RA: Soft, warm, “boggy”
Systemic Features:
OA: None
RA: Multiple extra-articular manifestations
Lab Findings:
OA: Normal blood tests
RA: Elevated RF and/or anti-CCP antibodies
Treatment Approach:
OA: Limited medical management, eventual joint replacement
RA: Aggressive medical management, rarely needs replacement
