Boron Deprivation Research Articles

Phenylboronic acid interacts with pectic rhamnogalacturonan-II and displays anti-auxinic effects during Arabidopsis thaliana root growth and development.

Boron dimerizes RG-II in the plant cell wall and is crucial for plant cell elongation. However, studying RG-II dimerization in plants is challenging because of the severe phenotypes or lethality of RG-II mutants. Boron deprivation abrogates both RG-II dimerization and plant growth, but whether or how these phenotypes are functionally linked has remained unclear. Boric acid analogues can serve as experimental tools to interfere with RG-II cross-linking. Here, we investigated RG-II dimerization and developmental phenotypes in Arabidopsis thaliana seedlings treated with a boric acid analogue, phenylboronic acid (PBA), to test whether the observed developmental phenotypes are attributable to alteration of RG-II dimerization or to other putative functions of boron in plants. We found that PBA treatment altered root development in seedlings while RG-II dimerization and distribution were not affected. Surprisingly, under low boron conditions, PBA treatment i) had no effect on root size but still prevented lateral root development and ii) restored RG-II dimerization. PBA treatment also disrupted auxin levels, potentially explaining the absence of lateral roots in seedlings treated with this analogue. We conclude that PBA interacts both with RG-II and other cellular targets such as auxin signaling components, and that the phenotypes caused by PBA arise from interference with multiple functions of boron.

PIN2/3/4 auxin carriers mediate root growth inhibition under conditions of boron deprivation in Arabidopsis.

The mechanistic basis by which boron (B) deprivation inhibits root growth via the mediation of root apical auxin transport and distribution remains elusive. This study showed that B deprivation repressed root growth of wild-type Arabidopsis seedlings, which was related to higher auxin accumulation (observed with DII-VENUS and DR5-GFP lines) in B-deprived roots. Boron deprivation elevated the auxin content in the root apex, coinciding with upregulation of the expression levels of auxin biosynthesis-related genes (TAA1, YUC3, YUC9, and NIT1) in shoots, but not in root apices. Phenotyping experiments using auxin transport-related mutants revealed that the PIN2/3/4 carriers are involved in root growth inhibition caused by B deprivation. B deprivation not only upregulated the transcriptional levels of PIN2/3/4, but also restrained the endocytosis of PIN2/3/4 carriers (observed with PIN-Dendra2 lines), resulting in elevated protein levels of PIN2/3/4 in the plasma membrane. Overall, these results suggest that B deprivation not only enhances auxin biosynthesis in shoots by elevating the expression levels of auxin biosynthesis-related genes but also promotes the polar auxin transport from shoots to roots by upregulating the gene expression levels of PIN2/3/4, as well as restraining the endocytosis of PIN2/3/4 carriers, ultimately resulting in auxin accumulation in root apices and root growth inhibition.

Boron-deficiency and aluminum toxicity activate antioxidant defense and disorganize the cell wall composition and architecture in trifoliate orange leaf

Boron (B)-deficiency and aluminum (Al) phytotoxicity are two main factors that influence the yield and quality of citrus. In this study, we investigated the effects of B-deficiency, Al stress, and double stress of B-deficiency and Al toxicity on antioxidant enzyme system and cell wall components in leaf of trifoliate orange seedlings. Boron deprivation and Al toxicity severely induced morphological and anatomical changes in leaves in terms of higher lipid peroxidation, inhibited photosynthesis and impeded seedling growth, and the damages was more pronounced by double stress. Boron-deficiency disturbed the distribution pattern of pectin in leaves, suppressing the content of alkali-soluble pectin and two types of 2-keto-3-deoxyoctanoic acid (KDO), thus reduced the binding of B to the leaf cell wall. Meanwhile, exposure of Al stress alone resulted in increased content of chelator-soluble pectin and alkali-soluble pectin, whilst an opposite trend was detected in the degree of methylation of the above two pectins. Transmission electron microscope (TEM) micrographs of –B and –B +Al-treated leaves showed destruction of chloroplasts and a distinct thickening of cell wall. Fourier-transform infrared spectroscopy (FTIR) and 13C-nuclear magnetic resonance spectroscopy (13C NMR) in conjunction with X-ray diffraction (XRD) exhibited cellulose accumulation while its crystallinity was reduced by Al toxicity and double stress. Taken together, our results reveal that B-deficiency and Al toxicity caused oxidative damage to plants, changed the pectin content and characteristics, and altered the cell wall components and architecture, which could be a major cause of deleterious seedling growth.

Programmed cell death induced by cadmium stress and/or boron deprivation in tobacco (Nicotiana tabacum L.) cultivar Bright Yellow 2 cells

Cadmium (Cd) is one of the most toxic and widespread heavy metal pollutants in soil. As an essential mineral nutrient, boron (B) plays critical roles in physiological processes of plants. In the present study, programmed cell death (PCD) induced by Cd stress and/or B deprivation was assessed and the underlying mechanisms were clarified in suspension-cultured Nicotiana tabacum L. cultivar Bright Yellow 2 (TBY-2) cells. The PCD in TBY-2 cells was analyzed by Hoechst 33258 staining and the terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) assay, and then, expression analysis of PCD-related genes was performed using quantitative real-time polymerase chain reaction (qPCR) assays. The production of reactive oxygen species (ROS) was determined using fluorescence microscopy of 2′,7′-dichlorofluorescein diacetate–labeled cells. The levels of lipid peroxides were quantified by the thiobarbituric acid–reactive substances (TBARS) method. Cadmium stress and/or B deprivation treatments induced PCD that was characterized by a significant increase in the percentage of cells stained with Hoechst 33258 or TUNEL-positive cells, and upregulation or downregulation of the expression of PCD-related genes. Treatments with Cd stress and/or B deprivation increased ROS production and the level of lipid peroxides compared to those of the control group. These data showed that in TBY-2 cells Cd stress and/or B deprivation activated ROS signaling pathways, leading to gene expression that was connected with the PCD process.

Boron deprivation induced inhibition of root elongation is provoked by oxidative damage, root injuries and changes in cell wall structure

Boron (B) is one of the essential micronutrients for the growth and development of higher plants and its deprivation inhibits root elongation. However, little is known about the mechanisms underlying inhibition of root elongation under B deficiency. The present study was carried out with three B levels (0, 5 and 10 μM B) to investigate the effect of B deprivation on the growth of trifoliate orange seedlings and to explore the possible mechanisms involved in the B deprivation induced root growth inhibition. The results indicated that B deprivation severely hampered primary and lateral root elongation with visible symptoms of leaf chlorosis. The B deprivation led to the accumulation of reactive oxygen species, membrane peroxidation and root cell injuries. Boron deprivation not only exhibited reduced concentrations of glutathione but also inhibited the activities of major antioxidant enzymes. Moreover, an elevated accumulation of Ca2+ ion and altered subcellular cell wall structure and disorganized homogalacturonan epitopes were observed in B deficient plants. Taken together, it is concluded that B deprivation leads to root cell injuries, changes in the cell wall structure and accumulates oxidative damage that could be possible causes of root growth inhibition of trifoliate orange under B deprivation.

Mechanism underlying rapid responses to boron deprivation in Arabidopsis roots

ABSTRACTTransferring hydroponically grown Arabidopsis plants (Arabidopsis thaliana L.) to boron (B)-free medium kills the cells in root tips within an hour. To understand the mechanism underlying the induced rapid cell death, the Arabidopsis response to B deprivation was characterized using inhibitors of presumably involved cellular processes. The results suggest that stretching of the plasma membrane and the influx of calcium ions through mechanosensitive channels triggered the responses and that reactive oxygen species were overproduced under B-deprived condition. In addition, nitric oxide was observed to be involved in cell death, suggesting that Arabidopsis root cells undergo programmed cell death upon B deprivation. RNA sequencing analysis revealed that B deprivation induced transcriptome changes that resembled pathogen-induced responses. In summary, we speculate that B deprivation induces hypersensitive responses in Arabidopsis roots as a response to defective cell wall structures.

Influence of boron deprivation on Hg stress-induced programmed cell death in suspension-cultured tobacco BY-2 cells

ABSTRACTSome agricultural regions in large areas deficient in Boron (B) also present a risk of contamination of soils with excess mercury (Hg). The purpose of this study was to explore whether Hg stress induces programmed cell death (PCD) in tobacco BY-2 (Nicotiana tabacum L. cv. Bright Yellow-2) cells and the influence of B deprivation on mercury (Hg) stress-induced PCD. It was shown that the BY-2 cells exposed to 30 μM mercury chloride (HgCl2) underwent PCDand in the meantime, the expression changes of PCD-related genes were found. Meanwhile, Hg stress in combination with B deprivation can cause much higher proportion of cells to undergo PCD than Hg stress alone. Accompanied with PCD, the HgCl2-stressed cells under B deprivation accumulated more H2O2 and lipid peroxides than control cells. Our results suggest that HgCl2 can induce PCD in tobacco BY-2 cells, that B deficiency would enhance this effect, and oxidative damage is directly involved in the PCD process.

Boron deficiency alters root growth and development and interacts with auxin metabolism by influencing the expression of auxin synthesis and transport genes

ABSTRACTBoron (B) deficiency inhibits and disturbs root growth and development by interacting with auxin (indole-3-acetic acid, IAA). However, the underlying mechanism of this interaction is still poorly understood. This study found that plants in a long-term boron deprivation treatment (∼0.25 µg L−1) had inhibited elongation of trifoliate orange roots, enlarged root tips and severe necrosis as well as a significant decrease in soluble boron and IAA content in seedling root tips. The results of a short-term boron deprivation treatment showed that a significant decrease in soluble boron and IAA content occurred after 3 hours of treatment (HOT) and 1 day of treatment (DOT), respectively. Moreover, the expression of IAA synthetic genes (TAA1, TAR2, YUC3 and YUC8) was strongly induced as early as 3 HOT and was then significantly reduced. The expression of rootward IAA transport genes (AUX1, PIN1 and PIN4) decreased significantly in the boron deprivation treatment, but the expression levels of shootward IAA transport genes (LAX1, ABCB1 and PIN3) were significantly increased. Taken together, the increase in IAA content before 1 DOT may be due to increased IAA synthesis caused by the induction of TAA1, TAR2, YUC3 and YUC8 expression; the subsequent decrease and the significantly lower final IAA content compared to the +B treatment (0.25 mg L−1 B) may be due to the reduced expression of IAA synthetic genes and rootward IAA transport genes and the increased expression of shootward IAA transport genes.Abbreviations: DAT: days after treatment; DOT: day of treatment; FW: fresh weight; HOT: hour of treatment; isB: insoluble boron; LC: liquid chromatography; LSD: least-significant difference; MS: mass spectrometry; PAT: polar auxin transport; qRT-PCR: quantitative real-time polymerase chain reaction; sB: soluble boron

Boron deficiency results in early repression of a cytokinin receptor gene and abnormal cell differentiation in the apical root meristem of Arabidopsis thaliana

The development of Arabidopsis thaliana was dramatically altered within few hours following boron (B) deprivation. This effect was particularly evident in the apical root meristem. The essentiality of boron in plants has been clearly linked to its structural role in the cell wall, however the diversity and rapidity alterations of plant organogenesis when the micronutrient is absent suggest that B deficiency could also affect gene regulation during plant development. Therefore, the effect of B deficiency on cell elongation, apical root meristem cell division, and early differentiation of root tissues was investigated in A. thaliana seedlings. Dark-growth experiments indicated that hypocotyl elongation was inhibited 2 days after removing B, but apical root growth ceased almost immediately following B deprivation. Detection of cycline B1 by GUS staining of a promoter-reporter construct revealed that low B led to a reduced zone of cell division. The expression of CRE1/WOL/AHK4, encoding an integral membrane protein with histidine kinase domain that mediates cytokinin signaling and root xylem differentiation, was inhibited under B deficiency resulting in arrested xylem development at the protoxylem stage. Because the transition from cell division to cell differentiation in apical root meristems is controlled by cytokinins, this result support the hypothesis that signaling mechanisms during cell differentiation and organogenesis are highly sensitive to B deficiency, and together with previous reports that link the micronutrient with auxin or ethylene control of root architecture, suggests that B could play a role in regulation of hormone mediated early plant development signaling.

Boron deprivation immediately causes cell death in growing roots of Arabidopsis thaliana (L.) Heynh.

Boron (B) is essential for the correct formation of cell wall structure because it is a component of borate-ester cross-links in pectin. Previously, we showed that removal of B from the culture medium immediately induced stress responses in suspension-cultured tobacco (Nicotiana tabacum L.) cells, but the mechanism by which cells exhibit such rapid responses remained unclear. In this study, we characterized the early responses of Arabidopsis thaliana (L.) Heynh. to B deprivation. Deprivation of B for 1 h caused cell death specifically in the root elongation zone. Reactive oxygen species accumulated in the same region, suggesting that the death was caused by oxidative damage. The B-deprivation treatment also induced the expressions of stress-responsive genes within 1 h. These results demonstrated that A. thaliana immediately senses and responds to the removal of B from the external medium. Similar responses were induced by calcium deprivation but not magnesium or potassium deprivation, suggesting that the failure of cross-linking in pectin molecules in growing cells triggers these rapid responses.

Proteomics reveals the adaptability mechanism of Brassica napus to short-term boron deprivation

Boron (B) is essential for the normal growth and development of oilseed rape. To gain better insight into the metabolic processes of Brassica napus in response to B starvation, a time course proteomics analysis of roots under conditions of hydroponic cultivation was carried out. Forty-six differentially expressed proteins were identified by MALDI-TOF/TOF MS. These proteins were classified into the following functional categories: carbohydrate and energy metabolism, stress response, signaling and regulation, cell wall, protein process, amino acid and fatty acid metabolism, nucleic acid metabolism. In general, the energy metabolism pathway and certain biosynthesis pathways were maintained at a relatively low level, while signaling, regulation and stress response pathways were dramatically induced in the absence of B. Eight genes were selected for qPCR analysis to detect the relationships among protein and gene expression patterns. Furthermore, analyses of lipid peroxidation and glutathione reductase activity revealed that oxidative damage was induced and the antioxidative system was activated under conditions of B deficiency. These results suggest that carbon flux is a putative modulating process that controls the response to B deficiency stress, and a stable cell wall structure, resistance to oxidative damage and a complex signaling network may contribute to the tolerance to B deficiency.

Expression of root glutamate dehydrogenase genes in tobacco plants subjected to boron deprivation

Recently it has been reported that boron (B) deficiency increases the expression of Nicotiana tabacum asparagine synthetase (AS) gene in roots, and that AS might play a main role as a detoxifying mechanism to convert ammonium into asparagine. Interestingly, glutamate dehydrogenase (GDH) genes, Ntgdh-NAD;A1 and Ntgdh-NAD;B2, were up-regulated when tobacco roots were subjected to B deprivation for 8 and 24h. In addition, aminating and deaminating GDH (EC 1.4.1.2) activities were higher in B-deficient than in B-sufficient plants after 24h of B deficiency. Ammonium concentrations were kept sufficiently low and with similar values in B-deficient roots when compared to control. Glucose and fructose contents decreased after 24h of B deprivation. This drop in hexoses, which was corroborated by metabolomic analysis, correlated with higher GDH gene expression. Furthermore, metabolomic profiling showed that concentrations of several organic acids, phenolics, and amino acids increased after 24h of B deficiency. Our results suggest that GDH enzyme plays an important role in metabolic acclimation of tobacco roots to B deprivation. A putative model to explain these results is proposed and discussed.

Boron Nutrition of Cultured Tobacco BY-2 Cells. VI. Calcium is Involved in Early Responses to Boron Deprivation

Boron (B) deprivation induces various responses in plant cells, some of which can be observed very early. However, it has been unknown what kind of signal is generated by the stress. We found that B deprivation induced the expression of stress-responsive genes within 1 h in suspension-cultured tobacco BY-2 cells. The induction was largely suppressed by withholding medium Ca(2+) or by adding a Ca(2+) channel blocker. Analysis using aequorin-expressing cells showed that B-deprived cells took up more Ca(2+) than control cells. These results suggest that Ca(2+) influx plays a role in B deprivation stress signaling.

Micronutrients in Parenteral Nutrition: Boron, Silicon, and Fluoride

Boron may be beneficial for bone growth and maintenance, central nervous system function, and the inflammatory response, and silicon may be beneficial for bone maintenance and wound healing. Fluoride is not an essential element but amounts provided by contamination may be beneficial for bone strength. Fluoride toxicity may be a concern in parenteral nutrition. Further studies are warranted to determine whether there are optimal amounts of boron and silicon that should be delivered to typical and special population patients receiving parenteral nutrition. In addition, further studies are needed to determine whether providing the dietary guideline of adequate intake amounts of fluoride parenterally would prevent or treat parenteral nutrition osteopenia.

Membrane-Associated, Boron-Interacting Proteins Isolated by Boronate Affinity Chromatography

Boron deficiency symptoms point to a role for boron in plant membranes, but the molecular partners interacting with boron have not yet been identified. The objective of the present study was to isolate and identify membrane-associated proteins with an ability to interact with boron. Boron-interacting proteins were isolated from root microsomal preparations of arabidopsis (Arabidopsis thaliana) and maize (Zea mays) using phenylboronate affinity chromatography, subsequently separated by two-dimensional gel electrophoresis and identified using MALDI-TOF (matrix-assisted laser desorption ionization-time of flight) peptide mass fingerprinting. Twenty-six boron-binding membrane-associated proteins were identified in A. thaliana, and nine in Z. mays roots. Additional unidentified proteins were also present. Common to both species were the beta-subunit of mitochondrial ATP synthase, several beta-glucosidases, a luminal-binding protein and fructose bisphosphate aldolase. In A. thaliana, binding of these proteins to boron was significantly reduced after 4 d of boron deprivation. The relatively high number of diverse proteins identified as boron interacting, many of which are usually enriched in membrane microdomains, supports the hypothesis that boron plays a role in plant membranes by cross-linking glycoproteins, and may be involved in their recruitment to membrane microdomains.

Boron deprivation decreases liver S-adenosylmethionine and spermidine and increases plasma homocysteine and cysteine in rats

Two experiments were conducted with weanling Sprague–Dawley rats to determine whether changes in S-adenosylmethionine utilization or metabolism contribute to the diverse responses to boron deprivation. In both experiments, four treatment groups of 15 male rats were fed ground corn-casein based diets that contained an average of 0.05 mg (experiment 1) or 0.15 mg (experiment 2) boron/kg. In experiment 2, some ground corn was replaced by sucrose and fructose to increase oxidative stress. The dietary variables were supplemental 0 (boron-deprived) or 3 (boron-adequate) mg boron/kg and different fat sources (can affect the response to boron) of 75 g corn oil/kg or 65 g fish (menhaden) oil/kg plus 10 linoleic acid/kg. When euthanized at age 20 (experiment 1) and 18 (experiment 2) weeks, rats fed the low-boron diet were considered boron-deprived because they had decreased boron concentrations in femur and kidney. Boron deprivation regardless of dietary oil increased plasma cysteine and homocysteine and decreased liver S-adenosylmethionine, S-adenosylhomocysteine, and spermidine. Plasma concentration of 8-iso-prostaglandin F 2α (indicator of oxidative stress) was not affected by boron, but was decreased by feeding fish oil instead of corn oil. Fish oil instead of corn oil decreased S-adenosylmethionine, increased spermidine, and did not affect S-adenosylhomocysteine concentrations in liver. Additionally, fish oil versus corn oil did not affect plasma homocysteine in experiment 1, and slightly increased it in experiment 2. The findings suggest that boron is bioactive through affecting the formation or utilization of S-adenosylmethionine. Dietary fatty acid composition also affects S-adenosylmethionine formation or utilization, but apparently through a mechanism different from that of boron.

Boron and fish oil have different beneficial effects on strength and trabecular microarchitecture of bone

An experiment was performed to determine whether boron deprivation would adversely affect vertebra (trabecular) bone microarchitecture, and whether any adverse effect would be modified by dietary fatty acid composition. Female rats were fed diets containing 0.1 mg (9 μmol) boron/kg in a factorial arrangement with variables of supplemental boron at 0 (boron-deprived) or 3 (boron-adequate) mg (278 μmol)/kg and fat sources of 75 g safflower oil/kg or 65 g fish (menhaden) oil/kg plus 10 g linoleic acid/kg. After 6 weeks, six females per treatment were bred. Dams and pups continued on their respective diets through gestation, lactation, and after weaning. At age 21 weeks, the microarchitecture of the fourth lumbar vertebrae from 12 randomly selected pups from each treatment was determined by microcomputed tomography. Boron deprivation decreased bone volume fraction and increased trabecular separation and structural model index. Boron deprivation decreased trabecular thickness when the dietary oil was safflower. A three-point bending test for bone strength found that boron deprivation decreased the maximum force needed to break the femur. Feeding fish oil instead of safflower oil decreased connectivity density in vertebrae of boron-deficient but not in boron-adequate rats. Fish oil instead of safflower oil increased the maximum force to break and the bending moment of the femur, especially in rats fed adequate boron. The findings confirm that boron and fish oil are beneficial to cortical bone strength, and show that nutritional intakes of boron are beneficial for trabecular bone microarchitecture and influence the beneficial effects of fish oil on bone.

Boron (B) deprivation increases plasma homocysteine and decreases liver S‐adenosylmethionine (SAM) and S‐adenosylhomocysteine (SAH) in rats

The diverse effects of B deprivation suggest that B affects a biomolecule involved in a variety of biochemical reactions. An experiment was conducted to determine whether dietary B affects the liver concentration of SAM, a frequently used enzyme substrate, especially for methylation reactions that yield SAH. SAH is hydrolyzed to yield homocysteine (Hcy). Weanling male rats (15 per treatment) were fed a ground corn‐casein based diet (0.15 mg B/kg) containing sucrose and fructose to increase oxidative stress. Experimental variables were dietary supplements of 0 and 3 mg B/kg and fat sources (affect the response to B) of 75 g corn oil, 75 g canola oil, or 65 g fish oil plus 10 g linoleic acid/kg. When euthanized at age 18 wk, rats fed the B‐low diet were considered B‐deprived because they had decreased B concentrations in femur, tibia, and kidney. Decreased plasma C‐reactive protein indicated that fish oil decreased oxidative stress; the decrease was more noticeable in B‐deprived rats. Boron deprivation regardless of dietary oil decreased liver SAM and SAH, and increased plasma Hcy. Fish oil decreased liver SAM, which attenuated the SAM response to B. Femur, tibia and liver iron (bound by SAM) was decreased in B‐supplemented and fish oil‐fed rats. The findings suggest that B is bioactive through affecting the formation or utilization of SAM, and this effect is enhanced by oxidative stress. (Supported by USDA)

Boron Nutrition of Tobacco BY-2 Cells. V. Oxidative Damage is the Major Cause of Cell Death Induced by Boron Deprivation

Boron (B) is an essential micronutrient for vascular plants. However, it remains unclear how B deficiency leads to various metabolic disorders and cell death. To understand this mechanism, we analyzed the physiological changes in suspension-cultured tobacco (Nicotiana tabacum) BY-2 cells upon B deprivation. When 3-day-old cells were transferred to B-free medium, cell death was detectable as early as 12 h after treatment. The B-deprived cells accumulated more reactive oxygen species and lipid peroxides than control cells, and showed a slight but significant decrease in the cellular ascorbate pool. Supplementing the media with lipophilic antioxidants effectively suppressed the death of B-deprived cells, suggesting that the oxidative damage is the immediate and major cause of cell death under B deficiency. Dead cells in B-free culture exhibited a characteristic morphology with a shrunken cytoplasm, which is often seen in cells undergoing programmed cell death (PCD). However, they did not display other hallmarks of PCD such as internucleosomal DNA fragmentation, decreased ascorbate peroxidase expression and protection from death by cycloheximide. These results suggest that the death of tobacco cells induced by B deprivation is not likely to be a typical PCD.

A histomorphometric study of alveolar bone modelling and remodelling in mice fed a boron-deficient diet

Objective Emerging evidence indicates that boron (B) plays a role in bone formation and maintenance. Thus, a study was performed to determine whether dietary B-deficiency affects periodontal alveolar bone modelling and remodelling. Design Weanling Swiss mice ( n = 30) were divided into three groups: control diet (GI, 3 mg B/kg); B-deficient diet (GII, 0.07 mg B/kg); and pair-fed with GII (GIII). The animals were maintained on their respective diets for 9 weeks and then sacrificed. The guidelines of the NIH for the care and use of laboratory animals were observed. The mandibles were resected, fixed, decalcified in 10% EDTA and embedded in paraffin. Buccolingually oriented sections were obtained at the level of the mesial root of the first lower molar and stained with H–E. Histomorphometric studies were performed separately on the buccal and lingual sides of the periodontal alveolar bone. Percentages of osteoblast surfaces (ObSs), eroded surfaces (ESs), and quiescent surfaces (QSs) were determined. Results No statistically significant differences in food intake and body weight were observed between the groups. When compared with GI and GIII mice, GII mice (B-deficient) had 63% and 48% reductions in ObS and 58% and 73% increases in QS in buccal and lingual plates, respectively. ES were not affected by B nutriture. Conclusion The results are evidence that dietary boron deprivation in mice alters periodontal alveolar bone modelling and remodelling by inhibiting bone formation.