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Mouse Cellular Cementum is Highly Dependent on Growth Hormone Status

¹ School of Dentistry,
² School of Biomedical Sciences, and
³ Institute for Molecular Bioscience, University of Queensland, St. Lucia, Brisbane, Queensland 4072, Australia;
⁴ Edison Biotechnology Institute; and
⁵ Department of Biomedical Sciences, College of Osteopathic Medicine, Ohio University, Athens, OH, USA;

^* corresponding author, j.smid{at}mailbox.uq.edu.au

	ABSTRACT

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Cementum is known to be growth-hormone (GH)-responsive, but to what extent is unclear. This study examines the effects of extremes of GH status on cementogenesis in three lines of genetically modified mice; GH excess (giant), GH antagonist excess (dwarf), and GH receptor-deleted (GHR-KO) (dwarf). Age-matched mandibular molar tissues were processed for light microscope histology. Digital images of sections of first molar teeth were captured for morphometric analysis of lingual root cementum. Cross-sectional area of the cellular cementum was a sensitive guide to GH status, being reduced nearly 10-fold in GHR-KO mice, three-fold in GH antagonist mice, and increased almost two-fold in giant mice (p < 0.001). Cellular cementum length was similarly influenced by GH status, but to a lesser extent. Acellular cementum was generally unaffected. This study reveals cellular cementum to be a highly responsive GH target tissue, which may have therapeutic applications in assisting regeneration of the periodontium.

KEY WORDS: cementum • growth hormone • GH transgenic mice • GH receptor knockout mice

	INTRODUCTION

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Cementum is the thin layer of mineralized tissue that attaches the periodontal ligament (PDL) to the tooth root surface. Its composition differs markedly from that of enamel and dentin, and is similar to that of bone (Saygin et al., 2000). Unlike bone, cementum does not undergo continuous remodeling, and continues to grow in thickness throughout life (Bosshardt and Selvig, 1997). Cementum is formed as primary acellular cementum and secondary cellular cementum (Cho and Garant, 2000). Acellular cementum, found on the cervical third and middle portions of the root, attaches the principle fibers of the PDL (Cho and Garant, 2000). Cellular cementum is found on the apical third of the root and surrounds the apical foramen (Cho and Garant, 2000).

There is evidence that growth hormone (GH) influences cementogenesis. Rats given daily injections of GH for many months develop molar tooth hypercementosis (Becks et al., 1948). Humans with pituitary gigantism display premature tooth eruption and hypercementosis (Schour and Massler, 1943), whereas those suffering pituitary dwarfism or GH insensitivity, Laron syndrome (LS), display hypodontia and delayed tooth eruption (Sarnat et al., 1988). There are no clinical observations on the cementum of these patients. A reduction in cellular cementogenesis is found in the molar teeth of hypophysectomized rats (Clayden et al., 1994), and this is ameliorated by injections of GH (Clayden et al., 1994; Li et al., 2001). Cementoblasts within cellular cementum display strong reactivity for GH receptor antibody, whereas cementocytes and cementoblasts associated with acellular cementum are negative or react poorly with GH receptor antibody (Zhang et al., 1992). Bone morphogenetic proteins (BMPs) -2 and -4 strongly up-regulate the expression of mineralization genes in cementoblasts (Saygin et al., 2000). In cementoblasts, GH increases the expression of BMP-2 and -4 and bone-related proteins, osteocalcin (OC) and osteopontin (OP) (Li et al., 2001). GH also up-regulates the expression of OC and OP in cellular cementoblasts, but not in cells contributing to acellular cementum (Li et al., 2001).

Several lines of mice have been genetically engineered to produce alterations in the growth hormone (GH) axis (Kopchick et al., 1999). These include the classic giant mouse carrying a bovine GH (bGH) transgene driven by the mouse metallothionein-I (MT) promoter (MT-bGH), leading to excess GH secretion (Kopchick et al., 1999). Another line of bGH transgenic mice carries a (bGH-G119K) transgene in which lysine 119 is substituted for glycine 119 (Chen et al., 1991b). This is a GH antagonist, so these mice are dwarfs (Chen et al., 1991a). In a third line, the GH receptor gene is disrupted or knocked out (GHR-KO), resulting in pronounced dwarfism (Zhou et al., 1997). These three mouse lines represent models for human pituitary gigantism, pituitary dwarfism, and GH insensitivity dwarfism, respectively. Notwithstanding that the first GH transgenic mouse was developed two decades ago, there are no published studies of the dentition in GH transgenic animals. Accordingly, this study compares the amount of cementum in the lower first molar teeth in these three mouse models of altered GH status (MT-bGH, bGH-G119K, and GHR-KO), using morphometric analysis.

	MATERIALS & METHODS

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Mouse Genotypes
MT-bGH mice with a B6/SJL background were crossed with female wild-type (Wt) animals of the same background, to yield giant bGH-expressing mice (GHXs phenotype) with the transgene acting in a dominant manner. Male bGH-G119K mice (C57BL/6J background) were mated with female Wt C57BL/6J mice to produce litters (GHAnt phenotype) with the dominant transgene. To produce GHR-KO mouse litters, we crossed 129OLA/BalbC male mice heterozygous (Het) for the GHR-KO mutation with Het female 129OLA/BalbC mice. Soon after birth, mouse pups were genotyped by polymerase chain-reaction (PCR) with tail DNA. All mice were maintained with the same dietary and lighting regimens and in specific pathogen-free conditions.

To study the GH excess condition, we used matched Wt and GHXs mice, with 6 males and 4 females for each phenotype. For the GH antagonist condition, matched Wt and GHAnt mice were used, with 4 males and 6 females for each phenotype. The GHR-KO consisted of Wt, Het, and Homozygous KO groups, and compared 5 males and 5 females for each phenotype (Table). All mice were killed at 45 days after birth. Prior to death, the mice were weighed, and the nose-rump body length was measured.

Tissue Preparation
Mouse heads were bisected sagittally and fixed in 4.0% paraformaldehyde in phosphate-buffered saline (PBS) for 24 hrs at 4°C. The left half-heads were then washed twice in PBS and demineralized (confirmed by radiography) in a neutral EDTA solution. Mandibular molar teeth blocks were then dissected from the left half-heads, trimmed, and embedded in paraffin wax. The molar blocks were embedded on their lingual surfaces. Five-µm-thick serial longitudinal sections with a mesio-distal aspect were cut with a microtome, with the use of ice-cold paraffin blocks. All sections were mounted on aminopropyltriethoxysilane (APES)-coated glass slides. Sections were then stained with hematoxylin and eosin.

Morphometric Analysis
Stained sections were selected for morphometric analysis of the cementum of the first mandibular molar tooth. Ideal sections for analysis included both first molar tooth roots in longitudinal section (see Fig. 1A). However, even with a stringent alignment of the tissue block, small variations in relative directions of the roots of the first molar tooth meant that the complete section of only one root was generally visible in a given section. Two section selection criteria were used for morphometric analysis: (1) a continuous pulp chamber lumen from the apical foramen to the pulp cavity of the tooth crown, and (2) a cementum layer, continuously visible from the gingival sulcus to the apical foramen. Either one (ideal) or two representative sections (one mesial and one distal root) were taken for morphometric analysis from each molar tooth block.

View larger version (47K): [in this window] [in a new window]   Figure 1. Photomicrographs of longitudinal sections of mandibular first molar teeth, stained with hematoxylin and eosin, from three lines of mice genetically engineered to produce alterations in the growth hormone (GH) axis. Magnification (19x) is the same for all images. (A) A section displaying a complete cross-section of both mesial (Mesial) and dorsal (Dorsal) roots. Black lines identify radicular cementum: line * to # is acellular cementum; line to * is cellular cementum; area C is apical cellular cementum. (B,C) Sections of mesial tooth roots of littermate mice of a GH excess (giant) mice line. (B) Wild-type (Wt) phenotype. (C) Giant (GHXs) phenotype. (D,E) Sections of mesial tooth roots of littermate mice of a GH antagonist excess (dwarf) mice line. (D) Wild-type (Wt) phenotype. (E) Dwarf (GHAnt) phenotype. (F-H) Sections of mesial tooth roots of littermate mice of a GH receptor-deleted (GHR-KO) (dwarf) mice line. (F) Wild-type (Wt) phenotype. (G) Heterozygous (Het) for the GHR-KO mutation. (H) Dwarf (KO) phenotype.

Cellular cementum cross-sectional areas (C, Fig. 1A), cellular cementum lengths ( to *, Fig. 1A), and acellular cementum lengths (* to #, Fig. 1A) were measured for both mesial and distal first mandibular molar tooth roots for each mouse. Measurements were made, on screen images of the selected stained sections, with the use of a morphometric analysis program (Scion Image, Scion Corporation, Frederick, MD, USA). The cementum morphometric data were analyzed statistically (ANOVA) with a statistics program (Minitab12, Minitab Inc., State College, PA, USA).

	RESULTS

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The Table illustrates the nearly three-fold range in body weight which can be achieved by genetic modification of the GH axis. Body length follows the same pattern, although the differences are not as extreme (Table).

Sections of molar teeth from each group of mice clearly demonstrated qualitative differences in the amount of cementum present on roots of the various teeth (Fig. 1).

Morphometric analysis revealed that the area of cellular cementum for the lower first molar mesial root (combined mesial areas labeled "C" in Fig. 1A) of Wt mice is approximately 0.1 mm² (Fig. 2); however, this area in bGH-G119K (C57BL/6J strain) Wt mice was slightly larger (Fig. 2). The presence of the bGH transgene markedly increased the area of cellular cementum, for both the mesial and distal roots (Fig. 2A). Conversely, the GH antagonist transgene significantly decreased cellular cemental area on both molar roots (Fig. 2B). In the absence of a functioning GH receptor (GHR-KO), the decrease in cellular cementum area was dramatic, for both mesial and distal roots (Fig. 2C).

View larger version (13K): [in this window] [in a new window]   Figure 2. Cross-sectional areas of mouse mandibular first molar tooth cellular cementum. These measurements are for mesial and distal lingual roots of three lines of mice genetically engineered to produce alterations in the growth hormone (GH) axis. (A) Bovine GH (MT-bGH) mice, with either giant mutant (GHXs) or wild-type (Wt) phenotype (both roots, n = 10). (B) Antagonist MT-bGH (bGH-G119K) mice, with either dwarf mutant (GHAnt) or Wt phenotype (both roots, n = 10). (C) GH receptor-deleted (GHR-KO) mice have three animal groups: Wt mice (mesial roots, n = 10; distal roots, n = 8); heterozygous (Het) mice (mesial roots, n = 8; distal roots, n = 9), and homozygous (KO) mice (mesial roots, n = 8; distal roots, n = 7). The areas were quantified by morphometric analysis of images of stained sections of mouse molar teeth by comparison with images of a 2.00-mm scalar. All mice were 45 days old. All areas are presented as mean ± 2SEM in mm2. ***p < 0.001, one-way ANOVA.

View larger version (17K): [in this window] [in a new window]   Figure 3. Lengths of mouse mandibular first molar tooth cementum. These measurements are of mesial and distal lingual roots of three lines of mice genetically engineered to produce alterations in the growth hormone (GH) axis. Data are of cellular cementum lengths, acellular cementum lengths, and total cementum lengths (cellular+acellular). (A) Cementum lengths of bovine GH (MT-bGH) mice, of either giant mutant (GHXs) or wild-type (Wt) phenotype (both roots, n = 10). (B) Cementum lengths of antagonist MT-bGH (bGH-G119K) mice, of either dwarf mutant (GHAnt) or Wt phenotype (both roots, n = 10). (C) Cementum lengths of GH receptor-deleted (GHR-KO) mice, either Wt mice (mesial roots, n = 10; distal roots, n = 8), heterozygous (Het) mice (mesial roots, n = 8; distal roots, n = 9), or homozygous dwarf (KO) mice (mesial roots, n = 8; distal roots, n = 7). The lengths were quantified by morphometric analysis of images of stained sections of mouse molar teeth by comparison with images of a 2.00-mm scalar. All mice were 45 days old. All lengths are presented as mean ± 2SEM in mm2. *p < 0.05; **p < 0.01; ***p < 0.001; one-way ANOVA

	DISCUSSION

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Our earlier demonstration of an increase in cementum formation following human GH administration (Clayden et al., 1994) was compromised by the absence of other pituitary hormones, such as thyroid-stimulating hormone and gonadotrophins, in hypophysectomized rats. The use of human GH, which also activates the prolactin receptor in rodents, also compromises interpretation of the data. In this study we have used mice with genetically defined alterations in their GH axis to obtain unequivocal data concerning the influence of GH status on molar cementum. Cellular cementum is a tissue highly responsive to GH status. Giant GHXs transgenic mice show an increase of approximately 80% in cellular cementum area in both mesial and distal roots. In contrast, body wt increases in males (26% increase) and females (57%) and body length increases (7% increase, males; 13% increase, females) are relatively modest (Table). The increase (about 30%) reported for cross-sectional area of cortical bone in femurs of MT-bGH mice (Eckstein et al., 2002) is also considerably less than the increases in cemental area observed here. GH antagonist mice show over 60% decrease in cellular cementum areas on both mesial and distal roots, whereas decreases in body wt (43%, males; 34%, females) and body length (21%, males; 16%, females) are more modest. Reductions in organ size in bGH-G119K mice are reported to be less than 50% (Knapp et al., 1994). In the GHR-KO mice, first molar teeth show virtually no cellular cementum, and morphometric analysis showed a > 90% decrease in area. Other tissues in GHR-KO dwarf mice show up to a 65% decrease in weight (Zhou et al., 1997). This reflects the decreases in body wt (55%, males; 46%, females) and in body length (33%, males; 34%, females).

Growth hormone appears to affect cellular cementum to a greater degree than acellular cementum (Fig. 3). There are marked differences between acellular and cellular cementum. Immunohistochemical studies of rat molar tissues show that acellular cementum is strongly immunoreactive for OP (Bronckers et al., 1994; Hashimoto et al., 2001), but it is weakly immunoreactive or negative for OC (Bronckers et al., 1994; Hashimoto et al., 2001; Li et al., 2001). In contrast, cellular cementum is strongly immunoreactive for OC (Li et al., 2001; Sasano et al., 2001), but only moderately so for OP (Hashimoto et al., 2001; Li et al., 2001). A feature of the disease cleidocranial dysostosis (CCD) is teeth which lack of cellular cementum, but have essentially normal acellular cementum (Fukuta et al., 2001). CCD is a genetic disease which arises from mutations in core-binding factor-1 (Cbfa1) gene (Ducy, 2000). This transcription factor, Cbfa1, normally activates the expression of several genes, including the OC gene (Ducy, 2000).

One reason for the unusual sensitivity of cementum to GH may be that cementum is deposited on mouse molar roots at the time of maximum GH effect, that is, after 20 days of post-natal age (Cohn, 1957; Lezot et al., 2000). Based on our previous ultrastructural study (Clayden et al., 1994), GH increases both cementoblast number and secretory activity. This is a particularly strong response, since only 10 days of GH treatment are sufficient to restore cementum to control levels in hypophysectomized rats (Clayden et al., 1994). Cementoblasts display GH receptor immunoreactivity, and cementoblasts which are most active in matrix formation possess the highest GHR immunoreactivity (Zhang et al., 1992). This observation indicates a direct role for GH in promoting cementum formation, but does not exclude the intermediacy of IGF-1 (either endocrine or paracrine in origin). Indeed, we have also showed that immunoreactive IGF-1 receptors are present on cementoblasts (Ong et al., 2001).

The increased number of cementoblasts observed after hGH treatment of hypophysectomized rats suggests an effect of GH on differentiation to cementoblasts (Clayden et al., 1994). This may involve the intermediacy of BMPs-2 and -4, since we have showed that GH is able to induce both of these odontogenic BMPs in periodontal ligament fibroblasts in vitro (Li et al., 1998) and in the periodontium of GH-deficient rats (Li et al., 2001). BMP-2 was recently reported to induce dental follicle cells to differentiate toward a cementoblast phenotype in vitro (Zhao et al., 2002). The increased number of cementoblasts may also be the result of GH-induced proliferation of stem cells in the dental follicle. GH treatment of GH-deficient dwarf rats causes a marked increase in proliferation of odontogenic mesenchyme within the lingual aspect of the rat dental organ, where cementoblast precursors occur (Young et al., 1993). The combined action of GH to promote precursor proliferation and differentiation, together with enhanced matrix secretion by mature cementoblasts, would account for the striking action of GH in promoting cementogenesis.

	ACKNOWLEDGMENTS

 
The assistance of Trish Hitchcock and Kym Kelly-Taylor (Animal House, School of Biomedical Sciences, University of Queensland) is acknowledged. Portions of this work were supported by a National Health and Medical Research Council of Australia Project Grant to MJW, and by an Australian Dental Research Foundation grant to WGY and JRS. JJK is supported, in part, by the state of Ohio’s Eminent Scholars’ Program that includes a gift by Milton and Lawrence Goll.

Received April 16, 2003; Last revision September 17, 2003; Accepted September 23, 2003

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This Article Abstract Figures Only Full Text (PDF) Services Similar articles in this journal Similar articles in ISI Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via ISI Web of Science (3) Citing Articles via Google Scholar Google Scholar Articles by Smid, J.R. Articles by Waters, M.J. Search for Related Content PubMed PubMed Citation Articles by Smid, J.R. Articles by Waters, M.J.