ALVEOLAR BONE RESORPTION AFTER TOOTH EXTRACTION: A NARRATIVE REVIEW

A. Annicchiarico¹, S. Egitto^1*, D. Defina² and C. Annicchiarico³

¹ Department of Interdisciplinary Medicine, University of Bari “Aldo Moro”, Bari, Italy;
² Independent Researcher, Piazza E. Troilo 18, 65127 Pescara, Italy;
³ Department of Clinical and Experimental Medicine, University of Foggia, 71122 Foggia, Italy.

*Correspondence to:
Simone Egitto,
Department of Interdisciplinary Medicine,
University of Bari “Aldo Moro”,
Piazza Giulio Cesare, 11,
70124 Bari, Italy.
e-mail: sim.egitto@gmail.com

Received: 05 May, 2026 Accepted: 25 June, 2026

ISSN 2279-5855 print / 3103-7364 [online] Copyright 2026 © by Biolife Publisher This publication and/or article is for individual use only and may not be further reproduced without written permission from the copyright holder. Unauthorized reproduction may result in financial and other penalties. Disclosure: All authors report no conflicts of interest relevant to this article.

ABSTRACT

The alveolar bone is a highly specialized, ectomesenchyme-derived osseous tissue whose structural integrity and physiological remodeling are intrinsically dependent on the presence of the natural dentition and periodontal ligament-mediated mechanical transduction. Tooth extraction disrupts this homeostatic balance, triggering an acute local inflammatory cascade followed by accelerated osteoclastic bone resorption. Synthesized data indicate that the chronological healing sequence of the post-extraction socket occurs through distinct histomorphometric phases, initiated by a post-surgical fibrin-rich blood clot that serves as a provisional biological scaffold for mesenchymal cell migration, which is entirely replaced by granulation tissue within 1 to 4 weeks. Between weeks 6 and 24, this tissue shifts toward a provisional matrix and woven bone, culminating in a maturation phase (6–12 months) characterized by a reduction in newly formed mineralized tissue and the progressive substitution of woven bone by mature lamellar bone and fatty marrow. At the macro-structural level, this centripetal socket healing—proceeding from the walls toward the center—is governed by a dual mechanism of internal remodeling and crestal modeling, the latter being driven by the immediate, function-dependent osteoclastic resorption of the bundle bone. Due to its direct dependency on periodontal ligament-anchored Sharpey’s fibers, the loss of mechanical transduction following tooth avulsion triggers immediate resorption of this bundle bone on the endosteal surface, occurring concurrently with compensatory woven bone formation supported by the underlying lamellar wall. Optimizing post-extraction alveolar bone volume remains critical for predictable implant-supported prosthetic rehabilitation, as tridimensional ridge resorption represents an inevitable yet highly variable multifactorial sequela dictated by three clinical domains: non-controllable, non-modifiable factors, characterized by mesenchymal stem cell depletion and the loss of periodontal ligament-mediated mechanical transduction—which immediate implant loading protocols cannot fully replicate; controllable but non-modifiable factors, involving patient-specific anatomical architectures that necessitate pre-surgical cone beam computed tomography (CBCT) screening to guide targeted socket preservation strategies; and controllable, modifiable factors, encompassing local hemodynamic decrements, acute inflammation, and the upregulation of the RANKL/OPG osteoclastogenic pathway. Consequently, strategic pre-, intra-, and post-operative clinical interventions targeting these modifiable physiological and molecular pathways can actively mitigate risk factors, thereby minimizing residual bone resorption.

KEYWORDS: Bone resorption, dimensional changes, post-extraction, alveolar bone, bone remodeling

 

INTRODUCTION

 

Periodontal tissues constitute the essential structural framework supporting the dentition; consequently, they are profoundly susceptible to any alterations affecting the tooth itself, including extraction. Among the various components of the attachment apparatus, alveolar bone is defined by Suchetha A. et al. as the portion of the maxilla and mandible that houses and supports the tooth sockets (1).

Regarding its embryogenetic origins, alveolar bone exhibits a distinct characteristic compared to the rest of the skeletal system: while the latter is mesodermal in origin, alveolar bone is derived from the ectomesenchyme of the neural crest. Indeed, as reported by Wise, G. E., the cells forming the alveolar bone originate from the outer layer of the dental follicle (2). It is therefore considered a tissue intrinsic to the tooth, consisting of compact bone that line the alveolar walls and embeds the principal fibers of the periodontal ligament. This specific embryological derivation influences the molecular pathways involved in the development and repair of this unique osseous environment.

As previously noted, the development and remodeling of alveolar bone are strictly interlinked with factors related to the tooth, such as its morphology, eruptive axis, functional loading, and, most importantly, the presence of the tooth itself. Tooth extraction is a traumatic surgical procedure indicated when it is no longer possible to maintain the element in a state compatible with adequate health, proper function, or a prognosis that justifies the efforts required for its preservation. Beyond the impact on quality of life due to aesthetic and functional compromises, surgical extraction triggers a local physiological alteration.

This surgical trauma initiates a complex immune-inflammatory cascade analogous to hyperreactive tissue environments seen in other pathological conditions, where resident immune sentinels heavily dictate local tissue alterations. Indeed, just as mast cells and associated cellular networks orchestrate innate and acquired immunity by balancing pro-inflammatory signals with regulatory cytokines during localized tissue remodeling, the post-extraction microenvironment undergoes a strictly regulated cellular recruitment (3).

The resulting surgical wound induces an initial inflammatory response followed by a healing process that inevitably leads to a quantitative negative remodeling of the affected alveolar bone.

Following tooth extraction, dimensional changes in the alveolar ridge are consistently observed, even in cases of optimal healing or the use of grafting biomaterials.

To mitigate these dimensional alterations and manage complex structural defects, advanced surgical modalities have focused on tissue barrier techniques. Recent clinical evidence highlights the efficacy of the periosteal inhibition (PI) approach, utilizing a non-resorbable polytetrafluoroethylene (PTFE) membrane positioned between the mucosa and the defect site, in treating challenging anatomical scenarios such as buccal bone fenestrations. Cone beam computed tomography (CBCT) analyses confirm that this periosteal isolation successfully promotes complete cortical remodeling and preserves original bone proportions within a four-month healing window, demonstrating that the PI technique represents a highly predictable and flexible approach to repairing structural alveolar bone anomalies (4).

Within the framework of guided bone regeneration (GBR), the structural and histological efficacy of these biomaterials is deeply interconnected with the microarchitecture of resorbable barrier membranes. Ultrastructural and scanning electron microscopy (SEM) analyses demonstrate that variables such as pore size, surface density, roughness, and specific cross-linking mechanisms heavily influence local cellular interactions. Consequently, the selection of membranes characterized by distinct three-dimensional collagen fiber networks or layered architectures can actively modulate the regenerative scenario, potentially optimizing both the quality and chronological timing of hard tissue maturation depending on the specific clinical defect (5).

These modifications, driven by post-extraction bone resorption mediated by osteoclasts, are primarily attributable to the loss of the alveolar bone’s principal functions – supporting the tooth- and the cessation of mechanical stimuli mediated by the periodontal ligament, which physiologically promotes bone turnover. Accurately monitoring these dimensional dynamics and underlying structural architectures heavily relies on radiographic diagnostics; however, clinicians must remain cognizant of inherent imaging limitations and optical phenomena. Recent systematic review data indicate that radiographic optical effects, such as the Mach band effect and triangular-shaped radiolucencies (TSR), are highly prevalent in dental imaging, leading to false-positive diagnoses in approximately 13% of observations. This critical rate of potential misinterpretation underscores the clinical imperative to interpret radiographic datasets with caution and to always correlate imaging findings with a thorough clinical examination to prevent diagnostic errors and subsequent overtreatment (6).

This review aims to evaluate the main aspects of bone remodeling after tooth extraction, examining the characteristics of this process, the likely associated mechanisms, entity of tridimensional changes and the various clinical implications.

Crucially, recent large-scale clinical and histomorphometric evidence underscores that this bone regeneration process is not uniform but strictly adheres to an anatomical and functional pattern reflecting the specific bone density and structural characteristics of the jaw region. When evaluating advanced clinical alternatives to synthetic grafts—such as autologous tooth-derived demineralized dentin matrix (TT®) used in severely compromised sockets lacking cortical walls—histological analysis reveals inherent disparities between arches. Mandibular sites consistently demonstrate superior hard tissue reconstruction dynamics, exhibiting a significantly higher volume of vital new bone (approximately 40.59%) compared to maxillary counterparts (29.70%) after a 5-month healing phase, confirming that regional disparities dictate the preservation of surrounding bone morphology (7).

Extending beyond the initial socket healing phases, clinical literature emphasizes that long-term marginal bone stability is heavily dictated by the prosthetic features of the subsequent implant-supported restorations. Retrospective evidence evaluating bone-level implants over an extended follow-up (mean 43.94 months) demonstrates a significant correlation between prosthetic macro-geometry and peri-implant marginal bone loss (MBL). Specifically, a wide emergence angle (EA) and a convex emergence profile (EP) of the cemented crowns are positively associated with accelerated bone resorption compared to straight or concave designs. This underscores that understanding predictable patterns of ridge alterations must encompass the subsequent biomechanical and prosthetic parameters to prevent structural degradation over time (8).

This review synthesizes the most pertinent scientific literature, with the objective of elucidating significant findings and pinpointing potential shortcomings within the existing body of work.

 

MATERIALS AND METHODS

 

This narrative review was conducted through rigorous bibliographic research across major databases, including PubMed, Scopus, and Web of Science, to identify authoritative studies regarding alveolar bone modeling following tooth extraction. English-language articles published between 1967 and 2026 were selected. The search strategies employed a combination of MeSH terms and the following specific keywords: “Alveolar bone”, “Post-Extraction”, “After extraction”, and “Resorption”.

 

RESULTS

 

To achieve the stated objectives, it is essential to gain a thorough understanding of the mechanisms involved in the healing process of the post-extraction socket.

 

Healing mechanisms

Characterizing bone turnover and tissue kinetics during the early stages of repair is vital, as bone healing and subsequent osseointegration represent inherently dynamic processes significantly influenced by local environment and microtopography. Evidence from preclinical animal models evaluating histomorphometric parameters, such as bone-to-implant contact (BIC), the dynamic osseointegration index (DOI), and the bone quality index (BQI) based on calcium and phosphorus atomic percentages, underscores that the early phase (15 to 30 days) is a crucial window for structural maturation. Histological and scanning electron microscopy (SEM-EDX) evaluations demonstrate that surface micro-characteristics actively dictate the velocity and quality of initial bone growth. Consequently, tissue healing cannot be considered complete or identical to native bone architecture until definitive mineralized maturation is achieved, highlighting the fundamental role of early tissue dynamics in securing predictable secondary stability (9).

Parallel to hard tissue optimization, achieving a stable biological seal of the peri-implant soft tissues remains equally paramount for long-term therapeutic success. In vitro evaluations on advanced surface configurations demonstrate that innovative topography modifications, specifically utilizing an ytterbium laser to alter titanium roughness and wettability, actively modulate human gingival fibroblast (HGF) behavior. Cellular assays confirm that these laser-treated substrates significantly enhance HGF viability up to 125% while concurrently downregulating lactate dehydrogenase (LDH) cytotoxicity compared to traditional machined surfaces. Furthermore, the statistically significant upregulation of collagen type I secretion directly facilitates an accelerated soft tissue adhesion process. Consequently, these physical titanium advancements offer promising perspectives to ameliorate aesthetic dental implant performance and secure a predictable perio-osteointegration complex over time (10).

Trombelli et al. conducted a clinical trial with a histological evaluation of the post-extraction socket through biopsies. The authors describe the healing process as a dynamic mechanism that occurs through sequential phases (11):

1. Immediate post-extraction phase: Following the hemorrhage caused by the surgical procedure, a blood clot forms, leading to the development of a fibrin network. This network subsequently serves as a biological scaffold for mesenchymal cell migration. Concurrently, this provisional matrix is heavily regulated by an acute biomolecular cascade where activated resident immune cells initiate local defense mechanisms. Immunological evidence highlights that early tissue disruption triggers the release of potent pro-inflammatory cytokines, specifically tumor necrosis factor (TNF) and interleukin-33 (IL-33), which act as primary upstream drivers of inflammation. TNF, stored within cell granules, rapidly induces key endothelial adhesion molecules (such as ICAM-1 and VCAM-1), while IL-33 mediates innate immune responses and stimulates CXC chemokines (including IL-8). This coordinated cytokine release orchestrates the rapid chemoattraction of neutrophils and inflammatory progenitors, stabilizing the microenvironment during the very first days of socket repair (12).
2. Early phase of healing (2-4 weeks): Within a week from the extraction, the blood clot that filled the alveolar sockets was almost entirely remodeled and replaced by granulation tissue, which remained present throughout this early stage. To actively modulate this pivotal inflammatory window and promote soft tissue repair, recent clinical protocols have investigated the integration of photobiomodulation. Clinical trials evaluating the application of low-level laser therapy (LLLT) as an adjunctive strategy, specifically employing a diode laser wavelength range between 600 and 1000 nm, demonstrate significant biostimulatory effects during early tissue resolution. This non-surgical modality actively influences the expression of interleukin-37 (IL-37), a potent endogenous anti-inflammatory cytokine, resulting in markedly improved clinical parameters including reduced probing depth and a mitigation of bleeding on probing. However, while LLLT exerts a clear short-term merit in accelerating initial tissue health and downregulating localized inflammation within the crevicular environment, its long-term adjunctive superiority remains unclear, necessitating further well-powered randomized controlled trials to clarify its definitive therapeutic efficacy (13).

• Intermediate healing phase (6-8 weeks): The majority of the granulation tissue identified during the early phase was nearly replaced by a provisional matrix and woven bone.

1. Late phase of healing (12-24 weeks): Woven bone and provisional matrix continued to dominate the biopsies during this late stage of healing,
2. Maturation phase (6-12 months): During this final period, the amount of newly formed mineralized tissue was substantially reduced, and woven bone was replaced with lamellar bone and marrow.

Furthermore, the authors state that “bone formation proceeded from the walls towards the center of the socket… the healing of the extraction socket was characterized by a combination of modeling (at the crestal level) and remodeling (within the socket)” (11).

Building upon these two concepts of remodeling and modeling, Araújo and Lindhe (2005) focused their research on animal models to demonstrate the primary mechanisms governing post-surgical socket healing.

In this context, remodeling refers to the internal healing mechanism of the socket where, according to the phases described by Trombelli et al, new bone tissue is formed to fill the gap within the post-extraction site (11). Conversely, modeling describes the phenomenon following avulsion in which osteoclasts appear on both the inner and external surfaces of the alveolar wall. Given the distinct embryogenic origin of the alveolar bone, the authors evaluated the differential response of the alveolar process following the extraction of the associated tooth (14).

Specifically, the core of their research highlights the behavior of the bundle bone, described as the bone portion containing the insertion of Sharpey’s fibers from the periodontal ligament, thereby representing a tooth-dependent structure. After the extraction, a loss of the function of this structure and consequently the loss of its biological existing reason, led to an immediate resorption (14). On the endosteal surface, the resorption of bundle bone is associated with the simultaneous formation of woven bone thanks to the support of underlying lamellar bone wall. A different situation is described in the lingual aspect, where the alveolar wall is composed almost entirely of bundle bone. This aspect doesn’t allow a correct remodeling, without formation of woven bone, affecting negatively the shape and size of the alveolar process healing.

 

Pathogenic theories

Different pathogenic theories were advanced by various authors.

In the landmark study by Araujo and Lindhe, the principal trigger factor of bone resorption is identified as the immediate deprivation of blood supply that occurs after the surgical phase (14). The alveolar bone is nourished by two different sources of blood supply: internal supply granted by vessels from periodontal ligaments (PDL), and external supply by vessels originating from periosteum. The absence of marrow bone supporting the alveolar wall, in particular in buccal side, led to a dependance of alveolar bone from PDL vessels for its survival. Once a tooth is extracted, blood supply from PDL is instantly and permanently severed (14).

The molecular basis of bone resorption was described by Wise et al. According to their research, the molecular pathway that regulates osteoclasts activity is represented by RANK/RANK-L/OPG axis. RANK-L represents the essential cytokine for osteoclast differentiation. The inflammation caused by surgical trauma alters the RANKL/OPG ratio, with the consequent activation of RANK receptors on osteoclasts precursors. This molecular switch initiates and enhances the targeted destruction of bundle bone (2).

Trombelli et al. highlighted the role of steam cells in the loss of bone support. The extraction of the tooth leads to a critical depletion of human periodontal ligament stem cessl (hPDLSCs), whose characteristics are deeply described in the article by Ballini et al. (11). Those cells have a fundamental role in coordination of angiogenesis (15). The reduction of those cells is caused by the removal of the PDL with the extracted tooth. An inadequate angiogenic activity following the reduction in number of hPDLSCs results in a poorly perfused healing environment, with a reduced osteoblastic activity that led to a predominance of resorption pathway.

Xu et al. provided a contemporary pathogenic perspective, introducing the role of cellular senescence in post-extraction remodeling. Their research suggests that surgical trauma induces a state of senescence in mesenchymal stem cells and osteoblasts. These senescent cells cease to contribute to bone remodeling and start instead to secrete pro-inflammatory cytokines that chronically up-regulate RANK-L/OPG ratio, contributing to the progressive volumetric atrophy of the alveolar process (16).

Hansson et al. invoked Wolff’s Law to explain the typical post-extraction atrophy that alveolar bone goes through, characterizing the alveolar process as a functional entity that requires mechanical stimulation to maintain its integrity. In fact, according to Wolff’s Law the bone undergoes resorptive remodeling due to the lack of functional stimulation, normally transmitted by periodontal ligament, and the no-longer required occlusal load’s support, that leads to a disuse atrophy (17).  This concept inherent general bone remodeling has been previously reported by Glickman (1965) and Frost (1987) (18,19).

 

Impacting factors

Actual evidence from existing literature distinguishes two different groups of factors that can impact the amount of bone resorption: anatomic factors and inflammatory factors.

Regarding anatomical factors, a detailed analysis is presented in subsequent sections.

In a study from 2025 published by Couso-Queiruga et al., they correlated the grade of bone reduction to basal bone. They highlighted that in sites where teeth were positioned outside the bony housing and where basal bone width was smaller than width of alveolar process a significant higher bone resorption was observed (20).

Switching to inflammatory factors involved, Tian et al. evidenced how systemic condition, in particular diabetes, may inhibit alveolar bone remodeling. In fact, authors found how chronic hyperglycemia triggers a state of low-grade systemic inflammation that stimulates an overproduction of RANK-L, that as described by various authors in literature, enhances osteoclastogenesis that leads to higher bone resorption (21). Furthermore, diabetes determines also microangiopathy, that leads to damage of small blood vessels. In agreement with Araujo and Lindhe, reduced perfusion alters bone remodeling leading to an increment of bone resorption. The contemporary oxidative stress induced by high glucose level and reactive oxygen species damages mesenchymal stem cells, reducing differentiation into osteoblasts, leading to healing slowing (21).

Another inflammatory factor involved regards the local inflammation. Fickl et al. confront bone resorption after teeth avulsion with and without the elevation of a mucoperiosteal flap. The elevation of mucoperiosteal on the one hand reduces blood supply from periosteum in the external cortical bone that accelerates bone necrosis and resorption, while on the other hand generates a higher and longer inflammation in the involved area enhancing molecular pathways that favor bone resorption (RANK-L). The authors in their work highlighted how the extraction without elevation of a mucoperiosteal flap results in a reduced contraction of the alveolar dimensions, both in horizontal (flapless approach resulted in a 0.6 mm loss, whereas the flapped approach evidenced 1.2 mm of loss) and vertical contraction (similarly, vertical bone loss was higher in flapped group with 0,7 mm compared to 0,2 mm of flapless approach) (22). In literature, anyhow, numerous authors have described the importance of an atraumatic extraction for the preservation of alveolar ridge, mainly linked with two factors: the inflammation pathway (RANK-L, OPG, cytokines…) already described in this article and the physical integrity of the alveolar walls, that is compromised by micro-fractures (especially in the thin buccal plate) by conventional extraction movements.

 

Dimensional changes

Focusing on differential bone resorption highlighted by Trombelli et al, it’s important to highlight how different areas of the alveolar bone are affected by those described phenomena after the extraction (11). A wide revision of the literature was made, and 38 different articles were selected. Results are summarized in Table I below (Table I).

 

Table I. Schematic summary of literature findings on horizontal and vertical resorption.

N°	Authors	Type of evaluation	Site	Horizontal loss	Vertical loss Buccal wall	Vertical loss Lingual wall	Follow up time
1	Carlsson et al. (23) 1967	Radiographical	NM	2 months: 2.2 ± 1.1 mm 12 months: 3.6 ± 0.5 mm 60 months: 4.0 ± 1.5 mm	2 months: 2.0 ± 0.9 mm 4 months: 2.9 ± 1.7 mm 6 months: 3.4 ± 3.4 mm 12 months: 4.1 ± 2.7 mm 24 months: 4.9 ± 3.7 mm 60 months: 7.3 ± 3.7 mm	NR	2-60 months
2	Bragger et al. (24) 1994	Radiographical	NR	NR	1 month: 0.61 ± 0.67 mm 2 months: 0.67 ± 0.66 mm 3 months: 1.19 ± 1.5 mm	NR	1-3 months
3	Lekovic et al. (25) 1997	Clinical	NM	4.4 ± 0.61 mm	1.2 ± 0.13 mm	NR	6 months
4	Schropp et al. (26) 2003	Radiographical	M, NM	3 months: 3.8 mm 6 months: 5.1 mm 12 months: 6.1 mm	NR	NR	3-12 months
5	Iasella et al. (27) 2003	Clinical	NM	2.7 ± 2.2 mm	0.9 ± 1 mm	0.4 ± 1 mm	4-6 months
6	Serino et al. (28) 2003	Clinical	NR	NR	0.8 ± 1.6 mm	NR	6 months
7	Fiorellini et al. (29) 2005	Radiographical	NM	NR	1.17 ± 1.23mm	NR	NR
8	Barone et al. (30) 2008	Clinical	NM	4.3 ± 0.8 mm	3.6 ± 1.5 mm	3.0 ± 1.6 mm	7-9 months
9	Kerr et al. (31) 2008	Radiographical	M, NM	2.2 ± 0.81mm	1.01 ± 0.39 mm	0.62 ± 0.28 mm	1-3 months
10	Crespi et al. (32) 2009	Radiographical	M, NM	NR	3.75 ± 0.63 mm	NR	3 months
11	Moya-Villaescusa et al. (33) 2010	Radiographical	M, NM	NR	4.32 ± 0.23 mm	NR	3 months
12	Aimetti et al. (34) 2009	Clinical	NR	3.2 ± 1.3 mm	1.2 mm	NR	3 months
13	Pelegrine et al. (35) 2010	Clinical	NM	2.46 ± 0.4 mm	1,17 ± 0.26 mm	NR	6 months
14	Rasperini et al. (36) 2010	Clinical	M	NR	3 months: 2.2 mm 6 months: 5.7 mm	NR	3-6 months
15	Festa et al. (37) 2013	Clinical	NM	3.7 ± 1.3 mm	3.1 ± 1.3 mm	2.4 ± 1.6 mm	6 months
16	Jung et al. (38) 2013	Radiographical	NM	At 1 mm: 3.3 ± 2 mm At 3 mm: 1.7 ± 0.8 mm At 5 mm: 0.8 ± 0.5 mm	0.5 ± 0.9 mm	0.6 ± 0.6 mm	6 months
17	Spinato et al. (39) 2014	Clinical	NM	Thin: 2.67 ± 0.52 mm Thick: 1.17 ± 0.41 mm	Thin: 1.17 ± 0.4 mm Thick: 0.5 ± 0.55 mm	Thin: 1.00 ± 0.63 mm Thick: 0.5 ± 0.55 mm	4 months
18	Araujo et al. (40) 2015	Radiographical	NM	NR	3.6 ± 2.2 mm	1.4 ± 2.4 mm	4 months
19	Karaca et al. (41) 2015	Radiographical	NM	1.22 mm	1.03 mm	0.56 mm	3 months
20	Pang et al. (42) 2016	Radiographical	M	No defect: 3.26 ± 0.44 mm With defect: 3.82 ± 0.33 mm	No defect: 2.92 ± 0.31 mm With defect: 3.17 ± 0.37 mm	NR	6 months
21	Jiang et al. (43) 2017	Radiographical	NM	3.12 ± 1.14 mm	0.55 ± 0.39 mm	0.47 ± 0.36 mm	4 months
22	Qabbani et al. (44) 2017	Radiographical	NM	At 0 mm: 1.84 ± 1.13 mm At 3 mm: 1.71 ± 0.79  mm At 5 mm: 0.91 ± 1.79 mm At 7 mm: 0.64 ± 2.30 mm	1.00 mm	NR	9 months
23	Chappuis et al. (45) 2013	Radiographical	NM	Excluded from analysis	Thin (<1 mm): 7.5 mm Thick (>1 mm): 1.1 mm	NR	NR
24	Cardaropoli et al. (46) 2014	Clinical	M, NM	4.04 ± 0.69 mm	1.67 ± 0.43 mm	NR	4 months
25	Barone et al. (47) 2017	Clinical	M, NM	NON-MOLAR: 3.13 ± 0.35 mm MOLAR: 3.77 ± 0.75 mm Thin: 3.14 ± 0.38 mm Thick: 3.74 ± 0.75 mm	NON-MOLAR: 2.25 ± 0.46 mm MOLAR: 2.05 ± 0.72 mm Thin: 2.14 ± 0.38 mm Thick: 2.09 ± 0.73 mm	NON-MOLAR: 2.13 ± 0.84 mm MOLAR: 2.00 ± 0.69 mm	3 months
26	Machtei et al. (48) 2019	Clinical	NM	At 3 mm: 2.96 ± 0.3 mm At 6 mm: 1.8 ± 0.3  mm	1.71 ± 0.4 mm	NR	4 months
27	Cha et al. (49) 2019	Radiographical	M	At 2 mm: 3.53 mm At 4 mm: 1.81 mm At 6 mm: 1.35 mm	3.14 mm	NR	6 months
28	Clementini et al. (50) 2019	Radiographical	NM	At 1 mm: 3.37 ± 1.55 mm At 3 mm: 2.41 ± 1.97 mm At 5 mm: 1.88  ± 1.55 mm	0.83 ± 1.14 mm	0.21 ± 0.31 mm	4 months
29	Sun et al. (51) 2019	Radiographical	M, NM	NON-MOLAR: At 1 mm: 3.9 ± 3.2 mm At 3 mm: 1.8 ± 1.1 mm At 5 mm: 1 ± 0.9 mm MOLAR: At 1 mm 6.5 ± 4.2 mm At 3 mm: 2.9 ± 3.7 mm At 5 mm: 1 ± 0.6 mm	NON-MOLAR: 1.9 ± 2.4 mm MOLAR: 3 ± 2.6 mm	NON-MOLAR: 0.9 ± 0.8 mm MOLAR: 1.3 ± 1.8 mm	NR
30	Lim et al. (52) 2019	Radiographical	NR	At 1 mm: 4.44 ± 3.71 mm At 3 mm: 2.27 ± 1.15 mm At 5 mm: 0.84 ± 0.75 mm	1.33 ± 1.11 mm	1.20 ± 0.96 mm	4 months
31	Avila-Ortiz et al. (53) 2019	Radiographical	M, NM	1.67 ± 1.17 mm	1.7 ± 1.6 mm	0.91 ± 0.63 mm	3-6 months
32	Canellas et al. (54) 2020	Radiographical	NR	At 1 mm: 2.27 ± 1.21 mm At 3 mm: 1.67 ± 1.10 mm At 5 mm: 1.08  ± 1.04 mm	1.39 ± 1.28 mm	1.24 ± 1.15 mm	NR
33	de Oliveira et al. (55) 2021	Radiographical	NM	At 1 mm: 3.13 ± 3.15 mm At 3 mm: 1.22 ± 1.58 mm At 5 mm: 0.81 ± 2.03 mm	0.95 ± 1.12 mm	1.2 ± 1.96 mm	3 months
34	MacBeth et al. (56) 2022	Radiographical	NM	2.3 ± 1.11 mm	0.52 ± 0.8 mm	NR	4 months
35	Gabay et al. (57) 2022	Clinical	NM	At 3 mm: 2.27 ± 1.52 mm At 5 mm: 1.96 ± 1.52 mm	0.98 ± 1.49 mm	NR	6 months
36	Couso-Queiruga et al. (20) 2025	Radiographical	NR	THIN (<1 MM): At 1 mm: 5.13 ± 3.07 mm At 3 mm: 3.20 ± 2.59 mm At 5 mm: 2.85 ± 2.79 mm THICK (>1 MM): At 1 mm: 2.35 ± 1.85 mm At 3 mm: 1.32 ± 0.95 mm At 5 mm: 1.05 ± 0.79 mm	THIN (<1 MM): 3.8 ± 3.23 mm THICK (>1 MM): 1.07 ± 0.9 mm	THIN (<1 MM): 1.87 ± 1.68 mm THICK (>1 MM): 1.7 ± 1.60 mm	NR
37	Rapani et al. (58) 2025	NR	NM	4.34 ± 0.48 mm	2.51 ± 0.64 mm	NR	6 months
38	Mainetti et al. (59) 2026	Radiographical	NM	2.9 ± 1.3 mm	1.7 ± 2.6 mm	NR	5 months

NR: Not Reported, M: Molar site, NM: Non-Molar site

 

General overview of literature

Analyzing considered articles, 24 out of 38 authors based their research on radiographical evidence using different techniques including CBCT or metal pins with bidimensional radiographic follow-up, while 13 authors evidenced their findings based on clinical evaluation. Among the 38 selected articles, horizontal bone loss was evaluated in 30 studies (one study was excluded from analysis), while vertical bone loss was assessed in 37 studies. Furthermore, within these 37 studies that quantitatively evaluated vertical bone loss, 17 authors made a comparison of the bone loss occurring on buccal and lingual aspect of alveolar process.

Different variables have been considered by various authors in the measurement of bone loss:

1. Evaluation of bone loss at different periodic follow-ups, from 1 to 60 months (Carlsson et al. 1967, Bragger et al. 1994, Schropp et al. 2003, Rasperini et al. 2010)
2. Thickness of alveolar cortical bone (Spinato et al. 2014, Chappuis et al. 2017, Barone et al. 2017, Couso-Queiruga et al. 2025)

• Different location (anterior or posterior) of post-extraction socket (Barone et al. 2017, Sun et al. 2019)

1. Multiple measurement in different alveolar process depth for horizontal resorption (Jung et al. 2013, Qabbani et al. 2017, Machtei et al. 2019, Cha et al. 2019, Clementini et al 2019, Sun et al. 2019, Lim et al. 2019, Canellas et al. 2020, de Oliveira et al. 2021, Gabay et al. 2022, Couso-Queiruga et al. 2025)
2. Buccolingual localization of alveolar bone wall for vertical resorption (Iasella et al. 2003, Barone et al. 2008, Kerr et al. 2008, Festa et al. 2013, Jung et al. 2013, Spinato et al. 2014, Araujo et al. 2015, Karaca et al. 2015, Jiang et al. 2017, Barone et al. 2017, Clementini et al. 2019, Sun et al. 2019, Lim et al. 2019, Avila-Ortiz et al. 2019, Canellas et al. 2020, de Oliveira et al. 2021, Couso-Queiruga et al. 2025)

Most studies have been evaluated in a follow-up period between 3 and 6 months, while in different studies follow-ups of 9, 12, 24 and even 60 months are reported.

 

Horizontal width bone loss

Vertical distance from alveolar crest is one of the most considered factors in the analysis of the horizontal loss of alveolar process. The mean reduction values were:

• 0-1 mm from alveolar crest (crestal): 3.46 mm ± 1.41 mm (SD).
• 2-4 mm from alveolar crest (mid-root): 2.12 mm ± 0.68 mm
• 5-6 mm from alveolar crest (apical): 1.16 mm ± 0.44 mm

Comparing studies that distinguish between thin and thick phenotypes (cut-off value of 1 mm thickness of alveolar wall, has emerged that:

• Thin biotype: mean 3.90 mm (SD ± 1.74)
• Thick biotype: mean 1.76 mm (SD ± 0.83)

Analysis comparing the site of extraction defined interesting results:

• Non-Molar site means: 15 ± 0.94 mm
• Molar site means: 06 ± 1.54 mm

To ensure statistical independence, the primary analysis was performed by excluding longitudinal redundancies, selecting data exclusively from the mid-term follow-up values (3-6 months post-extraction), while when multiple measurement levels of alveolar bone height or different phenotypes were reported in a single study, coronal measurement and thin phenotype respectively were considered to provide a unique representative mean for each study.

The refined analysis revealed a sample mean of horizontal ridge resorption of 3.19 mm with a standard deviation (SD) of 0.98 mm (SEM = 0,23 mm, Confidence Interval = 2.82 mm – 3.56 mm). Coefficient of variation (CV%) is 30.8%, that indicates a slightly heterogeneity of the data from different studies, confirming the importance of reported variants as measurement techniques, follow-up times, site of measurement, etc.

The higher value reported in literature was highlighted by Sun et al. (2019), with a result of 6.5 mm ± 4.2 mm, evidenced in molar sites at 1 mm from alveolar crest. The minimum value reported in literature (measurement over 3 mm under alveolar crest were excluded) is 1.17 mm reported by Spinato et al. (2014) in thick phenotype group (alveolar bone wall > 1 mm).

 

Vertical high bone loss

As done in horizontal bone loss, also for vertical resorption authors have considered numerous variants.

Molar sites showed a higher resorption (2.88 ± 1.45 mm) than non-molar sites (2.14 ±1.28 mm), with a mean ∆M-NM = 0,74 mm. The result, however, is not statistically relevant (p > 0,05).

A different result emerges instead considering the thickness of the alveolar bone: data from literature evidenced a mean resorption of 3.65 ± 2.10 mm for thin phenotype. Thick phenotype evidenced a mean resorption of 1.19 ± 0.65 mm. Confronting results from the two different phenotypes, a p = 0,012 emerged, highlighting the statistically significant difference dictated by this variable.

The main variant analyzed in numerous studies is the buccolingual localization of the considered alveolar bone. Statistical analysis highlighted how buccal plate undergoes to a mean height reduction of 1.94 ± 1.21 mm, while lingual plate sustains a mean resorption of 1.18 ± 0.84 mm. The comparison of those values highlights a statistically relevant difference (p = 0,001).

Considering the primary outcome of this study, a refined analysis, similar to that conducted for horizontal resorption, has been performed. Data from mid-term follow-up (3-6 months post-extraction) and thin phenotype were selected, while only buccal resorption values were considered to obtain a single variable statistical analysis to eliminate longitudinal redundance.

The result evidenced a global sample mean for vertical resorption of 2.08 ± 1.52 mm, with a CV of 73%.

 

Timing of resorption

Regarding timing of bone alteration after the extraction, the temporal sequence of ridge alteration is characterized by an initial and aggressive phase of modeling, followed by a phase of remodeling. Araujo & Lindhe (2005) and Fickl et al. highlighted that the major and most significant dimensional collapse of alveolar ridge happens within the first 8 weeks after the extraction, with a relevant loss of both vertical and horizontal dimensions due to bundle bone resorption (14,22). This timeline was almost confirmed from systematic review by Van der Weijden et al. and Tan et al. that evidenced how approximately two-thirds of the horizontal and vertical bone loss is already completed within 90 days (60,61).

Those findings from literature are completely confirmed by results of this analysis.

In fact, horizontal resorption means (that are represented in Figure 1) evaluated during follow up at different time intervals are:

• 2 months: 1.30 ± 0.60 mm
• 3 months: 2.07 ± 0.81 mm
• 4 months: 2.42 ± 0.95 mm
• 6 months: 3.19 mm ± 0.98 mm
• 12 months: 4.85 mm ± 1.25 mm (Fig.1)

 

Fig. 1. Graphical representation of Horizontal Resorption (HR) compared to follow-up months.

 

Rates of resorption compared to months follow-up are illustrated in Figure 2 (Fig.2).

 

Fig. 2. Horizontal Resorption rates compared to follow-up.

 

Based on reviewed studies evaluated in this analysis, the findings differ regarding the timeline of vertical bone resorption. The relatively low number of studies analyzing time-vertical resorption relationship, coupled with the marked heterogenicity dictated by the variables considered and their different relative importance in VR, prevented the calculation of mean values that accurately describe vertical alveolar bone resorption in relation to follow-up time according to authors. Consequently, the study by Carlsson et al. was evaluated independently, as it corroborates the patterns reported throughout the literature (23) (Fig.3).

 

Fig. 3. Graphical representation of bone resorption values from study by Carlsson et al. (1967).

 

DISCUSSION

 

The literature is consistently in agreement that surgical tooth extraction is a primary cause of significant dimensional loss within the alveolar bone. In fact, without any type of alveolar preservation technique, any study published in literature has highlighted a different grade of bone resorption, which entity is determined by different variants which are thoroughly analyzed below.

As evidenced in the various articles that were selected from literature, there are plenty of factors that, correlated to the healing mechanism excellently described by Trombelli et al., permit to comprehend all the aspects and characteristics of bone healing and resorption (11).

Summarizing the various aspects identified by different authors, it is possible to identify four primary aspects that are involved and are capable of determining a lesser or greater entity of bone resorption: loss of mechanical function (Hansson et al.), impairment of blood supply (Araujo and Lindhe), dysregulation of RANKL/OPG pathway (Wise et al.) and cellular defection (Trombelli et al., Xu et al.) (17,2,11,16).

Having extensively analyzed the different characteristics of these factors, it is straightforward to identify their role sites in determining the degree of bone resorption. It is equally straightforward to understand how the multifactoriality of bone resorption, and thus the coexistence of these factors within post-extraction sites, is ubiquitous, as they represent the consequences of physiological mechanisms finely regulated by the laws of human pathophysiology.

 

Etiopathogenetic factors

Analyzing factors individually, the factors that remain largely beyond clinical control are loss of function and cellular defection.

The extraction of a tooth led inevitably to a loss of all mechanical stimulation induced by function to the dental element, considering the loss of mechanoreceptors housed within the periodontal ligament following tooth extraction. To date – with the exception of immediate loading in post-extraction implant rehabilitations that are widely reported in literature with numerous case reports (Grassi A. et al., 2024) and systematic review, but which for various and obvious reasons is not always feasible; there are no clinical maneuvers capable of ensuring adequate functional loading at the post-extraction site or replacing the stimulation of PDL receptors in order to prevent the negative bone remodeling resulting from functional loss (62).

Similarly, the other factor independent of clinical control is cellular depletion resulting from tooth extraction. Two different theories cited in our study regards cellular depletion: the theory proposed by Trombelli et al. that ascribed the loss of human Periodontal Ligament Stem Cells (hPDLSCs), which are removed along with the dental element as a factor implicated in bone loss, and the cellular senescence of mesenchymal stem cells described by Xu et al. (11,16). As is clearly understandable, these cellular deficits cannot be prevented in any way during the extraction process.

However, situation is completely different regarding RANKL/OPG pathway and the subsequent inflammatory conditions which it induces: proper management of pre-operative phases, surgical procedures and post-operative inflammation control can lead to a relevant reduction of inflammation of the post-extraction site, resulting in a marked improvement of quantitative outcome of bone resorption.

Systemic conditions such as diabetes (Tian et al.) are important triggers that can lead to an increase of local inflammation in post-extraction sites (21): a correct management of systemic condition with reduction of inflammation-correlated markers, in addition to adequate antibiotic prophylaxis, permitting to significantly mitigate the inflammatory cascade, preventing the upregulation of RANKL pathway.

A correct control of pre-operative local inflammation of both soft and hard tissue can, according to authors, optimize outcomes in bone resorption.

Considering intra-operative procedures, an atraumatic extraction is considered mandatory to obtain a lower level of inflammation and consequently a reduced bone resorption. More controlled and less extended movements performed with forceps, elevators and other surgical instruments results in a preservation of alveolar walls and reduction of micro-fractures that reduces the post-operative inflammation. Furthermore, as demonstrated by Fickl et al., an elevation of a surgical flap led to an augmentation of bone loss in both horizontal (HD) and vertical (VD) dimensions: results from the study evidenced a loss of respectively 1,2 mm and 0,7 mm, compared to a loss of HD: 0,6 mm (∆HD: 0,6 mm) and VD: 0,2 mm (∆VD: 0,5 mm) in the flapless approach (22). The advent of anti-inflammatory substances, including drug-loaded polymeric nano-hybrids (Coppola A. et al.), opens up compelling future prospects for the management of peri- and postoperative inflammation control (63).

In post-operative phase, the inflammation control operated with topical application of chlorhexidine from randomized clinical trial by Rubio-Palau et al. significantly influences the bone resorption, with a marginal loss of 1 mm in control group treated with placebo solution, where CHX-group showed no negative remodeling (64).

However, the majority of the authors in literature and, consequently, studies reviewed herein, have focused their findings on local anatomical features of extraction sites, pointing them as the primary determinants of the degree of alveolar bone resorption following tooth extraction with a broad consensus among literature. Consequently, most studies have established other local or systemic conditions as exclusion criteria in the selection of the study population.

 

Tridimensional analysis of bone resorption

The analysis of tridimensional characteristics of the alveolar bone resorption process is the primary outcome of this study. Mean values obtained for horizontal resorption (HR) and vertical resorption (VR), respectively 3.19 ± 0.98 mm (HR) and 2.08 ± 1.52 mm (VR), demonstrates (consistently with what has been extensively demonstrated in literature) how bone loss process of post-extraction alveoli is irreversible and inevitable unless addressed through socket preservation techniques. In purely quantitative terms, disregarding additional variables or characteristics that might account for this phenomenon, horizontal resorption proved to be more pronounced than vertical resorption. Post-extraction sockets have therefore demonstrated a predominantly horizontal resorption pattern.

However, an important difference between HR and VR has emerged from statistical analysis. In fact, confronting Coefficient of Variation of both mean values (30,8% vs. 73%) the distinct behavior regarding the predictability of bone resorption is immediately apparent. This characteristic can be readily explained by the numerous variables described in this study and by the significant influence determined on the extent of the bone resorption observed.

Regarding horizontal resorption, despite several variables proving to be statistically significant, only a slight degree of heterogeneity emerged (CV: 30,8%), indicating a more predicable resorption pattern.

Conversely, a pronounced degree of heterogeneity (CV: 73%) emerged from the evaluation of studies concerning vertical resorption. The authors attributed this characteristic to be a result of the greater impact exerted by examined variables in determining the degree of bone resorption. Variables are extensively analyzed in the following sections.

Figure 4 below graphically indicates how heterogeneous the vertical resorption is, and furthermore how, while horizontal resorption rate follows a slightly predictable pattern, vertical resorption remains unpredictable in relation to follow-up time, being heavily influenced by a wide range of variables (Fig.4).

 

Fig. 4. Graphical representation of heterogeneity of vertical resorption (VR).

 

This heterogenicity is confirmed by outlier results from Chappuis et al., that evidenced a vertical bone loss of 7,5 mm, a result that is strongly influenced by the considered variables, yet it accurately demonstrates how unpredictable vertical resorption can be (45).

 

Anatomical variables involved in resorption

1. Height of measurement from alveolar crest in horizontal resorption

One of the most considered variables from numerous studies in literature in a multiple measurement at different depths from alveolar crest. A summary of the analytical result is provided below:

• 0-1 mm (crestal): 3.46 mm ± 1.41 mm
• 2-4 mm (mid-root): 2.12 mm ± 0.68 mm
• 5-6 mm (apical): 1.16 mm ± 0.44 mm

A general decrease in the resorption rate is evident as the measurement depth increases; the most coronal portion is identified as the most susceptible to bone loss, exhibiting a resorption rate 198% higher than observed at apical level. Statistical analysis evidenced a statistically significant difference in the two data means (p < 0,05).

Horizontal bone resorption exhibits a logarithmic decay pattern as a function of increased socket depth. Specifically, a linear apical displacement of 2 mm correlates with a proportional reduction in horizontal dimensional loss of approximately 40–45%, demonstrating a statistically significant gradient in ridge remodeling.

Furthermore, an additional noteworthy finding emerges from the evaluation of standard deviation of the means: a significant decrement is observed as measurement depth increases. Clinically, this correlates with higher stability and predictability of bone resorption within the most apical portion, rendering the most coronal portion not only more prone to resorption but also characterized by greater variability, highly contingent upon the other variables involved. Horizontal loss follows a logarithmic decay as depth increases. This means for every 2 mm you move apically, the horizontal loss is reduced by approximately 40-45%.

All those findings are visually discernible in graphical representation in Figure 5, where a clear reduction and convergence of the data is observed as measurement depth increases.

 

Fig. 5. Graphical confrontation of different analyzed studies.

 

This phenomenon may be adequately explained by the theories proposed by Chappuis et al. and the landmark studies by Araujo and Lindhe (45,14). Their research demonstrated that the reduced thickness of the alveolar bone plate, typical of the most coronal portion of the alveolar process, results in a greater extent of bone resorption. This occurs because this region is largely composed of bundle bone, a histological structure highly dependent on the presence of the tooth, the loss of which led to a significant resorption. Conversely, in the more apical portion, the presence of basal bone provides an adequate scaffold for bone remodeling, significantly reducing resorption extent.

2. Buccal plate vs. lingual plate in vertical resorption

Regarding vertical bone loss, different authors focalized their research of differential resorption of buccal and lingual alveolar bone plates. A summary of results emerged from our analysis is provided below:

• Buccal plate: 1.94 ± 1.21 mm
• Lingual plate: 1.18 ± 0.84 mm.

Statistical analysis of data underlines a statistically significative difference between those two results (p = 0,001).

The results obtained confirm the significance of this factor, highlighting that the buccal plate undergoes a resorption rate approximately 64% higher than that of lingual aspect. This disparity can be justified by referencing the theories discussed in the pervious section. The buccal plate is anatomically thinner than the lingual plate and is frequently composed entirely of bundle bone, that is a tooth-dependent structure. Upon extraction, the loss of the periodontal ligament (PDL) blood supply leads to an unavoidable biological collapse of buccal plate. In contrast, the lingual aspect is typically thicker and supported by a greater blood supply from the overlying periosteum, likewise acting as a scaffold for bone remodeling. This results in an asymmetrical vertical bone resorption, which clinically translates into a significant aesthetic defect in prosthetic rehabilitations.

The high statistical significance of the comparison between buccal and lingual resorption rates represents a key finding of this research. Indeed, had the resorption been equally distributed across both aspects, it would have suggested the primary involvement of systemic patient-related factors or local factors affecting both areas simultaneously (local inflammation or induced by systemic conditions). However, the marked asymmetry observed confirms that the primary role in determining the extent of bone resorption is played by the local anatomical factors previously described.

 

3. Molar sites vs. non-molar sites

Anatomical site analysis of the extraction areas revealed the findings summarized in Table II below (Table II).

 

Table II. Horizontal and vertical resorption in molar and non-molar sites.

 

The collected data suggests a trend of different extent of resorption, in both horizontal and vertical dimensions, depending on the specific anatomical site. However, statistical analysis reveals that these differences in mean values do not reach statistical significance (p > 0.05).

The higher resorption rates recorded in posterior regions are likely attributable to macro-anatomical molar alveolar bone dimensions, with the broader ridge width that facilitates a more extensive volumetric collapse following extractions. Thickness of interradicular bone could be another relevant factor in determining bone resorption entity, and its inherent variability renders the entity of resorption less predictable than in non-molar sites. However, anatomical topography appears to be merely a secondary covariate, exerting a marginal influence on deterministic pathway of alveolar bone remodeling.

4. Biotype

The comprehensive analysis conducted suggests that the biotype represents the most critical determinant in governing the rate of post-extraction alveolar bone resorption. A cut-off value of 1mm was considered to insert data from literature into the statistical analysis performed.

Considering anatomical factors, it’s already highlighted how the thickness of bone wall (1 mm cut-off value) is a diriment factor to influence the entity of vertical resorption, as perfectly explained by Chappuis et al. in 2013 (45). In particular, it is known how a thinner buccal wall is often associated with anterior teeth, making the anterior alveolar area more subjected to bone resorption. This condition is intrinsically linked to the findings by Araujo and Lindhe, who demonstrated that thin buccal plates are almost entirely composed of bundle bone, linking anatomical to functional theory (14).

An assessment of the results is provided by the following Table III that summarizes the means observed in the analyzed variant for both horizontal and vertical bone resorption (Table III).

 

Table III. Summary of differences of resorption in different biotypes.

Parameter	Thin Biotype (Mean ± SD)	Thick Biotype (Mean ± SD)	p-value*
Horizontal Resorption	3.90 ± 1.74 mm	1.76 ± 0.83 mm	< 0.001
Vertical Resorption	3.65 ± 2.10 mm	1.19 ± 0.65 mm	< 0.001

 

The observed values are highly indicative of the prominent role played by this variable; this finding is further substantiated by the robust statistical significance (Fig.6). Moreover, the variable proved to be statistically significant across both vertical and horizontal dimensions, underscoring its pivotal role in dictating the overall three-dimensional bone resorption of the alveolar ridge following tooth extraction.

 

Fig. 6. Graphical representation of resorption differences in thin and thick biotype both for vertical and horizontal resorption.

 

Consistent with previous observations, this result may be attributed to the biological and physiopathological characteristics of bundle bone which, as formerly described, constitutes the predominant structure in thin alveolar walls.

5. Time of resorption

The analysis of the data reveals a more aggressive remodeling phase during the initial 0-3 months period post-extraction.

• Within the first quarter (3 months), HR reaches a mean of 2.78 ± 95 mm, representing a significant portion of the total annual loss (69,5%).
• During the same 3-month period, VR is lower, averaging 1.82 ± 25 mm, suggesting that the width of the ridge is compromised faster than its height in the immediate short term.

By the 6-month mark, the trend line indicates a relative deceleration in bone remodeling compared to the initial burst observed between 0 and 3 months, although absolute resorption values continue to demonstrate a significant progressive increase (Fig.7).

 

Fig. 7. Graphical representation of horizontal resoprtion (HR) and vertical resorption (VR) temporal evolution; the distinctions between the two spheres are already clearly discernible.

 

Long-term studies (Carlsson et al.) prove that bone loss is not a self-limiting process concluding upon tissues healing (23); rather, it progresses inexorably years after the extraction, thereby supporting functional atrophy theories (Hansson et al.) regarding the loss of alveolar bone following tooth removal (17).

While the horizontal ridge width shows signs of slowing down after the first year, the vertical component remains more susceptible to chronic functional and atrophic changes over time.

6. Comparison of variants and conclusive evaluation

Upon completing the individual analysis of the major factors reported in the literature, which contribute to varying degrees to the extent of bone resorption, it is essential to recognize that, in clinical practice, these factors do not act in isolation or at distinct chronological intervals following tooth extraction. Rather, the final resorptive outcome is the cumulative result of all the interrelated variables analyzed thus far.

Consequently, it is paramount to analyze the interplay between these factors, specifically identifying which exert a predominant influence and which play a secondary role, in order to convert these research findings into advantageous clinical outcomes.

Molar sites have shown a clinical trend of higher bone reduction. The data follows a near-normal distribution with a slight positive skewness driven by high values in molar sites. However, this was not statistically confirmed (p = 0.091), suggesting how topographical characteristics should not be considered as a prognostic marker.

Having established that site-specific topography, despite its undeniable contribution, plays a minor role in the overall extent of bone resorption and their statistical significance remains secondary, it is imperative to recognize that a comprehensive evaluation of all concurrent variables is essential for clinical practice and remains fundamental in managing post-extraction sites intended for functional and aesthetic rehabilitation.

A rigorous analysis of the obtained data demonstrates that the most significant resorption occurs within the thin biotype, specifically at the most coronal aspect of the alveolar bone, for the well-established reasons previously discussed in detail.

The most significant statistical finding is the convergence of biotype and depth.

• At 1 mm depth: The difference between thin and thick biotypes is at its maximum (2.78 mm difference).
• At 5 mm depth: The difference narrows significantly (1.80 mm difference).
• Conclusion: Statistical significance (p-value < 0.05) is highest at the crestal level. If a patient has a thin biotype, the risk of horizontal collapse is almost 3 times higher in the first 1 mm than in the apical 5 mm, obviously.

As observed, crestal resorption appears significantly more pronounced compared to measurements taken at more apical levels. This discrepancy may have introduced a ‘measurement BIAS’ in the results reported in literature, particularly in studies where the extent of resorption is documented without a standardized vertical reference point (e.g., Lekovic at 4.4 mm vs. Karaka at 1.22 mm).

Nevertheless, the evaluations conducted converge toward a single conclusion. Within three of the analyzed variables (Height of measurement for HR, buccal vs. lingual wall in VR, and biotype), the extent of resorption is dictated by a single common denominator: the thickness of the alveolar bone. By adopting a holistic perspective across these three variables, the following insights emerge:

• Height of measurement: In the comparison of mean measurements of horizontal bone resorption obtained at different depths of the alveolar wall, the most pronounced HR was observed at the coronal portion, which anatomically represents the area of least thickness.
• Buccal vs lingual wall: regarding the differential values observed in vertical resorption, the data indicates that the most significant vertical bone loss occurs at the buccal wall. Histologically and anatomically, this wall is considerably thinner than its lingual counterpart.
• Biotype: this represents the variable that most effectively investigates the common denominator. Indeed, the results observed in both vertical and horizontal resorption leave no room for alternative interpretations; in the thin biotype, mean values are substantially higher than in the thick biotype, which conversely acts as a protective factor against bone resorption. A thin bone plate (<1 mm) is the single greatest risk factor for catastrophic alveolar bone collapse.

The outlier value in dataset, Chappuis (7.5 mm of VR for thin plates), highlights a critical clinical reality; when the buccal plate is extremely thin, the resorption isn’t just a remodeling but a complete structural collapse (45). The data from Chappuis et al. acts as a statistical outlier but is biologically plausible in cases of extreme buccal plate low thickness (45). When this study is excluded from analysis, the p-value for the phenotype comparison remains significant (p < 0.05), proving that bone thickness is a stable and reliable predictor of bone resorption.

 

CONCLUSIONS

 

One of the primary reasons of the necessity of a consistent bone volume after a correct healing of the post-surgical alveolar bone in modern dentistry is represented by treatment plan that includes implants placement for a consequent prosthetic rehabilitation of the partially or fully edentulous dental arch.

Considering all the numerous studies, clinical trials and review among literature, it is well known and demonstrated how surgical teeth extraction is a primary cause of bone modeling, that lead to important dimensional changes that affect the post-extraction alveolar bone. It is equally known that the entity of resulting bone loss depends on different factors (systemic and local) and the anatomical-histological characteristics of the specific alveolar bone area under consideration.  In our study, we evidenced how among different factors that are determinant for the quantity of bone resorption, it is possible to divide factors into three different categories:

• Not controllable and not modifiable factors: the loss of functional and mechanical stimulation of alveolar bone, and cellular depletion related to a loss of PDL and mesenchymal stem cells. These factors are not clinically controllable and modifiable by clinicians before, during and after surgical treatments. It is appropriate to cite the immediate loading in post-extraction implant placement which, although it represents a means of determining a functional load (despite all the necessary consideration which must inevitably be carried out considering this treatment option), it differs significantly from the physiological functional load transmitted by teeth through periodontal ligament to alveolar bone.
• Controllable but not modifiable factors: anatomical characteristics of both dental elements and alveolar bone. It is possible to have a general overview of anatomical situation before surgical extraction through modern three-dimensional radiographic techniques. The execution of CBCT, which unavoidably involves a biological cost, is justified and, moreover, fundamental in cases where extraction will be followed by surgical planning and positioning of dental implants. Knowing the thickness of alveolar wall and all the characteristics that are deeply analyzed in this study can help clinicians to be aware in advance of correlated risk in terms of bone resorption and to strategically be able to prevent them with adequate socket preservation technique.
• Controllable and modifiable factors: decrement of bloody supply, upregulation of RANKL/OPG pathway and the consequent inflammation. These factors are controllable with a correct anamnesis and objective exam that let the clinician know eventual situation that can improve the bone resorption. In modern clinical workflows, the optimization of this diagnostic phase is increasingly dependent on the transition from traditional paper medical records to advanced electronic health records (EHRs). Evidence demonstrates that EHR interfaces significantly enhance patient safety and clinical efficiency, enabling practitioners to identify critical systemic conditions and risk factors more rapidly and with greater accuracy, thereby virtually eliminating diagnostic oversights (65). Furthermore, clinicians have the possibility to intervene by modifying these factors during pre-operative, intra-operative and post-operative procedures that primarily led to a significant reduction of risk factors and, consequently, to a minimization of bone resorption.

In conclusion, bone resorption represents an inevitable collateral effect of tooth extraction but as described, it comprises characteristics and contributing factors that can be easily modified by clinicians. In light of this, when an adequate bone volume is requested, proper management through all clinical phases of the surgical treatment can help the clinician to minimize, but not to completely avoid, bone resorption.

 

Conflict of interest

The authors declare that they have no conflict of interest.

 

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