The interrelationship of orthodontic tooth movement in patients with periodontitis and Diabetes mellitus

A inter-relação do movimento dentário ortodôntico em pacientes com periodontite e Diabetes mellitus

ABSTRACT

Orthodontic tooth movement is a mechanically induced bone remodeling process aimed at aligning malpositioned teeth. Periodontitis is a polymicrobial infection of the supporting tissues of the teeth that results in the destruction of the periodontium. Diabetes Mellitus is a metabolic disorder that contributes to several types of comorbidities and even premature death of an individual. Due to the high demand of diabetic patients with periodontitis and the need for orthodontic therapy to achieve better periodontal health, we aimed to carry out a bibliographic review on orthodontic tooth movement in patients with periodontitis and diabetes mellitus. The search for articles in this literature review took place between February 2022 and March 2023. The articles were researched, selected and extracted through the database: PUBMED, LILACS and GOOGLE SCHOLAR available online, in the range of years between 1990 and 2022. Diabetes and periodontitis may adversely affect bone remodeling in orthodontic tooth movement. However, despite the need for further long-term studies to elucidate the mechanism of orthodontic tooth movement in diabetic patients with a history of periodontitis, the literature suggests that if there is a well-established periodontal-orthodontic therapy associated with the patient’s glycemic control, the treatment will be successful.

Indexing terms
Diabetes Mellitus; Orthodontics; Periodontitis

RESUMO

A movimentação dentária ortodôntica é um processo de remodelação óssea induzida mecanicamente com o objetivo de alinhar dentes mal posicionados. A periodontite é uma infecção polimicrobiana dos tecidos de suporte dos dentes que resulta na destruição do periodonto. O Diabetes Mellitus é um distúrbio metabólico que contribui para vários tipos de comorbidades e até mesmo a morte prematura de um indivíduo. Devido a grande demanda de pacientes diabéticos com periodontite e apresentando a necessidade da terapia ortodôntica para atingir melhor saúde periodontal, tivemos como objetivo realizar uma revisão bibliográfica sobre a movimentação dentária ortodôntica em pacientes com periodontite e diabetes mellitus. A busca pelos artigos desta revisão de literatura ocorreu entre fevereiro de 2022 e março de 2023. Os artigos foram pesquisados, selecionados e extraídos por meio das bases de dados: PUBMED, LILACS e GOOGLE SCHOLAR disponíveis online, no intervalo entre 1990 até 2022. Diabetes e periodontite podem afetar adversamente a remodelação óssea na movimentação dentária ortodôntica. No entanto, apesar da necessidade de mais estudos a longo prazo para elucidar o mecanismo da movimentação dentária ortodôntica em pacientes diabéticos com histórico de periodontite, a literatura nos sugere que se houver uma terapia periodontal-ortodôntica bem estabelecida associada ao controle glicêmico do paciente, o tratamento será bem-sucedido.

Termos de indexação
Diabetes Mellitus; Ortodontia; Periodontite

INTRODUCTION

Orthodontic tooth movement (OTM) is basically a phenomenon of bone remodeling. The aim of OTM is to align malpositioned teeth by applying external forces (“orthodontic forces”) to the teeth and thus stimulate bone remodeling. The ability of teeth to move through bone depends on the periodontal ligament, which attaches the tooth to the adjacent bone. During OTM, mechanical stimulation triggers complex aseptic inflammatory, cellular and molecular processes, causing remodeling of surrounding tissues, leading to bone resorption on the pressure side and bone formation on the tension side [¹].

Periodontitis is a chronic inflammatory condition in response to biofilm that can lead to irreversible damage to the supporting structures surrounding the teeth, potentially causing tooth loss being one of the most common oral diseases. It is typically characterized by inflammatory infiltration in the periodontal tissues (gum, periodontal ligament, alveolar bone and cementum) causing damage and loss of alveolar bone. Common features of periodontitis include gingival inflammation, clinical attachment loss, radiographic evidence of alveolar bone loss, probing depth sites, mobility, bleeding on probing, and pathologic tooth migration [²].

Diabetes Mellitus (DM) is characterized by hyperglycemia, inflammation and high oxidative stress, which leads to systemic complications. This chronic disorder has a negative effect on most metabolic pathways and contributes to the pathophysiology and complications of the disease. Other examples of complications of chronic diseases are retinopathy, neuropathy, cardiovascular disease, and nephropathy. In addition to these complications, oral diseases can also be expected in diabetic patients. It is already well documented in many reviews and epidemiological studies that diabetes and periodontitis have a bidirectional relationship [³].

The aim of this work is to report the interrelationship between OTM, periodontitis and DM through a literature review, to obtain a better understanding in the treatment of patients who present this scenario.

The search for articles in this literature review took place between February 2022 and March 2023. The articles were researched, selected and extracted through the database: PUBMED, LILACS and GOOGLE SCHOLAR available online, in the range of years between 1990 and 2022. Of the 253 articles initially found, the 30 most relevant articles on OTM, periodontitis and DM were selected to carry out this review. The main descriptors used were: Orthodontics, Tooth Movement Techniques, Periodontitis.

Orthodontic tooth movement (OTM)

The OTM causes complex remodeling in dentoalveolar biological tissue. Since the first publication on the OTM mechanism in 1911, several theories have been proposed. So far, the pressure-tension theory is the most accepted and proposes that cellular responses are modulated by cytokines, released from the blood flow or from cells in situ, in response to mechanical stress imposed on the periodontal ligament and alveolar bone [⁴].

The ability of teeth to move through bone depends on the periodontal ligament, which attaches the tooth to the adjacent bone. The periodontal ligament is a highly specialized connective tissue, including a population of heterogeneous cells and a fibrous extracellular matrix. Most of the periodontal ligament space is occupied by bundles of collagen fibers (mainly type I) that are embedded in the intercellular substance. Cellular changes in the periodontal ligament are the first events after OTM activation. Inflammatory mediators such as prostaglandins (PGs), interleukins (ILs; IL-1, -6 and -17), the tumor necrosis factor (TNF)-α superfamily and the expression of the receptor activator of nuclear factor-kappa B (RANK)/ receptor activator of nuclear factor-κappa B ligand (RANKL)/ osteoprotegerin (OPG) system are increased in the periodontium [⁴]. Secretion of cytokines and decreased oxygen tension lead to temporary sterile inflammation. Abundant inflammatory cytokines are released by periodontal ligament cells into the gingival crevicular fluid and periodontal environment, recruiting immune cells that regulate regional bone metabolism [⁵].

Bone is continually reabsorbed by osteoclasts and newly formed by osteoblasts to maintain bone volume and calcium homeostasis throughout the lifespan of vertebrates. In OTM, the RANK/RANKL/OPG system is the key regulator for bone remodeling. Udagawa et al. [⁶] explain that osteoclasts are multinucleated cells that derive from cells of the monocyte/macrophage lineage. These so-called pre-osteoclastic cells present the RANK receptor, which when associated with the RANKL ligand become osteoclasts and activate osteoclastogenesis, consequently promoting bone resorption. In contrast, osteoblasts mediate osteoclastogenesis by expressing RANKL, which is expressed as a membrane-associated cytokine. OPG is a soluble RANKL decoy receptor that is predominantly produced by osteoblasts, and which prevents osteoclast formation and osteoclastic bone resorption by inhibiting RANK/RANKL interaction. RANK/RANKL signaling regulates the formation, activation and survival of osteoclasts in bone modeling and remodeling under normal conditions and in a variety of pathological conditions characterized by increased bone resorption [⁴]. OPG protects bone from excessive resorption by binding to RANKL and preventing it from binding to RANK [⁷].

During an OTM, the “pressure/tension theory” describes that the surface of the lamina dura that is being compressed, specifically, the surface on which the tooth is applying pressure, is resorbed by pressure associated osteoclasts, while bone replacement by the osteoblasts is associated by tension along the tensioned surface of the periodontal ligament fibers. Other participants in bone remodeling in OTM are different types of matrix metalloproteinases (MMPs) and their tissue inhibitors of matrix metalloproteinases (TIMPs), both secreted by periodontal ligament fibroblasts. MMPs cause manipulation of extracellular matrix proteins such as collagen and elastin and can be regulated by TIMPs, and the MMP/TIMP ratio generally determines the extent of extracellular matrix protein manipulation and tissue remodeling [⁸].

Several systemic factors can adversely affect orthodontic treatment. Studies have revealed hypercalciuria and decreased intestinal calcium absorption in diabetic individuals, indicating increased bone demineralization [⁹]. The presence of factors that modify the inflammatory response, such as diabetes, can also alter the host’s response to orthodontic force. Animal studies [⁹,¹⁰] demonstrated that diabetes can accelerate periodontal collapse during OTM in diabetic animals and in animals that had greater alveolar bone loss during orthodontic treatment than in healthy animals.

The installation of fixed orthodontic appliances can compromise patients’ oral environment due to the presence of additional surfaces, making oral hygiene procedures difficult, and may affect the balance of the oral microbiota. Due to difficulty in brushing, plaque may accumulate around the brackets, resulting in halitosis, decalcification of tooth surfaces, periodontal diseases. Patients undergoing orthodontic treatment must be aware of this risk and follow appropriate measures to prevent it. Based on the difficulty of maintaining oral hygiene, the oral microbiota can also be influenced by orthodontic appliances. These variables can cause microbial dysbiosis, causing a change in increased colonization by pathogenic bacteria that have potent virulence factors that contribute to gingival inflammation, destruction of periodontal support and changes in the enamel surface. Therefore, orthodontic patients are considered “risk” patients [¹¹].

In addition to periodontal implications, plaque retention in the presence of orthodontic appliances has also been associated with increased susceptibility to caries and is influenced by transient/permanent qualitative and quantitative changes in the oral microbiota, responsible for the appearance of oral infections, with systemic effects on oral health and well-being , thus predisposing orthodontic patients to suffer various pathologies with greater probability than non-orthodontic patients [¹²].

Periodontitis

Periodontitis is a complex immuno-inflammatory condition characterized by rupture of the periodontal ligament and subsequent formation of periodontal pockets, alveolar bone loss and often resulting in tooth loss [²]. It is defined by stage and degree of the disease: the stage represents the severity, extent and distribution of the disease, as well as the expected complexity of its management; Grade represents the additional biological dimensions of the disease, including the observed and/or predicted rate of progression, the predicted outcomes of treatment, and the risk that the disease or its treatment will negatively affect the patient’s overall health [¹³]. Disease progression depends not only on bacteria, but also on the host’s immune response, as inadequate immune response to microorganisms can accelerate the development and progression of periodontitis. Periodontal pathogens enter the circulatory system, producing endotoxins that cause systemic infections, thus leading to an increase in inflammatory cytokines stimulated by bacterial lipopolysaccharides (LPS)2. LPS, in association with other virulence factors of these periodontal pathogens, stimulate host macrophages and other constituent inflammatory cells, triggering the production of a series of pro-inflammatory cytokines, such as TNF-α, IL-1β, which produce a synergistic effect. by increasing the synthesis of IL-6, resulting in increased activation of Th17 cells and prostaglandin E2 (PGE 2) [¹⁴]. The presence of these pro-inflammatory cytokines and virulence factors stimulate the production of MMPs by macrophages, fibroblasts, junctional epithelial cells and neutrophils. The MMPs are a large family of zinc endopeptidase enzymes that are involved in the degradation of extracellular proteins and are responsible for the destruction of collagen fibers in periodontal tissues, especially periodontal ligament fibers. Furthermore, pro-inflammatory cytokines induce RANKL in osteoblasts and T helper cells. The resulting RANKL on osteoblasts and T helper cells then interacts with RANK on preosteoclasts, which results in the genesis of osteoclasts and their maturation. Mature osteoclasts mediate alveolar bone resorption. In periodontitis, an imbalance in the RANK/RANKL/OPG system occurs, as it is a unique osteoimmune disease in which RANKL links the antibacterial immune response to bone destruction [¹⁵].

Current standard therapy in both gingivitis and periodontitis aims to remove pathogenic microbial biofilm through mechanical debridement (scaling and root planing). Treatment of periodontitis involves a non-specific reduction of the bacterial load below the gingival margin, which can be achieved through non-surgical periodontal therapy (NSPT), oral hygiene instructions and supportive periodontal therapy (SPT) [¹⁶]. The main objective of NSPT is to reduce inflammation and restore periodontal health through the removal of biofilm and supra- and subgingival plaque using a closed approach. Likewise, SPT has been shown to be effective in maintaining periodontal health and preventing tooth loss in patients with periodontitis. Vertical periodontal bone defects (intraosseous defects) have been associated with a greater risk of progression and eventually tooth loss. Therefore, they are considered sites that require therapy, often in addition to NSPT [¹⁷].

Due to the significant morbidity of periodontitis and associated diseases, there is an urgent need to develop new therapeutic approaches to support currently used strategies, which focus on limiting bacterial challenge (scaling and root planing or root surface debridement) [¹⁶].

Pathological migration of teeth is a common complication of periodontitis, due to bone loss and manifests as the tilting, projection and separation of anterior teeth. Patients with periodontitis often present several sequelae, such as: 1) inadequate angulation; 2) excessive mouth projection; 3) extrusion of one or more incisors; and 4) development of single or multiple diastemas in anterior teeth, with progressive incisor spacing, often fan-shaped [¹⁸]. Teeth with significant loss of supporting periodontal tissue are especially prone to occlusal trauma, which has been defined as secondary occlusal trauma. After adequate periodontal therapy, orthodontic treatment can improve both the alveolar bone and periodontal soft tissues. Orthodontic correction of pathologically malpositioned teeth can alleviate occlusal trauma, stabilize the dentition and improve periodontal status [¹⁹].

Diabetes Mellitus (DM)

The DM is a metabolic disorder that slowly but continuously contributes to premature death and various types of comorbidities [³]. DM is also called non-insulin-dependent diabetes (NIDD) and is characterized by a deficiency of insulin receptors. In patients with DM, chronic hyperglycemia or glycemia peaks in the postprandial period promote the non-enzymatic modification of several macromolecules, enabling the generation of advanced glycation end products (AGEs) [²⁰].

The AGEs are formed when the carbonyl component of a sugar reacts with a free amino group of an amino acid in a series of non-enzymatic processes known collectively as the Maillard reaction. Approximately 30% of AGEs are absorbed into the systemic circulation through gastrointestinal absorption and the influence of systemic load. The AGEs circulating in the bloodstream bind to receptors for AGE (RAGE), which are transmembrane pattern recognition receptors belonging to the superfamily of immunoglobulin genes, present on the cell surface and promote the generation of reactive oxygen species (ROS), with activation of nuclear factor kappa B [²¹].

One of the main mechanisms for the development of diabetes complications is through oxidative stress. Oxidative stress is defined as a disturbance in the balance between ROS production and antioxidant defense systems (ADS) and develops when the rate of ROS formation exceeds ADS, resulting in the toxic effects of free radicals [²²]. This distortion in the cell’s redox balance results in damage to membranes and vital biomolecules such as DNA, proteins and lipids. There is a large body of evidence to suggest that AGEs play a significant role in the pathogenesis of macro- and microvascular diabetic complications [²¹].

Diabetic patients, even those treated with insulin, present changes in bone metabolism [²⁰], with periodontal disease being considered a complication of DM [³]. Diabetes also prolongs the duration of alveolar bone degradation, remodeling, and resorption of the periodontal ligament. The MMPs play a crucial role in remodeling the extracellular matrix of the periodontal ligament and alveolar bone. Intense expression of MMP-9 was observed in patients with diabetes and periodontitis [²³]. As DM has a considerable negative effect on bone remodeling, the teeth of diabetic patients are very likely to be misaligned and require dental correction [³]. The presence of factors that modify the inflammatory response, such as diabetes, can also alter the host’s response to orthodontic force [²⁴].

DISCUSSION

DM and periodontitis are chronic non-communicable diseases, closely related and have a high prevalence in the world, seriously compromising the quality of life of the affected population. Periodontitis becomes more serious and frequent in the presence of DM [³]. In recent years, orthodontic treatment has become popular among both juvenile and adult patients. Especially for adult patients, systemic factors must be taken into consideration when orthodontic treatment is performed [⁹].

To restore functional and facial aesthetics, orthodontic treatment triggers tooth movement and involves multiple biological processes. During OTM, orthodontic force causes aseptic inflammation, leading to bone resorption in the region of pressure and bone formation in the region of tension. Eventually, the periodontium is reconstructed and the tooth is moved. Therefore, well-controlled inflammation is essential in OTM [²⁵].

DM can modulate the host response to periodontal pathogens, altering their structure and AGE metabolites, cytokines, bone metabolism and immune response, in addition to participating in the immune regulation of diabetes to periodontitis microflora. The combination of RAGE receptors expressed by macrophages and AGEs produced by DM can activate monocytes, macrophages and endothelial cells and induce the release of pro-inflammatory cytokines. The effect of DM on periodontitis may involve the adipose factor, AGE/RAGE and RANK/RANKL pathways [²¹].

Boas Nogueira et al. [²⁶], demonstrated that OTM, in the presence of periodontitis, increases the levels of inflammatory cytokines, damaging periodontal tissue. Santamaria Jr et al. [⁹], showed a lower organization of collagen fibers in diabetic rats, regardless of the presence of periodontitis during OTM. Other studies suggest that diabetes not only induces greater alveolar bone resorption, but also alters OTM [²⁷]. Rapid disorganization of the periodontal ligament was observed in diabetic animals during OTM [¹⁰]. Patients with diabetes present intense collagenase activity and decreased fibroblast collagen synthesis in gingival tissue [⁹]. Altered collagen metabolism may predispose diabetic patients to periodontitis and imperfect healing. Almeida et al. [²³] evaluated the levels of (MMPs) -1, -2, -3, -7, -8, -12 and -13 in the gingival crevicular fluid of teeth compromised by periodontitis at different times during OTM and suggest that orthodontic movement in teeth compromised by periodontitis without active pockets did not result in significant changes in MMP levels in gingival crevicular fluid.

Zasčiurinskienė et al. [²⁸] in a randomized clinical study with 50 patients comparing two treatment strategies in relation to the effect of orthodontic treatment in patients with plaque-induced periodontitis, but with the disease stabilized, concluded that orthodontic treatment, concomitant with periodontal treatment and SPT, can be used in the routine treatment of patients with plaque-induced periodontitis.

Diabetes is not a contraindication for orthodontic interventions. However, diabetic patients must establish very tight control of their glycemic states and be kept under adequate monitoring before starting active orthodontic treatment [²⁹]. Due to the low blood flow to the teeth and supporting tissues that occurs in diabetic patients, dentists must take into consideration that the teeth and periodontium of these patients are negatively compromised and, therefore, must apply physiological forces as light as possible [³⁰]. A combined orthodontic-periodontal therapy may be necessary for a functionally and aesthetically satisfactory treatment result. Some clinical studies have been dedicated to this combined therapy and have proven that patients treated with periodontitis can be treated orthodontically with successful results [²⁸].

CONCLUSION

The DM and periodontitis can adversely affect bone remodeling and tooth movement during the application of orthodontic forces. Despite the need for more long-term and well-designed studies to understand OTM in patients with DM and a history of periodontitis, the literature suggests that if there is a well-established periodontal-orthodontic therapy associated with the patient’s glycemic control, the treatment will be well -successful.

How to cite this article

• Bernardo DV, Guimarães GS, Camargo GACG. The interrelationship of orthodontic tooth movement in patients with periodontitis and Diabetes mellitus. RGO, Rev Gaúch Odontol. 2024;72:e20240011. http://dx.doi.org/10.1590/1981-86372024002220240011

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Edited by

• Assistant editor: Luciana Butini Oliveira

Publication Dates

• Publication in this collection
  07 Oct 2024
• Date of issue
  2024

History

• Received
  28 Feb 2024
• Reviewed
  09 June 2024
• Accepted
  27 June 2024