Dental implants have a strong track record, yet the rumor persists that they inevitably cause gums to recede. I hear it from new patients every month, often from someone whose friend had a crown that looked longer over time and assumed the implant was to blame. The truth is more nuanced. Implants do not inherently cause gum recession. Tissue changes around implants happen for specific reasons, some preventable and some rooted in biology. When treatment is planned with the same rigor a structural engineer brings to a bridge, the pink and white esthetics can remain stable for years, even decades.
This piece unpacks where the myth comes from, what actually drives soft-tissue loss around implants, and how design decisions, surgical technique, maintenance, and patient habits shape outcomes. I will also flag where implants differ from natural teeth, because that is where misunderstandings often begin.
Where the myth came from
Gum recession around natural teeth is common. Thin biotypes, aggressive brushing, orthodontic movement, lip or frenum pulls, and chronic inflammation from plaque can all lower the gum line. When a person later gets an implant in the same mouth, ongoing recession gets blamed on the new device. Another source is comparison. On a central incisor, a half millimeter of tissue change reads as a longer tooth in photos and mirrors. If the implant crown emerges from a thicker porcelain collar than its neighbor, the discrepancy feels like recession even if the gum margin barely moved.
Early implant dentistry added fuel. In the 1990s and early 2000s, immediate implant placement was less common, platform switching had not yet become standard, and soft-tissue grafting around implants was not routine. Some cases healed with marginal tissue changes. Those stories lingered. Modern protocols, better surfaces, and a more conservative philosophy have measurably improved soft-tissue stability.
Teeth and implants are not the same, and that matters
A natural tooth is suspended by the periodontal ligament, a shock absorber that also hosts blood vessels and nerve fibers. Collagen fibers from the ligament insert into the root cementum, splaying outward like guy wires that help maintain the crest of the bone. The gingival fibers interdigitate with this system. When plaque-induced inflammation flares, the ligament responds with increased blood flow and immune activity. It is dynamic tissue.
An implant has no periodontal ligament. Osseointegration means bone grows directly onto the titanium or zirconia surface. The gum fibers around an implant run parallel to the surface rather than inserting into it. Blood supply is slightly less robust at the implant collar than around a tooth. This difference does not doom the gum, but it does change the rules. Stable bone height is crucial. The design of the abutment and crown, down to fractions of a millimeter, influences how the tissue drapes, seals, and resists micro-movements that can trigger remodeling.
Understanding this anatomy is central to preventing recession. If you try to treat an implant like a tooth, you set yourself up for disappointment.
What actually causes gum recession around implants
Recession is rarely a single-cause issue. The final picture tends to be a blend of site biology, surgical technique, prosthetic design, and behavior over time. The most common contributors I see are:
- Thin tissue biotype with poor volume. When the gum is naturally thin and scalloped, even subtle bone remodeling telegraphs as a drop in the margin or a translucent shine-through of titanium. Buccal bone deficiency or dehiscence. If the outer wall of bone is missing or too thin, the gum above it lacks a scaffold and recedes. This is the fastest way to an exposed abutment or a long-looking crown. Excessive implant diameter or mispositioning. Pushing a wide implant too facially to chase primary stability compresses the buccal plate and leads to collapse later. Depth errors follow the same pattern. Too shallow, and the implant-abutment junction sits near the gum margin, which invites inflammation and recession. Microgap and platform design. A microgap at the crest, especially with a non-platform-switched connection, creates a small bacterial niche. Chronic low-grade inflammation around this junction can remodel 1 to 2 mm of bone, which then reflects in the soft tissue. Prosthetic emergence profile and contour. A bulky emergence profile pressing into the tissue starves blood supply. A concave, cleansable emergence helps tissues thrive. Over-contoured crowns make hygiene nearly impossible, and plaque wins. Habits and host factors. Smoking, uncontrolled diabetes, and bruxism put the soft tissues under constant stress. Parafunction in particular drives micromovements that can erode marginal bone if the screw joint or prosthesis lacks stability. Inadequate maintenance. Implants are not “set and forget.” Biofilm builds differently on titanium than enamel. Interdental cleaning and periodic professional maintenance matter more than the ad campaigns suggest.
Notice what is not on that list: the implant itself, in isolation. The device does not cause recession. Design, execution, and biology do.
The three stages where tissue stability is won or lost
When counseling someone about gum esthetics around implants, I think in three phases. Each phase offers ways to protect tissue and avoid recession.
Phase 1: Site preparation before implant placement
If a patient loses a front tooth to a vertical root fracture, there is often a missing buccal plate hiding under the gum. If we extract and walk away for three or four months, the ridge collapses. Later, even a flawless implant placement struggles to recreate a youthful gum line. Ridge preservation after tooth extraction makes a measurable difference. A collagen membrane and a slow-resorbing graft can maintain the ridge width by 1 to 3 mm compared with extraction alone, which is often the difference between a natural emergence and a compromised one.
For thin biotypes, soft-tissue augmentation before or during implant placement pays dividends. A subepithelial connective tissue graft increases tissue thickness, which increases resistance to recession. Think of it as building a thicker blanket over the bone so the contour holds.
Orthodontic site development is another overlooked tool. Slow tooth movement can drift bone in favorable directions, especially in the esthetic zone. Moving a hopeless lateral incisor palatally over months, then extracting, can leave a fuller facial plate that receives an implant more gracefully.
Phase 2: Surgical placement and timing
Implant position, depth, and angulation determine whether tissues will behave. I have little tolerance for chasing initial torque by shoving an implant too facially. If the bone says no, accept it, graft, and return. On upper anterior teeth, a palatal bias with a slight angulation toward the cingulum preserves the buccal plate and allows a concave emergence profile later.
Depth is decisive. The implant platform typically needs to sit 2 to 3 mm apical to the planned facial gingival margin. Too shallow risks visible titanium or abutment margins; too deep can complicate hygiene and lead to gray show-through if the tissues are thin. Cone beam imaging helps plan this in three dimensions, and guided surgery can translate the plan with precision.
Timing matters. Immediate placement can preserve soft-tissue architecture by maintaining the socket shape, but only when the buccal plate is intact and the implant achieves stable engagement apically. A gap graft between the implant and the socket wall supports the tissue. If the buccal plate is deficient, delayed placement with staged bone grafting often yields better soft-tissue results. The thrill of same-day teeth is not worth a compromised gum line.
Phase 3: Prosthetic design and maintenance
Once the implant is integrated, the prosthesis becomes the dominant influence. Abutment material and shade influence how the tissue looks, especially in thin biotypes. A zirconia abutment or a titanium abutment with a zirconia collar can eliminate gray shine-through. Platform switching, where the abutment is narrower than the implant platform, moves the microgap inward and encourages a stable soft-tissue cuff.
The emergence profile should be gentle and cleansable. I like to think of it as an umbrella supporting the gum, not a tent pole stretching it. For provisional crowns, contouring the cervical third to sculpt the tissue is a quiet art. Small adjustments over a few weeks train the papillae and margin to a pleasing architecture. Skip this step and the final crown often looks like an implant.
Screw-retained restorations reduce the risk of cement-induced peri-implant disease. If cement is used, it must be minimal, retrievable, and verifiably removed. Excess cement is still one of the most preventable causes of inflammation and recession around implants.
Long term, professional maintenance should be calibrated to the individual. A healthy non-smoker with excellent home care might do well on six-month intervals. A bruxer with previous peri-implant mucositis is better seen every three or four months. Hygienists should use implant-safe instruments and, when appropriate, low-abrasive air polishing. The goal is biofilm control without traumatizing the tissue.
What to expect over time
Even when everything is done right, biological systems Tooth extraction remodel. Radiographic studies show a small amount of crestal bone remodeling in the first year, often 0.5 to 1.0 mm, followed by long periods of stability. In thick tissue, that bone remodeling does not translate to visible recession. In thin tissue, half a millimeter can be visible. Patients should hear that truth up front. It is easier to accept a tiny change when it was predicted than when it arrives as a surprise.
Parafunction and occlusion play a quiet role. Repeated micromovements at the implant-abutment interface can aggravate the microgap and bone crest. A well-designed occlusal scheme with lighter contact in excursions, plus a night guard when indicated, protects both bone and tissue.
Systemic health holds the rest of the keys. Poorly controlled diabetes and smoking double the risk of peri-implantitis in some cohorts. Anyone investing in implants should also invest in lifestyle changes that support healing, including tobacco cessation and sleep health. For patients with sleep apnea, treating the airway can reduce bruxism, which helps the implant environment. A dental office that routinely screens and refers for sleep apnea treatment does its implant patients a favor.
Addressing fear with design choices
Fear of recession often lives in the esthetic zone. I approach upper anterior implants with a default plan that prioritizes tissue:
- Thicken the tissue if the biotype is thin. A 1 to 2 mm connective tissue graft changes the equation. Platform switch the connection and choose an abutment color that disappears under the gum. Sculpt the provisionals until the papillae and margin settle. Rushing to final risks a flat, unaesthetic emergence. Favor screw retention to eliminate the cement variable. Build a cleansable shape and teach the hygiene routine with the provisional in place so the patient can practice before the final is delivered.
In posterior sites, the conversation shifts to function and maintenance. A molar implant with stable tissue still needs a patient who will clean around a broader emergence profile. This is where tools matter. Some do well with interproximal brushes sized correctly for the embrasure. Others prefer water flossers. I’m agnostic about brands. What matters is consistent use and a comfortable technique that does not traumatize the gum.
When recession already exists
Suppose a patient walks in with a high smile line and an implant lateral incisor that looks too long. The first step is diagnosis, not repair. Cone beam imaging can confirm the buccal plate status, the implant depth, and whether a prosthetic fix is feasible. If the contour is over-bulky, a new provisional with a softer emergence can coax the tissue coronally over weeks. If the tissue is too thin, a subepithelial connective tissue graft may restore volume and bring the margin up slightly. These soft-tissue moves can gain 0.5 to 1.5 mm in experienced hands, enough to harmonize in many smiles.
When the implant sits too facially or too shallow, prosthetic band-aids rarely satisfy. Explantation and site reconstruction may be the honest path. It is a tough conversation but better than chasing a problem that physics will not allow you to solve.
Do whitening, fillings, or other dental treatments affect implant tissues?
People often ask whether routine procedures threaten implant gums. Teeth whitening does not harm implant surfaces or gum tissue around them when used as directed. Whitening gels do not change the shade of the crown or abutment, though, so shade matching considerations remain. Dental fillings near implants are straightforward, provided isolation and hygiene are solid. Tooth extraction elsewhere in the mouth has no direct effect on a healed implant site. Fluoride treatments are safe, and in high-caries-risk patients they protect the adjacent natural teeth that share the oral environment with the implant.
Root canals on neighboring teeth follow the usual playbook. The only extra step is careful imaging and planning if posts or crowns will sit near the implant to avoid occlusal overload on either structure. For anxious patients, sedation dentistry can make longer grafting or implant visits more tolerable, which indirectly helps tissue health by allowing meticulous, unhurried work.
Laser dentistry sometimes appears in discussions about peri-implant mucositis or soft-tissue recontouring. The right wavelength and settings can reduce inflammation and decontaminate surfaces. The wrong settings can overheat or damage tissue. Lasers, including erbium devices like a waterlase system often marketed for gentle soft-tissue work, are tools, not magic. Operator skill determines the result.
For patients using clear aligners like Invisalign, timing is important. Tooth movement changes occlusion and can redistribute forces on an implant crown. Aligners should be planned with the implant in mind, often as an anchor point without orthodontic movement. Communication between the restorative dentist and the orthodontist prevents surprises.
If a crown chips or a screw loosens on a weekend, seek an emergency dentist who understands implant systems. Temporary measures that respect the soft tissue prevent a cascade of inflammation that could otherwise invite recession.
Daily habits that protect implant gums
Implants thrive when the environment stays calm and clean. What you do at home matters more than what happens in the operatory twice a year. Here is a short, practical checklist I give patients who just received a final implant crown:
- Use a soft brush with small, circular motions at the gum line. Two minutes, twice a day. Clean the implant’s sides daily. Interdental brushes sized to the space, or a water flosser angled from the cheek and tongue sides, work well. If you clench or grind, wear the night guard. It protects the bone and the prosthesis. Do not smoke. If you do, get help to quit. Even a reduction cuts risk. Keep maintenance visits. Early signs of mucositis are silent and easy to reverse when caught.
A note on cost and value
Tissue-focused planning adds steps. Ridge preservation at the time of tooth extraction, soft-tissue grafting, provisionalization to sculpt the gum, and custom abutments all carry fees. They also buy stability. Skipping them can look cheaper in year one and far more expensive in year five if recession forces revisions. When you price an implant, ask for a complete plan that includes site development and tissue management. Cheaper is often a mirage.
How dentists evaluate risk before saying yes
Before recommending an implant, a conscientious dentist evaluates risk for recession and peri-implant disease the same way a cardiologist evaluates risk before clearing someone for a marathon. The assessment includes:
- Biotype and smile line. Thin gums in a high smile are high stakes. The plan changes accordingly. Ridge anatomy in three dimensions. Cone beam imaging is not optional in esthetic zones. Systemic health and habits. A smoker with diabetes needs a different conversation and timeline than a nonsmoker with controlled health. Occlusion and parafunction. Signs of wear, muscle tenderness, or headaches point toward protective therapy as part of the plan. Hygiene history. Past behavior predicts future maintenance. If daily cleaning has been a challenge, the prosthesis must be designed with bigger embrasures and simpler access.
Positioning implants is the easy part. Saying no to a site that is not ready takes more judgment. A dentist who recommends a staged approach or suggests orthodontics first is not upselling. They are protecting your future gum line.
Clearing the record
Implants do not inherently cause gum recession. Recession around implants reflects a mix of initial site anatomy, surgical and prosthetic choices, systemic health, habits, and maintenance. With thoughtful planning, gentle surgery, disciplined prosthetic design, and supportive home care, the soft tissues around implants can stay full and healthy for the long term.
If you are weighing implants and still worry about your gum line, sit with your dentist and walk through your specific risks. Ask to see similar cases from their practice, including photos six months and three years out. A clinician comfortable with tissue management will be candid about trade-offs, explain the steps to thicken or preserve the gum, and map a maintenance plan that fits your life. That conversation, not the myth, should shape your decision.