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Host Modulation Therapy (HMT)
Used in addition to scaling and root planing (SP) and surgery.
Modifies or reduces destructive aspects and upregulates protective aspects of the host response
Adjunctive approach to conventional periodontal therapy targeting the patient’s immune-inflammatory response, which drives tissue breakdown
purpose of Host Modulation Therapy (HMT)
aims to reduce excessive inflammation
enhance wound healing
periodontal stability
Risk Factors of Host Modulation Therapy (HMT)
Addresses factors that adversely affect host response (e.g., smoking, diabetes, genetic susceptibility)
addresses the host side of the host-bacterial interaction, ameliorates excessive inflammatory processes to enhance wound healing and periodontal stability
drug classes that evaluated as HMTs:
NSAIDs
bisphosphonates
tetracyclines
enamel matrix proteins
growth factors
BMPs
comprehensive management of host modulation therapy
patient education
bacterial reduction (SP)
site-specific antibacterial treatment
risk factor modification
surgery if needed.
Host Modulation Therapy (HMT) Agents
NSAIDs
Bisphosphonates
sub-antimicrobial-dose doxycycline (SDD)
NSAIDs
Systemic use can significantly slow alveolar bone loss.
Inhibit Prostaglandin E2 (PGE2), which upregulates bone resorption
Stopping it may cause a “rebound effect” with accelerated bone loss
Not indicated as adjunctive HMT due to serious side effects and the need for long-term daily use.
risk of NSAIDs
GI problems
hemorrhage
higher fragility of bone
—due to daily use for up to 3 years showed benefits however these can be an effect
Bisphosphonates
inhibits osteoclast activity, shown to enhance alveolar bone status in studies.
bone-seeking agents that inhibit bone resorption by disrupting osteoclast activity.
not approved for periodontal disease; discouraged due to risk primarily with intravenous use
risk of bisphosphonates
osteonecrosis of the jaws (ONJ)
sub-antimicrobial-dose doxycycline (SDD)
must not be used as monotherapy
can be combined with local antimicrobial delivery systems
acts via MMP (MMP-8 and MMP-9) inhibition, enzyme, cytokine reduction, osteoblast stimulation—not an antibiotic effect
only FDA-approved systemically administered HMT adjunct to SRP for chronic periodontitis
MMP → matrix metalloproteinases
ex: Periostat
indications of sub-antimicrobial-dose doxycycline (SDD)
for chronic and aggressive periodontitis as adjunct to SRP
useful in refractory cases and high-risk patients (smokers, diabetics, osteoporotic, genetically susceptible)
contraindications of sub-antimicrobial-dose doxycycline (SDD)
allergy to tetracycline
pregnancy / lactation
children <12 yeats
disadvantage: may reduce efficacy of oral contraceptives
benefits of sub-antimicrobial-dose doxycycline (SDD)
gains in attachment
reduced probing depth
stimulates osteoblasts
no resistance risk at 20mg dose
effective even in high-risk patients (e.g., smokers)
dosage of sub-antimicrobial-dose doxycycline (SDD)
20mg BID for 3–9 months → first round of SRP
SDD + local delivery (atridox) + SRP
demonstrated >2mm improvement in attachment gains and probing depth reductions vs SRP alone (p<0.0001) in a 6-month, 180 patient trial
Locally Administered HMTs
Used as adjuncts to surgical procedures to stimulate regeneration
Topical NSAIDs have not been approved
examples of FDA-approved Locally Administered HMTs
Enamel Matrix Proteins (Emdogain)
Recombinant human platelet-derived growth factor-BB (GEM 215)
Bone Morphogenetic Proteins (rhBMP-2 / INFUSE)
Osseointegration
clinically defined as asymptomatic rigid fixation
direct structural and functional connection between living bone and implant surface without soft tissue.
initial healing of osseointegration
Mirrors bone fracture repair
Immobility: Movement greater than 150 μm prevents osteoblast differentiation → fibrous scar tissue → nonintegration
Temperature: Bone necrosis occurs if overheating during drilling exceeds 47°C for 1 minute.
Bone Maturation
Steady remodeling state reached after ~18 months
Progresses from fast-growing, poorly mineralized woven bone to slow-growing, dense lamellar bone.
Primary stability (placement) of osseointegration
depends on implant geometry and bone quantity/quality.
Secondary stability (over time) of osseointegration
depends on implant surface and percentage of bone contact.
peri-implant soft tissues
includes oral epithelium, sulcular epithelium, a sulcus, long junctional epithelial attachment, and underlying connective tissue — similar to teeth
Implants
Bone is in direct contact with the implant
lack a periodontal ligament (PDL), cementum, and Sharpey’s fibers.
Long junctional epithelium
attaches to titanium via basal lamina and hemidesmosomes.
Peri-implant “Biologic Width”
Combined height of epithelial attachment and supracrestal connective tissue
~3–4 mm or 4–4.5 mm
Connective Tissue Fibers
Cannot insert into the implant surface.
Run mostly parallel or in a cuff-like circular orientation, forming a soft tissue “seal.”
Keratinized Tissue
Not required for long-term success.
may cause pain or discomfort during oral hygiene due to mobility of nonkeratinized mucosa.
Vascular Supply
Scarcer than around teeth; no contribution from PDL.
Peri-implant tissues respond to plaque with inflammation similar to periodontal tissues
probe stops in healthy tissue
~1.5 mm coronal to alveolar crest (above the bone)
Clinical Consequences (Teeth vs. Implants)
Lack of Resiliency:
Implants lack a PDL, so they are rigidly attached and cannot move to compensate for occlusal disharmony.
Overload can cause microfractures and bone loss.
Growth:
Implants placed before growth completion will not migrate or erupt with natural teeth.
Can lead to occlusal problems; therefore, contraindicated in growing patients.
Maintenance:
Long-term success requires meticulous plaque control.
Frequent maintenance visits are recommended (e.g., every 3–4 months).
comprehensive periodontal management
patient education & oral hygiene
high-quality SRP + local delivery
host modulation (SDD)
risk factor modification
surgery + HMT if indicated