Other names
Types
Causes
Symptoms and everyday effects
Diagnostic tests
Non-pharmacological treatments (therapies & others)
Drug treatments
Dietary molecular supplements
Immunity-booster / Regenerative / Stem-cell” drugs
Surgeries (procedures and why they are done)
When to see doctors/dentists
What to eat and what to avoid
Frequently asked questions

Selective tooth agenesis-5 (often shortened to STHAG5) is a genetic form of “missing teeth from birth.” In this condition, one or more permanent teeth never form during early development. Wisdom teeth are not counted when doctors measure the problem. STHAG5 points to a mapped spot on chromosome 10q11–q21 linked to tooth agenesis; the exact causal gene at this locus has not yet been firmly identified. Clinically, STHAG5 looks like nonsyndromic hypodontia/oligodontia (missing a few teeth or many teeth) without other medical problems. Researchers group STHAG5 with other “selective tooth agenesis” types that are numbered (STHAG1, STHAG3, STHAG4, etc.) by gene or chromosomal region. onlinelibrary.wiley.com+1

Selective Tooth Agenesis-5 (STHAG5) is a genetic condition where some permanent teeth never form. People may be born missing one tooth or many teeth (often front incisors, premolars, or second premolars), while other teeth are normal. Baby teeth may be present but can be lost normally with no permanent replacements underneath. “Selective” means only certain teeth are missing; the jaws and other body systems are usually normal. STHAG5 has been linked to changes in a gene that helps control the Wnt signaling pathway (often LRP6), which guides tooth bud formation. It is different from teeth lost by decay or trauma—here the teeth never develop at all. The condition can affect chewing, speech, facial appearance, bite balance, and self-confidence, but it can be managed well with modern dentistry. (Evidence: genetic reviews on nonsyndromic tooth agenesis and Wnt/LRP6; AAPD/AO restorative and orthodontic care guidelines.)

During early face and jaw development, tooth buds need precise signals to start, grow, and form enamel/dentin. If a key signal (like Wnt) is weaker or mistimed because of a gene variant (e.g., LRP6, WNT10A, AXIN2, MSX1, PAX9 in other subtypes), some buds never start. That is why certain teeth are absent while others are fine. (Evidence: dental development and Wnt-pathway literature; reviews of hypodontia genes.)

To understand STHAG5, it helps to know the broader picture: selective tooth agenesis is common (if third molars are included, up to ~20% of people have some missing tooth), and many cases are genetic. Several genes are already proven in related types (for example MSX1, PAX9, WNT10A, AXIN2, LRP6, WNT10B, EDA, GREM2, TSPEAR), while STHAG5 remains a mapped locus with ongoing gene discovery. scielo.isciii.es+1

Other names

Selective tooth agenesis-5
STHAG5
Tooth agenesis linked to 10q11–q21 (nonsyndromic)
A mapped locus of nonsyndromic hypodontia/oligodontia at 10q
These terms all refer to the same diagnostic “bucket”: congenital absence of specific permanent teeth due to a locus at 10q11–q21, with no consistent extra-oral features. onlinelibrary.wiley.com

Types

Doctors classify selective tooth agenesis by how many permanent teeth (excluding wisdom teeth) are missing:

Hypodontia – fewer than six teeth missing.
Oligodontia – six or more teeth missing.
Anodontia – all teeth missing (rare; usually syndromic and not typical for STHAG5).

STHAG5 usually presents as hypodontia or oligodontia. These definitions are standard across the tooth agenesis literature. scielo.sa.cr+1

Causes

Because STHAG5 is a mapped chromosomal region rather than a single confirmed gene, the “causes” below explain the likely mechanisms for STHAG5 and the well-proven causes of closely related selective tooth agenesis types. Together they show how this condition arises.

A DNA change (variant) at 10q11–q21 that affects tooth formation
STHAG5 designates a region on chromosome 10 associated with missing teeth. A pathogenic change here may disrupt a gene or its regulatory switches needed for early tooth bud formation. onlinelibrary.wiley.com
Polygenic effects (more than one gene)
Selective tooth agenesis can reflect the combined impact of multiple small-effect variants; STHAG5 might modify risk together with changes in known tooth genes (e.g., MSX1, PAX9, WNT10A). NCBI
Disruption of tooth-patterning genes (MSX1, PAX9) in the family background
Even if the main signal maps to 10q (STHAG5), background variants in MSX1 and PAX9—classic tooth-patterning genes—can influence which teeth fail to form. Wikipedia
WNT signaling imbalance
WNT pathways guide tooth initiation and shape. Variants in WNT genes (e.g., WNT10A in STHAG4, WNT10B in STHAG8) are proven causes of selective tooth agenesis; a 10q factor in STHAG5 may intersect these same pathways. PMC+1
Recessive or semidominant inheritance with reduced penetrance
Some tooth agenesis genes show semidominant behavior: one variant gives a mild pattern; two variants give many missing teeth. Penetrance can be incomplete, so relatives may carry a variant but have normal teeth. NCBI
Regulatory (noncoding) variants
Changes in enhancers/switches near the causal 10q gene could silence normal tooth-development programs without altering the protein code itself. (This mechanism is common in developmental disorders.) sciencedirect.com
Copy-number changes (small deletions/duplications) at 10q
A small deletion or duplication within 10q11–q21 could remove or duplicate a critical segment, disturbing gene dosage and tooth bud initiation. NCBI
Modifier genes that change which teeth are most vulnerable
Studies show specific teeth (e.g., upper lateral incisors, second premolars) are often missing; modifiers help explain these patterns, even within the same family. Nature
Gene–gene interaction between WNT and EDA pathways
Cross-talk between WNT10A and EDA signaling influences ectodermal organ development (teeth, hair, glands). Interactions can magnify tooth agenesis risk. PLOS
Ethnic and population risk alleles
Certain populations carry common variants that increase risk (for example, the WNT10A p.Phe228Ile variant is relatively frequent globally and modifies tooth patterns, illustrating how common alleles can shape risk). NCBI
De novo variants
A new change can appear in the child even if parents are unaffected, a known pattern in developmental dental anomalies. sciencedirect.com
Epigenetic influences
Chromatin and methylation changes during craniofacial morphogenesis may alter expression of tooth genes within the 10q region. sciencedirect.com
Gene–environment interaction
Environmental stressors can amplify effects of borderline genetic variants—helping explain variable expressivity within families. scielo.isciii.es
In-utero exposures that perturb early ectoderm
Severe systemic illness, certain medications, or radiation in early pregnancy can disturb tooth lamina formation in genetically susceptible fetuses (not a primary cause of STHAG5, but can worsen outcomes). scielo.isciii.es
Cleft-related developmental pathways
Genes shared between clefting and tooth agenesis (e.g., WNT and MSX1 networks) show how facial patterning and tooth absence can co-occur in some families. SpringerLink
AXIN2 pathway changes
AXIN2 variants are a recognized cause of selective tooth agenesis; background AXIN2 status may shape the STHAG5 phenotype.
LRP6 receptor pathway changes
LRP6 (STHAG7) acts in WNT signaling; variants cause nonsyndromic oligodontia and illustrate how core WNT receptors influence tooth count. NCBI
WNT10B pathway differences
WNT10B (STHAG8) causes a tooth-loss pattern distinct from WNT10A. Such locus-specific patterns suggest STHAG5 may have its own signature once the exact gene is confirmed. NCBI
GREM2 (BMP antagonist) variation
GREM2 (STHAG9) affects BMP–WNT balance crucial for tooth initiation; background variation may modulate STHAG5 expression. NCBI
TSPEAR variants
TSPEAR (STHAG10) is another nonsyndromic hypodontia gene; awareness of this spectrum helps clinicians interpret gene panels when STHAG5 is suspected but not molecularly solved. NCBI

Symptoms and everyday effects

Some permanent teeth never erupt
Children or teens simply never develop specific permanent teeth (often laterals or premolars), while baby teeth may persist longer. scielo.isciii.es
Spacing and gaps
Spaces appear where teeth are missing, changing smile lines and food flow during chewing. scielo.isciii.es
Delayed eruption or altered sequence
Present teeth may erupt later than peers, and the normal order can shift. PMC
Small or peg-shaped teeth near the gaps
Teeth next to missing ones can be smaller or conical because the same pathways shape size and number. scielo.isciii.es
Malocclusion (bite problems)
Missing anchors change the bite, sometimes causing over-eruption of opposing teeth or midline shifts. scielo.isciii.es
Chewing inefficiency
Less contact area makes certain foods harder to process, which can nudge diet choices. scielo.isciii.es
Speech differences
S-, F-, and V-sounds may change when anterior teeth are absent. scielo.isciii.es
Aesthetic concerns and self-confidence issues
Visible gaps—especially in the front—can affect social confidence in school-age years. scielo.isciii.es
Prolonged retention of baby teeth
Deciduous teeth may remain for years if no permanent successor exists, then loosen or resorb unpredictably. scielo.isciii.es
Short roots or taurodontism in some families
Tooth-formation genes also influence root architecture, so short roots or enlarged pulp chambers can be seen. jpccr.eu
Altered dental age
Dental maturity may be delayed compared with chronological age in WNT-pathway tooth agenesis; this affects treatment timing. PMC
Shifting or tipping of neighboring teeth
Adjacent teeth may drift into empty spaces, complicating later orthodontics or implant placement. scielo.isciii.es
Plaque trapping and caries risk in unusual sites
Gaps and tooth shape changes create new niches for plaque until hygiene is adapted. scielo.isciii.es
Periodontal stress in remaining teeth
Fewer teeth share the load, which can increase functional stress on existing teeth over time. scielo.isciii.es
Family recurrence
Multiple relatives may have similar tooth patterns (variable expressivity), consistent with a genetic basis. NCBI

Diagnostic tests

A) Physical examination

Comprehensive intra-oral exam
The dentist counts teeth, records which ones are missing, and notes shape/size changes. This basic step defines the phenotype. scielo.isciii.es
Dental charting and tooth numbering
Teeth are mapped using a standard numbering system to compare with age-expected eruption charts. scielo.isciii.es
Assessment of eruption and dental age
Clinicians compare observed eruption to age norms; in WNT-pathway cases, dental age can be delayed. PMC
Facial and occlusal evaluation
Overbite/overjet, midlines, and vertical dimension are recorded to plan orthodontic or prosthetic care. scielo.isciii.es
Screen for subtle ectodermal features
Even in nonsyndromic cases, clinicians look at hair, nails, and skin to rule out ectodermal dysplasias that share pathways with tooth agenesis. PMC

B) Manual / chairside functional tests

Space analysis with calipers (arch length vs. tooth size)
Manual measurements predict whether orthodontics can close spaces or if prosthetic replacement is needed. scielo.isciii.es
Occlusal contact mapping (articulating paper/wax)
Marks show where teeth meet (or don’t), guiding bite correction plans. scielo.isciii.es
Study models (alginate or digital impressions)
Physical or digital casts help visualize space, simulate tooth movement, and plan implants/bridges. scielo.isciii.es
Percussion/mobility checks of retained baby teeth
Tapping and gentle movement help decide if a retained deciduous tooth is stable for near-term function. scielo.isciii.es

C) Laboratory & pathological/genetic tests

Targeted nonsyndromic tooth agenesis gene panel
Sequencing covers known genes (MSX1, PAX9, AXIN2, LRP6, WNT10A, WNT10B, EDA, GREM2, TSPEAR). A negative result with a family pattern supports a mapped-locus diagnosis like STHAG5. NCBI
Sanger sequencing for family segregation
When a variant is found, relatives can be tested to see if it tracks with missing teeth patterns. NCBI
Copy-number analysis (array CGH or NGS-CNV) around 10q11–q21
Detects small deletions/duplications that could explain STHAG5. NCBI
Single-gene reflex testing when phenotype suggests a gene
For example, if the pattern strongly suggests WNT10A or PAX9, reflex full-gene sequencing may be done; this helps rule in other STHAG types. NCBI
Genetic counseling session and documented pedigree
A three-generation family tree clarifies inheritance, penetrance, and recurrence risk. NCBI

D) Electrodiagnostic tests

Electric pulp testing (EPT)
Although not required to diagnose agenesis, EPT helps assess vitality of adjacent teeth before orthodontics or prosthetics. scielo.isciii.es
Bite-force measurement (chairside electronic gauges)
In selected cases, recording bite force helps plan occlusal rehabilitation when many teeth are missing. scielo.isciii.es
Quantitative sensory testing for oral function (selected cases)
If there are complaints of altered sensation from malocclusion changes, basic sensory tests can document baseline before treatment. scielo.isciii.es

E) Imaging tests

Panoramic radiograph (OPG)
The most useful first image: it shows tooth buds, unerupted teeth, root shape/length, and confirms true agenesis. scielo.isciii.es
Periapical radiographs
Close-up images assess retained baby teeth, root form, and alveolar bone near gaps. scielo.isciii.es
Bitewings
Helpful for posterior spacing and caries surveillance when occlusion is altered. scielo.isciii.es
Cone-beam CT (CBCT)
Three-dimensional planning for implants or guided orthodontics, and evaluation of bone volume where teeth are missing. scielo.isciii.es
Cephalometric radiograph
Assesses skeletal relationships and growth—important when deciding timing of orthodontic space closure versus prosthetic replacement. scielo.isciii.es
Intraoral and extraoral photography
Documents baseline appearance and assists with aesthetic planning and outcome tracking. scielo.isciii.es
Digital smile design imaging (simulation)
Planned restorations can be previewed to align expectations and guide multidisciplinary care. scielo.isciii.es

Non-pharmacological treatments (therapies & others)

Note: There is no approved medicine that makes a new adult tooth bud appear. Care focuses on prevention, growth-aware orthodontics, and prosthetic/implant rehabilitation. (Evidence: AAPD guidelines; orthodontic and prosthodontic consensus statements.)

Early dental assessment and growth-aware care plan
Description: A first visit in early childhood (by age 1–2, then regular checks) confirms which teeth are missing using exam and X-rays. Teams map out timing for baby tooth retention, space maintenance, and when to consider braces, adhesive restorations, or implants after growth. Parents learn brushing, fluoride use, and injury prevention. Purpose: Prevent avoidable decay, protect existing teeth, and plan the bite and smile as the child grows. Mechanism: Continuous monitoring + radiographs guide decisions on when to keep or close spaces and how to stage orthodontics and prosthetics safely. (Evidence: AAPD periodicity schedule; hypodontia care pathways.)
Fluoride hygiene program (toothpaste/varnish; professional cleanings)
Description: Regular brushing with fluoride toothpaste (twice daily) and professional cleanings reduce cavities around the fewer existing teeth, which must do more chewing work. High-risk patients may receive fluoride varnish applications at the clinic. Purpose: Keep the remaining teeth strong to avoid extra tooth loss. Mechanism: Fluoride strengthens enamel by forming fluorapatite and slowing demineralization; it also promotes remineralization of early white-spot lesions. (Evidence: caries prevention guidelines; AAPD fluoride recommendations.)
Fissure sealants on at-risk molars
Description: Clear or tooth-colored resin is flowed into deep grooves of molars to “seal” them from plaque acids. Purpose: Prevent decay on chewing surfaces in a dentition where each tooth is precious. Mechanism: Physical barrier blocks food/bacteria; reduces demineralization. (Evidence: Cochrane reviews on sealants; prevention guidelines.)
Dietary counseling for low-sugar, tooth-protective habits
Description: Counsel on limiting sugary snacks/drinks and frequent grazing. Promote water and balanced meals with calcium, vitamin D, and protein. Purpose: Reduce caries risk, protect enamel, and support bone health for future implants or orthodontics. Mechanism: Less sugar exposure lowers acid attacks; adequate nutrients support enamel and bone metabolism. (Evidence: caries risk management (CAMBRA) concepts; bone health nutrition statements.)
Space maintenance (band-and-loop, lingual arch, etc.)
Description: If a baby tooth is lost early where no adult successor exists, a small appliance holds the space to prevent neighboring teeth drifting. Purpose: Preserve room for future prosthetic tooth or orthodontic movement. Mechanism: Passive wire/band transfers chewing forces while maintaining arch length/width. (Evidence: AAPD space maintenance guideline.)
Composite resin build-ups/edge bonding for shape and symmetry
Description: Tooth-colored composite can widen small (“peg”) laterals or reshape teeth to improve appearance and contact points. Purpose: Cosmetic balance; functional contacts for proper bite and phonetics. Mechanism: Micromechanical bonding to enamel/dentin; layered composite mimics natural tooth. (Evidence: adhesive dentistry reviews.)
Adhesive resin-bonded bridges (“Maryland” bridges)
Description: A ceramic/metal wing attaches to the back of an adjacent tooth to hold a small false tooth with minimal drilling. Purpose: Interim or definitive replacement of a missing incisor/premolar when implants are delayed due to growth. Mechanism: Acid-etch/adhesive bonding; conservative retention via wings. (Evidence: prosthodontic consensus on resin-bonded prostheses.)
Removable partial dentures (RPDs) for growing patients
Description: Lightweight acrylic plates with prosthetic teeth replace multiple missing teeth and can be adjusted as the child grows. Purpose: Restore chewing, speech, smile, and support lip/cheek contours during growth years. Mechanism: Mechanical retention on remaining teeth/soft tissue; adjustable base/flange. (Evidence: pediatric prosthodontics texts; hypodontia management reviews.)
Orthodontic space closure (camouflage)
Description: Braces or clear aligners close spaces by moving neighboring teeth into agenesis areas (e.g., moving canine into lateral incisor position and reshaping it). Purpose: Achieve tooth symmetry without prosthetics in selected cases. Mechanism: Controlled tooth movement through bone remodeling (pressure/tension sides) guided by brackets/aligners and elastics. (Evidence: orthodontic literature on space closure for congenitally missing laterals.)
Orthodontic space opening and root parallelism for future implants
Description: Where an ideal tooth must be replaced, orthodontics re-opens/holds space and tips roots parallel to create safe implant sites. Purpose: Prepare precise mesiodistal and vertical dimensions for implant placement after growth. Mechanism: Biologic tooth movement with careful anchorage and 3-D control. (Evidence: interdisciplinary ortho-implant guidelines.)
Digital smile design and 3-D guided planning
Description: Photos, scans, and CBCT imaging allow virtual wax-ups and surgical/prosthetic guides. Purpose: Predictable esthetics and implant/prosthesis positioning with less guesswork. Mechanism: CAD/CAM planning translates planned tooth positions to surgical and restorative steps. (Evidence: digital dentistry consensus papers.)
Alveolar ridge preservation (socket grafting) when extractions are needed
Description: If a compromised tooth must be removed, the socket is gently grafted and covered to limit bone shrinkage, keeping options open. Purpose: Maintain volume for future implant or bridge pontic. Mechanism: Bone graft/biomaterial acts as scaffold while natural bone fills the socket. (Evidence: ridge preservation RCTs and systematic reviews.)
Guided bone regeneration (GBR) before implants
Description: When bone is thin, particulate grafts and a barrier membrane rebuild width/height. Purpose: Create a stable site for long-term implant success and emergence profile. Mechanism: Membrane excludes soft tissue; osteogenesis/osteoconduction fill the defect. (Evidence: GBR systematic reviews.)
Soft-tissue grafting and pink-esthetics management
Description: Connective tissue grafts or soft-tissue substitutes increase keratinized tissue and contour. Purpose: Healthier peri-implant/abutment tissues and natural gingival profile. Mechanism: Grafts increase tissue thickness and blood supply; better seal around teeth/implants. (Evidence: periodontal plastic surgery literature.)
Tooth autotransplantation (selected cases)
Description: A developing premolar or third molar is transplanted into an agenesis site (e.g., replacing a missing incisor), often in teens. Purpose: Biological tooth with PDL that remodels and erupts. Mechanism: Viable periodontal ligament cells on the root enable reattachment and continued development. (Evidence: autotransplantation cohort studies and reviews.)
Occlusal therapy and splints when bite is imbalanced
Description: Custom night guards or occlusal adjustments protect teeth from grinding/clenching that may concentrate forces on fewer teeth. Purpose: Reduce wear, fractures, and TMJ strain. Mechanism: Appliance redistributes load; neuromuscular deprogramming may reduce parafunction. (Evidence: occlusal therapy guidelines.)
Speech therapy support if anterior gaps affect sounds
Description: Collaboration with a speech-language pathologist can improve “s,” “z,” and certain labiodental sounds impacted by missing incisors. Purpose: Clearer speech and confidence. Mechanism: Targeted articulation exercises and compensatory placements. (Evidence: speech therapy best practices.)
Psychosocial support and shared decision-making
Description: Counseling and expectations management for children/teens and families. Purpose: Reduce stigma, support adherence to multi-year plans. Mechanism: Motivational interviewing and realistic timelines improve outcomes. (Evidence: pediatric patient-reported outcome literature.)
Long-term maintenance program
Description: 3–6-month recalls, hygiene reinforcement, prosthesis checks, and occlusion reviews. Purpose: Keep the system healthy for life. Mechanism: Early detection of caries, gingivitis, chipping, or screw loosening. (Evidence: maintenance guidelines for prosthodontics/implants.)
Definitive dental implants (post-growth) and ceramic restorations
Description: After facial growth completes (late teens/early adulthood), implants can replace missing teeth with crowns/bridges. Purpose: Durable, esthetic, and functional rehabilitation. Mechanism: Osseointegration (titanium bonds with bone); ceramic crowns restore form/function. (Evidence: implant consensus statements; timing after growth completion.)

Drug treatments

Important truth first: There are no FDA-approved drugs that make new adult teeth form in STHAG5. Medicines are used around dental care—for pain control, infection management, oral hygiene, sedation, and procedure support. Below are commonly used, evidence-based options with FDA labeling for their general dental uses. Doses are typical adult ranges unless noted; individual dosing depends on age, weight, kidney/liver function, interactions, and clinician judgment. Always follow your dentist/physician’s instructions. (Evidence: FDA package inserts; AAPD/American Dental Association guidance.)

Ibuprofen (NSAID)
Class: NSAID. Dosage/Time: 200–400 mg every 6–8 h PRN (max per label); pediatric weight-based dosing. Purpose: First-line dental pain and inflammation control after procedures. Mechanism: COX-1/COX-2 inhibition lowers prostaglandins → analgesic/anti-inflammatory effect. Side effects: Stomach upset, bleeding risk, kidney effects; avoid in certain GI/renal states. (Evidence: FDA label for ibuprofen; ADA analgesic guidance.)
Acetaminophen (paracetamol)
Class: Analgesic/antipyretic. Dosage/Time: 500–1,000 mg every 6–8 h (do not exceed daily max on label). Purpose: Pain control; can be combined with NSAIDs. Mechanism: Central prostaglandin modulation. Side effects: Liver toxicity if overdosed or with heavy alcohol use. (Evidence: FDA label for acetaminophen; ADA guidance.)
Ibuprofen + Acetaminophen (alternating or together per clinician)
Class: Non-opioid combination. Dosage/Time: Staggered or combined per instructions. Purpose: Superior dental pain relief vs opioids in many trials. Mechanism: Peripheral + central pathways. Side effects: As above; adhere to maximum daily doses. (Evidence: ADA dental pain recommendations; comparative trials.)
Amoxicillin
Class: Penicillin antibiotic. Dosage/Time: Typical 500 mg every 8 h for acute odontogenic infections per clinical judgment. Purpose: Treat bacterial dental infections when indicated. Mechanism: Inhibits bacterial cell-wall synthesis. Side effects: Allergy, GI upset, rash. (Evidence: FDA label for amoxicillin; dental infection guidance.)
Amoxicillin–Clavulanate
Class: Beta-lactam + beta-lactamase inhibitor. Use: Broader coverage in select infections. Mechanism: Cell-wall inhibition + enzyme blocker. Side effects: GI upset, diarrhea, allergy. (Evidence: FDA label; antimicrobial stewardship guidance.)
Azithromycin (for penicillin-allergic patients when appropriate)
Class: Macrolide. Purpose: Alternative for certain infections or prophylaxis indications. Mechanism: Inhibits bacterial protein synthesis (50S). Side effects: GI upset, QT prolongation risk. (Evidence: FDA label; ADA antibiotic stewardship.)
Clindamycin
Class: Lincosamide. Use: Select alternative; rising C. difficile risk → use cautiously. Mechanism: 50S ribosomal inhibition. Side effects: Diarrhea, C. difficile colitis risk. (Evidence: FDA label; ADA cautions.)
Metronidazole
Class: Nitroimidazole. Use: Anaerobic coverage as adjunct in specific infections. Mechanism: DNA strand breakage in anaerobes. Side effects: Metallic taste, disulfiram-like reaction with alcohol. (Evidence: FDA label; dental infection protocols.)
Chlorhexidine gluconate 0.12% oral rinse
Class: Antiseptic rinse (Rx). Dosage/Time: Rinse 15 mL for 30 s twice daily, short courses. Purpose: Reduce plaque/gingivitis, improve healing around surgeries. Mechanism: Binds bacterial membranes, broad antimicrobial effect. Side effects: Tooth/tongue staining, taste alteration. (Evidence: FDA/monograph labeling; periodontal guidelines.)
Sodium fluoride varnish (e.g., 5% NaF) or high-fluoride toothpaste
Class: Topical fluoride (varnish Rx; toothpaste OTC/Rx strengths). Purpose: Caries prevention for remaining teeth. Mechanism: Remineralization, acid resistance. Side effects: Rare if used as directed; avoid swallowing. (Evidence: FDA OTC monograph for fluoride dentifrices; AAPD fluoride guidance.)
Topical anesthetics (benzocaine or lidocaine gels)
Class: Local anesthetic topical. Purpose: Numbing of mucosa before injections or minor procedures. Mechanism: Blocks sodium channels in nerve endings. Side effects: Benzocaine: rare methemoglobinemia caution; lidocaine: numbness/biting risk if over-used. (Evidence: FDA labels; safety communications.)
Lidocaine with epinephrine (local anesthetic injection)
Class: Amide anesthetic + vasoconstrictor. Purpose: Profound local pain control. Mechanism: Sodium channel blockade; epinephrine prolongs action and reduces bleeding. Side effects: Tachycardia if intravascular; dose limits exist. (Evidence: FDA label for lidocaine/epi.)
Articaine with epinephrine (local anesthetic)
Class: Amide anesthetic (thiophene ring) + vasoconstrictor. Purpose: Infiltration with excellent bone penetration for restorative/implant stages. Mechanism: Sodium channel blockade. Side effects: Paresthesia risk debated; follow dose limits. (Evidence: FDA label for articaine/epi.)
Dexamethasone (peri-operative anti-inflammatory, Rx)
Class: Corticosteroid. Purpose: Reduce post-op swelling and trismus after surgeries/grafts. Mechanism: Inhibits inflammatory gene transcription. Side effects: Transient hyperglycemia, immunomodulation. (Evidence: FDA label; oral surgery RCTs.)
Tranexamic acid (mouthrinse or systemic in select bleeding-risk patients)
Class: Antifibrinolytic. Purpose: Help control post-op bleeding in anticoagulated patients per physician protocol. Mechanism: Blocks plasminogen activation. Side effects: Thrombosis risk if misused; use under medical guidance. (Evidence: FDA label; dental anticoagulation protocols.)
Nitrous oxide/oxygen inhalation (conscious sedation)
Class: Inhaled anxiolytic/analgesic for minimal sedation. Purpose: Anxiety control for prolonged procedures. Mechanism: CNS modulation; rapid on/off. Side effects: Nausea; avoid in certain sinus/ear conditions. (Evidence: FDA device gas labeling; sedation guidelines.)
Midazolam (oral/intranasal/IV) for procedural sedation (specialist use)
Class: Benzodiazepine. Purpose: Anxiolysis/sedation in pediatric or anxious patients by trained providers. Mechanism: GABA-A modulation. Side effects: Respiratory depression; requires monitoring and reversal plan. (Evidence: FDA label; sedation standards.)
Amoxicillin prophylaxis (only for select cardiac indications)
Class: Antibiotic. Purpose: Endocarditis prophylaxis per AHA in a small subset of cardiac conditions. Mechanism: Bactericidal vs oral streptococci. Side effects: Allergy, GI upset. (Evidence: FDA label; AHA/ADA endocarditis prophylaxis guideline.)
Hydrogen peroxide 1.5% OTC rinse (short-term use)
Class: Antiseptic oral rinse. Purpose: Temporary debridement/gingival inflammation relief. Mechanism: Oxidative cleansing and effervescence. Side effects: Mucosal irritation with overuse. (Evidence: FDA OTC monograph.)
Opioid-sparing policy (avoid routine opioids)
Class: Stewardship approach (not a drug). Purpose: Prefer non-opioids (ibuprofen+acetaminophen) which work as well or better for dental pain and reduce harm. Mechanism: Evidence-based analgesic synergy. Side effects: Fewer opioid-related adverse events. (Evidence: ADA 2018+ statements; comparative trials; FDA safety communications.)

Dietary molecular supplements

Supplements may support oral and bone health but do not create new teeth. Discuss with your clinician, especially for children, pregnancy, kidney disease, or when on medicines.

Vitamin D3 – helps calcium absorption and bone metabolism; deficiency is common and linked with caries risk. Typical adult 1,000–2,000 IU/day; tailor to serum 25-OH-D levels. (Evidence: endocrine/odontology reviews.)
Calcium (diet first, supplement if needed) – 1,000–1,200 mg/day total intake supports jawbone; split dosing enhances absorption. (Evidence: bone health guidelines.)
Phosphorus – partner mineral in hydroxyapatite; aim for balanced intake via diet (protein, dairy, legumes). Excess cola phosphoric acid is not helpful. (Evidence: nutrition texts.)
Magnesium – cofactor in bone/mineral metabolism; diet-first (nuts/greens); supplement only if low. (Evidence: bone mineral literature.)
Vitamin K2 (MK-7) – supports carboxylation of bone proteins (e.g., osteocalcin); emerging adjunct evidence; discuss if on anticoagulants. (Evidence: bone metabolism reviews.)
Vitamin A (retinol/beta-carotene) – needed for epithelial health; avoid excess in pregnancy; prefer colorful vegetables. (Evidence: nutrition/teratology guidance.)
Zinc – supports wound healing and immunity; excessive zinc can impair copper status. (Evidence: micronutrient reviews.)
Folate/B12 (if deficient) – supports cell turnover; check levels before supplementing. (Evidence: hematologic/epithelial health data.)
Collagen peptides/adequate protein – provides amino acids for connective tissue/soft-tissue healing after grafts. (Evidence: wound-healing nutrition.)
Omega-3 fatty acids (EPA/DHA) – anti-inflammatory adjunct for periodontal health; food sources preferred. (Evidence: periodontal adjunct literature.)

(Each statement draws from standard nutrition/bone/periodontal reviews and clinical consensus.)

Immunity-booster / Regenerative / Stem-cell” drugs

There are no FDA-approved regenerative or stem-cell drugs to create new teeth in STHAG5. The items below are research directions only; they are not clinical treatments you can (or should) take today.

Wnt-pathway agonists (experimental) – Aim: stimulate tooth bud formation/regrowth; Risk: off-target effects (tumorigenesis). Not approved. (Evidence: preclinical odontogenesis studies.)
BMPs (bone morphogenetic proteins) locally for bone—not teeth – Used experimentally/under strict indications to regenerate bone, not to create teeth. Not for routine pediatric use. (Evidence: surgical literature; FDA label for specific BMP devices has strict indications/warnings.)
FGF/SHH signaling modulators (experimental) – Concept: rescue initiation stages; no approved dental bud therapy. (Evidence: developmental biology research.)
Dental pulp stem cells (DPSC) / stem cell-based bio-roots (experimental) – Tissue engineering for future tooth-like structures; clinical reality is years away. (Evidence: tissue-engineering reviews.)
Gene therapy (LRP6/WNT10A correction) (experimental) – Conceptual precision therapy; not available. (Evidence: gene-editing research in craniofacial development.)
Scaffold-based whole-tooth organ engineering (experimental) – Lab-grown tooth germs; not clinical. (Evidence: organ engineering reviews.)

(Clear disclosure: research-only; no approved dosing. Follow clinical dentistry solutions listed above.)

Surgeries (procedures and why they are done)

Dental implant placement (after growth completion) – Titanium implant placed in healed/grafted bone to carry a crown. Why: permanent, natural-looking replacement with high long-term success. (Evidence: implant consensus.)
Guided bone regeneration (GBR) – Bone graft + membrane to widen/thicken the ridge before/with implants. Why: create sufficient bone volume and ideal prosthetic position. (Evidence: GBR systematic reviews.)
Sinus floor elevation (posterior maxilla) – Lift sinus membrane and place graft to gain vertical height for molar/premolar implants. Why: safe implant length/stability. (Evidence: sinus lift reviews.)
Block bone grafting / ridge augmentation – Autogenous or allogeneic blocks fixed to deficient ridge. Why: rebuild major defects for esthetic zone implants. (Evidence: augmentation literature.)
Tooth autotransplantation – Move a suitable donor tooth (often a developing premolar) into an agenesis site. Why: provide living tooth with PDL in selected growing patients. (Evidence: autotransplantation cohorts.)

Preventions

You cannot “prevent” a genetic tooth from being absent, but you can prevent extra problems.

Early dental visit and periodic X-rays to plan.
Daily fluoride toothpaste; professional fluoride if high risk.
Limit sugary snacks/drinks; water is default beverage.
Use sealants on deep grooves of molars.
Protect teeth during sports (mouthguard).
Do not smoke or vape; avoid secondhand smoke exposure.
During pregnancy: prenatal care, avoid retinoid excess and smoking/alcohol.
Keep gums healthy (brushing, interdental cleaning).
Manage grinding with splints if needed.
Keep all recall/prosthesis checks so small problems are fixed early. (Evidence: prevention and caries-risk management guidelines; general prenatal and tobacco health guidance.)

When to see doctors/dentists

If a child’s baby front teeth fall out and no permanent tooth erupts after the normal window.
If spaces widen, teeth drift/tilt, or bite feels “off.”
If chewing, speech, or confidence is affected by gaps.
Before adolescence to plan braces and eventual tooth replacement timing.
If pain, swelling, or gum bleeding develops around prostheses or adjacent teeth.
Before planning implants: to confirm growth completion and bone readiness. (Evidence: pediatric eruption charts; orthodontic/implant planning guidance.)

What to eat and what to avoid

Eat more of:

Water; milk or fortified alternatives (calcium + vitamin D).
Chewy but tooth-friendly proteins (eggs, fish, beans, yogurt).
Leafy greens, nuts/seeds (magnesium, K).
High-fiber fruits/vegetables (saliva flow).
Whole grains; balanced meals, not constant snacking.

Avoid/limit:

Sugary drinks/juices/sports drinks; frequent candies.
Sticky sweets (toffee/caramel) that cling to teeth.
Constant grazing—give teeth rest between exposures.
High-acid drinks (soda, energy drinks); if used, rinse with water.
Tobacco/alcohol (adolescents/adults). (Evidence: caries and erosion prevention literature; nutrition guidance.)

Frequently asked questions

Can a medicine make a missing adult tooth grow?
No. There is no approved drug that creates a new tooth. Care uses orthodontics and prosthetics, with implants after growth. (Evidence: clinical consensus.)
Is STHAG5 the same as losing a tooth from decay?
No. In agenesis the tooth never formed; decay/trauma remove formed teeth. (Evidence: developmental dentistry.)
Will my child outgrow this?
No new teeth form later. Planning early helps achieve a great, stable smile. (Evidence: eruption biology.)
What age is best for implants?
Usually after facial growth finishes (late teen years); earlier placement risks infraocclusion/misalignment as the jaws grow. (Evidence: implant timing consensus.)
Can braces close all spaces so I need no prosthetic?
Sometimes, yes—especially missing lateral incisors. Your orthodontist will assess bite/face symmetry. (Evidence: orthodontic literature.)
Are adhesive bridges strong?
They can last years, especially with good bite design and enamel bonding, and are conservative. (Evidence: resin-bonded bridge studies.)
What if bone is too thin for an implant?
GBR or grafting can rebuild bone; digital planning helps. (Evidence: GBR reviews.)
Will missing teeth harm speech?
Anterior gaps can affect certain sounds; speech therapy and restorations help. (Evidence: speech literature.)
Are RPDs only temporary?
They can be interim during growth or definitive if implants are not desired/possible. (Evidence: prosthodontic guidance.)
Do I need antibiotics for every dental procedure?
No. Antibiotics treat infections when indicated; prophylaxis is only for specific heart conditions. (Evidence: ADA/AHA guidelines.)
Are opioids necessary after dental surgery?
Usually not; ibuprofen ± acetaminophen works as well or better. (Evidence: ADA statements; clinical trials.)
Do supplements regrow teeth?
No, but adequate vitamin D/calcium/protein supports bone and soft-tissue health. (Evidence: nutrition/bone health literature.)
Is autotransplantation safe?
In selected cases and skilled hands, yes, with good long-term outcomes. (Evidence: cohort studies.)
Will implants look natural?
With careful planning and soft-tissue management, results can be highly esthetic. (Evidence: prosthetic/implant outcomes.)
How often should I follow up?
Typically every 3–6 months during active phases; at least twice per year for hygiene/maintenance. (Evidence: maintenance guidelines.)

Disclaimer: Each person’s journey is unique, treatment plan, life style, food habit, hormonal condition, immune system, chronic disease condition, geological location, weather and previous medical history is also unique. So always seek the best advice from a qualified medical professional or health care provider before trying any treatments to ensure to find out the best plan for you. This guide is for general information and educational purposes only. Regular check-ups and awareness can help to manage and prevent complications associated with these diseases conditions. If you or someone are suffering from this disease condition bookmark this website or share with someone who might find it useful! Boost your knowledge and stay ahead in your health journey. We always try to ensure that the content is regularly updated to reflect the latest medical research and treatment options. Thank you for giving your valuable time to read the article.

The article is written by Team RxHarun and reviewed by the Rx Editorial Board Members

Last Updated: November 01, 2025.

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Selective Tooth Agenesis-5 (STHAG5)