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Alveolar Bone: and It's Associated Pathologies
Alveolar Bone: and It's Associated Pathologies
Inorganic matrix
Alveolar bone is 67% inorganic material by weight. The inorganic
material is composed mainly of the minerals calcium and
phosphate. The mineral content is mostly in the form of calcium
hydroxyapatite crystals.
Organic matrix
The remaining alveolar bone is organic material (33%). The
organic material consists of collagen and non-collagenous
material. The cellular component of bone consists of
osteoblasts, osteocytes and osteoclasts.
• Osteoblasts are usually cuboidal and slightly elongated in shape.
They synthesise both collagenous ad non-collagenous bone
proteins. These cells have a high level of alkaline phosphatase on
the outer surface of their plasma membrane. The functions of
osteoblasts are bone formation by synthesising the organic matrix
of bone, cell to cell communication and maintenance of bone
matrix.
• Osteocytes are modified osteoblasts which become entrapped in
lacunae during the secretion of bone matrix. The osteocytes have
processes called canaliculi that radiate from the lacunae. These
canaliculi bring oxygen and nutrients to the osteocytes through
blood and remove metabolic waste products.
• Osteoclasts are multinucleated giant cells. They are found in
Howship’s lacunae.
Alveolar Bone Loss
Bone is lost through the process of resorption which involves
osteoclasts breaking down the hard tissue of bone. A key
indication of resorption is when scalloped erosion occurs. This is
also known as Howship’s lacuna. The resorption phase lasts as
long as the lifespan of the osteoclast which is around 8 to 10
days. After this resorption phase, the osteoclast can continue
resorbing surfaces in another cycle or carry out apoptosis. A
repair phase follows the resorption phase which lasts over 3
months. In patients with periodontal disease, inflammation lasts
longer and during the repair phase, resorption may override any
bone formation. This results in a net loss of alveolar bone.
Alveolar bone loss is closely associated with periodontal disease.
Periodontal disease is the inflammation of the gums. Studies in
osteoimmunology have proposed 2 models for alveolar bone
loss. One model states that inflammation is triggered by a
periodontal pathogen which activates the acquired immune
system to inhibit bone coupling by limiting new bone formation
after resorption. Another model states that cytokinesis may
inhibit the differentiation of osteoblasts from their precursors,
therefore limiting bone formation. This results in a net loss of
alveolar bone.
Alveolar Bone Loss In Osteoporosis
Bone Remodeling
The maintenance of bone is achieved by a fine balance between
bone formation and bone resorption. The differentiation and
activation of osteoclasts are tightly regulated by osteoblasts.
Osteoblasts express at least two cytokines essential for
osteoclast differentiation; they are receptor activator of NF-
kappaB ligand (RANKL) and macrophage colony stimulating
factor (M-CSF). On the other hand, differentiation of osteoblasts
is regulated by the transcription factors Runx2 and Osterix. The
recent progress of genetic experiments has revealed that
osteoclasts also regulate the differentiation of osteblasts in vivo.
This review describes the recent studies on the communication
between osteoblasts and osteoclasts in the process of bone
remodeling.
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