Oral and dental health vocabulary

From another article from the June 2016 issue of the magazine きょうの健康 .

  • 歯周病 ししゅうびょう  periodontal disease
  • 歯周病菌 ししゅうびょうきん  periodontal disease bacteria
  • 歯ぐき はぐき  gums
  • 歯肉 しにく  gingiva
  • 奥歯 おくば  molars; back teeth
  • ネバつく  to be sticky; to be stringy; to be glutinous
  • グラつく  to be unsteady
  • 歯槽骨 しそうこつ  alveolar process
  • 歯肉炎 しにくえん  gingivitis
  • 歯周炎 ししゅうえん  periodontitis
  • 境目 さかいめ  border; boundary line; crisis
  • 歯垢 しこう  dental plaque
  • プラーク  plaque
  • 腫れる はれる  to swell (from inflammation); to become swollen
  • 歯周ポケット ししゅうぽけっと  periodontal pocket
  • 破骨細胞  はこつさいぼう  osteoclast
  • 活溌 かっぱつ  vigour; active; lively
  • 目安 めやす  criterion; standard; rough estimate; approximation
  • 歯石 しせき  dental calculus; tartar (of the teeth)
  • むずがゆい creepy; itchy
  • 口臭 こうしゅう  bad breath; halitosis
  • しみる  to sting (wound or sensitive area, etc.)
  • 露出 ろしゅつ  exposure; disclosure
[In] the male, estrogen (not androgen) derived from direct testicular secretion (approximately 20%) and from extragonadal aromatization of testosterone and androstenedione (approximately 80%), is the critical sex hormone in the pubertal growth spurt, skeletal maturation, accrual of peak bone mass, and the maintenance of bone mass in the adult. Estrogen stimulates chondrogenesis in the epiphyseal growth plate increasing pubertal linear growth. At puberty, estrogen promotes skeletal maturation and the gradual, progressive closure of the epiphyseal growth plate, possibly as a consequence of both estrogen-induced vascular and osteoblastic invasion and the termination of chondrogenesis. In addition, during puberty and into the third decade, estrogen has an anabolic effect on the osteoblast and an apoptotic effect on the osteoclast, increasing bone mineral acquisition in axial and appendicular bone. In the adult, estrogen is important in maintaining the constancy of bone mass through its effects on remodeling and bone turnover.
—  Estrogen, Bone, Growth and Sex: A Sea Change in Conventional Wisdom, MM Grumbach, (2000) Journal of Pediatric Endocrinology and Metabolism 13 (Supplement), 1439-1456

Lack of estrogen causes a decrease in osteoprotegerin.

Osteoprotegerin (OPG), also known as osteoclastogenesis inhibitory factor (OCIF), is a cytokine and a member of the tumor necrosis factor (TNF) receptor superfamily.

Osteoprotegerin inhibits the differentiation of macrophages into osteoclasts and also regulates the resorption of osteoclasts.
Mnemonic: Osteoprotegerin protects bone (By preventing macrophage differentiation into osteoclasts.)

Osteoprotegerin, a RANK homolog, works by binding to the RANK-ligand on Osteoblast/Stromal cells, thus blocking the RANK-RANK lingand interaction between Osteoblast/Stromal cells and Osteoclast precursors. This has the effect of inhibiting the differentiation of the Osteoclast Precursor into a mature Osteoclast.
Mnemonic: Osteoprotegerin ranks high in protecting bones.

So, estrogen kinda inhibits the osteoclasts which causes osteoporosis is the moral of the story?


Extra: Recombinant human osteoprotegerin specifically acts on bone, increasing bone mineral density and bone volume. Osteoprotegerin has been used experimentally to decrease bone resorption in women with postmenopausal osteoporosis and in patients with lytic bone metastases.

That’s all!


Boney remodeling is a chronic process of replacement with minimal change in the gross shape of the bone structure. Osteoblasts and osteoclasts together are referred to as bone remodeling units. They work in concert together, coordinated via paracrine signaling by the osteoblasts. The constant remodeling allows for calcium homeostasis and the repair of microscopic daily stressors. The histology slide show demonstrates bone remodeling with osteoclasts resorbing one side of a bony trabecula and osteoblasts depositing new bone on the other side.

Osteoclasts (shown) resorb bone over a period of weeks, and are especially active during periods of rapid remodeling (eg, after menopause). Because osteoclasts work faster than osteoblasts, the rate of bone loss may outpace the rate of bone production. During these periods, the newly produced bone is at increased risk for fracture because it is less densely mineralized, collagen has not matured, and resorption sites are temporarily unfilled.